nitrogen-dioxide and Body-Weight

Middle East Respiratory Syndrome (MERS) is a novel respiratory illness firstly reported in Saudi Arabia in 2012. It is caused by a new corona virus, called MERS corona virus (MERS-CoV). Most people who have MERS-CoV infection developed severe acute respiratory illness.. This work is done to determine the clinical characteristics and the outcome of intensive care unit (ICU) admitted patients with confirmed MERS-CoV infection.. This study included 32 laboratory confirmed MERS corona virus infected patients who were admitted into ICU. It included 20 (62.50%) males and 12 (37.50%) females. The mean age was 43.99 ± 13.03 years. Diagnosis was done by real-time reverse transcription polymerase chain reaction (rRT-PCR) test for corona virus on throat swab, sputum, tracheal aspirate, or bronchoalveolar lavage specimens. Clinical characteristics, co-morbidities and outcome were reported for all subjects.. Most MERS corona patients present with fever, cough, dyspnea, sore throat, runny nose and sputum. The presence of abdominal symptoms may indicate bad prognosis. Prolonged duration of symptoms before patients' hospitalization, prolonged duration of mechanical ventilation and hospital stay, bilateral radiological pulmonary infiltrates, and hypoxemic respiratory failure were found to be strong predictors of mortality in such patients. Also, old age, current smoking, smoking severity, presence of associated co-morbidities like obesity, diabetes mellitus, chronic heart diseases, COPD, malignancy, renal failure, renal transplantation and liver cirrhosis are associated with a poor outcome of ICU admitted MERS corona virus infected patients.. Plasma HO-1, ferritin, p21, and NQO1 were all elevated at baseline in CKD participants. Plasma HO-1 and urine NQO1 levels each inversely correlated with eGFR (. SnPP can be safely administered and, after its injection, the resulting changes in plasma HO-1, NQO1, ferritin, and p21 concentrations can provide information as to antioxidant gene responsiveness/reserves in subjects with and without kidney disease.. A Study with RBT-1, in Healthy Volunteers and Subjects with Stage 3-4 Chronic Kidney Disease, NCT0363002 and NCT03893799.. HFNC did not significantly modify work of breathing in healthy subjects. However, a significant reduction in the minute volume was achieved, capillary [Formula: see text] remaining constant, which suggests a reduction in dead-space ventilation with flows > 20 L/min. (ClinicalTrials.gov registration NCT02495675).. 3 组患者手术时间、术中显性失血量及术后 1 周血红蛋白下降量比较差异均无统计学意义（. 对于肥胖和超重的膝关节单间室骨关节炎患者，采用 UKA 术后可获满意短中期疗效，远期疗效尚需进一步随访观察。.. Decreased muscle strength was identified at both time points in patients with hEDS/HSD. The evolution of most muscle strength parameters over time did not significantly differ between groups. Future studies should focus on the effectiveness of different types of muscle training strategies in hEDS/HSD patients.. These findings support previous adverse findings of e-cigarette exposure on neurodevelopment in a mouse model and provide substantial evidence of persistent adverse behavioral and neuroimmunological consequences to adult offspring following maternal e-cigarette exposure during pregnancy. https://doi.org/10.1289/EHP6067.. This RCT directly compares a neoadjuvant chemotherapy regimen with a standard CROSS regimen in terms of overall survival for patients with locally advanced ESCC. The results of this RCT will provide an answer for the controversy regarding the survival benefits between the two treatment strategies.. NCT04138212, date of registration: October 24, 2019.. Results of current investigation indicated that milk type and post fermentation cooling patterns had a pronounced effect on antioxidant characteristics, fatty acid profile, lipid oxidation and textural characteristics of yoghurt. Buffalo milk based yoghurt had more fat, protein, higher antioxidant capacity and vitamin content. Antioxidant and sensory characteristics of T. If milk is exposed to excessive amounts of light, Vitamins B. The two concentration of ZnO nanoparticles in the ambient air produced two different outcomes. The lower concentration resulted in significant increases in Zn content of the liver while the higher concentration significantly increased Zn in the lungs (p < 0.05). Additionally, at the lower concentration, Zn content was found to be lower in brain tissue (p < 0.05). Using TEM/EDX we detected ZnO nanoparticles inside the cells in the lungs, kidney and liver. Inhaling ZnO NP at the higher concentration increased the levels of mRNA of the following genes in the lungs: Mt2 (2.56 fold), Slc30a1 (1.52 fold) and Slc30a5 (2.34 fold). At the lower ZnO nanoparticle concentration, only Slc30a7 mRNA levels in the lungs were up (1.74 fold). Thus the two air concentrations of ZnO nanoparticles produced distinct effects on the expression of the Zn-homeostasis related genes.. Until adverse health effects of ZnO nanoparticles deposited in organs such as lungs are further investigated and/or ruled out, the exposure to ZnO nanoparticles in aerosols should be avoided or minimised.

Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor Proteins, Signal Transducing; Adenine; Adenocarcinoma; Adipogenesis; Administration, Cutaneous; Administration, Ophthalmic; Adolescent; Adsorption; Adult; Aeromonas hydrophila; Aerosols; Aged; Aged, 80 and over; Aging; Agriculture; Air Pollutants; Air Pollution; Airway Remodeling; Alanine Transaminase; Albuminuria; Aldehyde Dehydrogenase 1 Family; Algorithms; AlkB Homolog 2, Alpha-Ketoglutarate-Dependent Dioxygenase; Alzheimer Disease; Amino Acid Sequence; Ammonia; Ammonium Compounds; Anaerobiosis; Anesthetics, Dissociative; Anesthetics, Inhalation; Animals; Anti-Bacterial Agents; Anti-HIV Agents; Anti-Infective Agents; Anti-Inflammatory Agents; Antibiotics, Antineoplastic; Antibodies, Antineutrophil Cytoplasmic; Antibodies, Monoclonal, Humanized; Antifungal Agents; Antigens, Bacterial; Antigens, CD; Antigens, Differentiation, Myelomonocytic; Antimetabolites, Antineoplastic; Antineoplastic Agents; Antineoplastic Combined Chemotherapy Protocols; Antioxidants; Antitubercular Agents; Antiviral Agents; Apolipoproteins E; Apoptosis; Arabidopsis; Arabidopsis Proteins; Arsenic; Arthritis, Rheumatoid; Asthma; Atherosclerosis; ATP-Dependent Proteases; Attitude of Health Personnel; Australia; Austria; Autophagy; Axitinib; Bacteria; Bacterial Outer Membrane Proteins; Bacterial Proteins; Bacterial Toxins; Bacterial Typing Techniques; Bariatric Surgery; Base Composition; Bayes Theorem; Benzoxazoles; Benzylamines; beta Catenin; Betacoronavirus; Betula; Binding Sites; Biological Availability; Biological Oxygen Demand Analysis; Biomarkers; Biomarkers, Tumor; Biopsy; Bioreactors; Biosensing Techniques; Birth Weight; Blindness; Blood Chemical Analysis; Blood Gas Analysis; Blood Glucose; Blood Pressure; Blood Pressure Monitoring, Ambulatory; Blood-Brain Barrier; Blotting, Western; Body Mass Index; Body Weight; Bone and Bones; Bone Density; Bone Resorption; Borates; Brain; Brain Infarction; Brain Injuries, Traumatic; Brain Neoplasms; Breakfast; Breast Milk Expression; Breast Neoplasms; Bronchi; Bronchoalveolar Lavage Fluid; Buffaloes; Cadherins; Calcification, Physiologic; Calcium Compounds; Calcium, Dietary; Cannula; Caprolactam; Carbon; Carbon Dioxide; Carboplatin; Carcinogenesis; Carcinoma, Ductal; Carcinoma, Ehrlich Tumor; Carcinoma, Hepatocellular; Carcinoma, Non-Small-Cell Lung; Carcinoma, Pancreatic Ductal; Carcinoma, Renal Cell; Cardiovascular Diseases; Carps; Carrageenan; Case-Control Studies; Catalysis; Catalytic Domain; Cattle; CD8-Positive T-Lymphocytes; Cell Adhesion; Cell Cycle Proteins; Cell Death; Cell Differentiation; Cell Line; Cell Line, Tumor; Cell Movement; Cell Nucleus; Cell Phone Use; Cell Proliferation; Cell Survival; Cell Transformation, Neoplastic; Cell Transformation, Viral; Cells, Cultured; Cellulose; Chemical Phenomena; Chemoradiotherapy; Child; Child Development; Child, Preschool; China; Chitosan; Chlorocebus aethiops; Cholecalciferol; Chromatography, Liquid; Circadian Clocks; Circadian Rhythm; Circular Dichroism; Cisplatin; Citric Acid; Clinical Competence; Clinical Laboratory Techniques; Clinical Trials, Phase I as Topic; Clinical Trials, Phase II as Topic; Clostridioides difficile; Clostridium Infections; Coculture Techniques; Cohort Studies; Cold Temperature; Colitis; Collagen Type I; Collagen Type I, alpha 1 Chain; Collagen Type XI; Color; Connective Tissue Diseases; Copper; Coronary Angiography; Coronavirus 3C Proteases; Coronavirus Infections; Cost of Illness; Counselors; COVID-19; COVID-19 Testing; Creatine Kinase; Creatinine; Cross-Over Studies; Cross-Sectional Studies; Cryoelectron Microscopy; Cryosurgery; Crystallography, X-Ray; Cues; Cultural Competency; Cultural Diversity; Curriculum; Cyclic AMP Response Element-Binding Protein; Cyclin-Dependent Kinase Inhibitor p21; Cycloparaffins; Cysteine Endopeptidases; Cytokines; Cytoplasm; Cytoprotection; Databases, Factual; Denitrification; Deoxycytidine; Diabetes Complications; Diabetes Mellitus; Diabetes Mellitus, Experimental; Diabetes Mellitus, Type 1; Diabetes Mellitus, Type 2; Diagnosis, Differential; Diatoms; Diet; Diet, High-Fat; Dietary Exposure; Diffusion Magnetic Resonance Imaging; Diketopiperazines; Dipeptidyl Peptidase 4; Dipeptidyl-Peptidase IV Inhibitors; Disease Models, Animal; Disease Progression; Disease-Free Survival; DNA; DNA Damage; DNA Glycosylases; DNA Repair; DNA-Binding Proteins; DNA, Bacterial; DNA, Viral; Docetaxel; Dose Fractionation, Radiation; Dose-Response Relationship, Drug; Down-Regulation; Doxorubicin; Drosophila; Drosophila melanogaster; Drug Carriers; Drug Delivery Systems; Drug Liberation; Drug Repositioning; Drug Resistance, Bacterial; Drug Resistance, Multiple, Bacterial; Drug Resistance, Neoplasm; Drug Screening Assays, Antitumor; Drug Synergism; Drug Therapy, Combination; Edema; Edible Grain; Education, Graduate; Education, Medical, Graduate; Education, Pharmacy; Ehlers-Danlos Syndrome; Electron Transport Complex III; Electron Transport Complex IV; Electronic Nicotine Delivery Systems; Emergency Service, Hospital; Empathy; Emulsions; Endothelial Cells; Endurance Training; Energy Intake; Enterovirus A, Human; Environment; Environmental Monitoring; Enzyme Assays; Enzyme Inhibitors; Epithelial Cells; Epithelial-Mesenchymal Transition; Epoxide Hydrolases; Epoxy Compounds; Erythrocyte Count; Erythrocytes; Escherichia coli; Escherichia coli Infections; Escherichia coli Proteins; Esophageal Neoplasms; Esophageal Squamous Cell Carcinoma; Esophagectomy; Estrogens; Etanercept; Ethiopia; Ethnicity; Ethylenes; Exanthema; Exercise; Exercise Test; Exercise Tolerance; Extracellular Matrix; Extracorporeal Membrane Oxygenation; Eye Infections, Fungal; False Negative Reactions; Fatty Acids; Fecal Microbiota Transplantation; Feces; Female; Femur Neck; Fermentation; Ferritins; Fetal Development; Fibroblast Growth Factor-23; Fibroblast Growth Factors; Fibroblasts; Fibroins; Fish Proteins; Flavanones; Flavonoids; Focus Groups; Follow-Up Studies; Food Handling; Food Supply; Food, Formulated; Forced Expiratory Volume; Forests; Fractures, Bone; Fruit and Vegetable Juices; Fusobacteria; G1 Phase Cell Cycle Checkpoints; G2 Phase Cell Cycle Checkpoints; Gamma Rays; Gastrectomy; Gastrointestinal Microbiome; Gastrointestinal Stromal Tumors; Gefitinib; Gels; Gemcitabine; Gene Amplification; Gene Expression; Gene Expression Regulation; Gene Expression Regulation, Bacterial; Gene Expression Regulation, Neoplastic; Gene Expression Regulation, Plant; Gene Knockdown Techniques; Gene-Environment Interaction; Genotype; Germany; Glioma; Glomerular Filtration Rate; Glucagon; Glucocorticoids; Glycemic Control; Glycerol; Glycogen Synthase Kinase 3 beta; Glycolipids; Glycolysis; Goblet Cells; Gram-Negative Bacterial Infections; Granulocyte Colony-Stimulating Factor; Graphite; Greenhouse Effect; Guanidines; Haemophilus influenzae; HCT116 Cells; Health Knowledge, Attitudes, Practice; Health Personnel; Health Services Accessibility; Health Services Needs and Demand; Health Status Disparities; Healthy Volunteers; Heart Failure; Heart Rate; Heart Transplantation; Heart-Assist Devices; HEK293 Cells; Heme; Heme Oxygenase-1; Hemolysis; Hemorrhage; Hepatitis B; Hepatitis B e Antigens; Hepatitis B Surface Antigens; Hepatitis B virus; Hepatitis B, Chronic; Hepatocytes; Hexoses; High-Throughput Nucleotide Sequencing; Hippo Signaling Pathway; Histamine; Histamine Agonists; Histidine; Histone Deacetylase 2; HIV Infections; HIV Reverse Transcriptase; HIV-1; Homebound Persons; Homeodomain Proteins; Homosexuality, Male; Hospice and Palliative Care Nursing; HSP70 Heat-Shock Proteins; Humans; Hyaluronan Receptors; Hydrogen; Hydrogen Peroxide; Hydrogen-Ion Concentration; Hydrolysis; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Hypoglycemia; Hypoglycemic Agents; Hypoxia; Idiopathic Interstitial Pneumonias; Imaging, Three-Dimensional; Imatinib Mesylate; Immunotherapy; Implementation Science; Incidence; INDEL Mutation; Induced Pluripotent Stem Cells; Industrial Waste; Infant; Infant, Newborn; Inflammation; Inflammation Mediators; Infliximab; Infusions, Intravenous; Inhibitory Concentration 50; Injections; Insecticides; Insulin-Like Growth Factor Binding Protein 5; Insulin-Secreting Cells; Interleukin-1; Interleukin-17; Interleukin-8; Internship and Residency; Intestines; Intracellular Signaling Peptides and Proteins; Ion Transport; Iridaceae; Iridoid Glucosides; Islets of Langerhans Transplantation; Isodon; Isoflurane; Isotopes; Italy; Joint Instability; Ketamine; Kidney; Kidney Failure, Chronic; Kidney Function Tests; Kidney Neoplasms; Kinetics; Klebsiella pneumoniae; Knee Joint; Kruppel-Like Factor 4; Kruppel-Like Transcription Factors; Lactate Dehydrogenase 5; Laparoscopy; Laser Therapy; Lasers, Semiconductor; Lasers, Solid-State; Laurates; Lead; Leukocyte L1 Antigen Complex; Leukocytes, Mononuclear; Light; Lipid Peroxidation; Lipopolysaccharides; Liposomes; Liver; Liver Cirrhosis; Liver Neoplasms; Liver Transplantation; Locomotion; Longitudinal Studies; Lopinavir; Lower Urinary Tract Symptoms; Lubricants; Lung; Lung Diseases, Interstitial; Lung Neoplasms; Lymphocyte Activation; Lymphocytes, Tumor-Infiltrating; Lymphoma, Mantle-Cell; Lysosomes; Macrophages; Male; Manganese Compounds; MAP Kinase Kinase 4; Mass Screening; Maternal Health; Medicine, Chinese Traditional; Melanoma, Experimental; Memantine; Membrane Glycoproteins; Membrane Proteins; Mesenchymal Stem Cell Transplantation; Metal Nanoparticles; Metalloendopeptidases; Metalloporphyrins; Methadone; Methane; Methicillin-Resistant Staphylococcus aureus; Mexico; Mice; Mice, Inbred BALB C; Mice, Inbred C57BL; Mice, Inbred ICR; Mice, Knockout; Mice, Nude; Mice, SCID; Mice, Transgenic; Microarray Analysis; Microbial Sensitivity Tests; Microbiota; Micronutrients; MicroRNAs; Microscopy, Confocal; Microsomes, Liver; Middle Aged; Milk; Milk, Human; Minority Groups; Mitochondria; Mitochondrial Membranes; Mitochondrial Proteins; Models, Animal; Models, Molecular; Molecular Conformation; Molecular Docking Simulation; Molecular Dynamics Simulation; Molecular Epidemiology; Molecular Structure; Molecular Weight; Multilocus Sequence Typing; Multimodal Imaging; Muscle Strength; Muscle, Skeletal; Muscular Diseases; Mutation; Mycobacterium tuberculosis; Myocardial Stunning; Myristates; NAD(P)H Dehydrogenase (Quinone); Nanocomposites; Nanogels; Nanoparticles; Nanotechnology; Naphthalenes; Nasal Cavity; National Health Programs; Necrosis; Needs Assessment; Neoadjuvant Therapy; Neonicotinoids; Neoplasm Invasiveness; Neoplasm Metastasis; Neoplasm Proteins; Neoplasm Recurrence, Local; Neoplasm Staging; Neoplasm Transplantation; Neoplasms; Neoplastic Stem Cells; Netherlands; Neuroblastoma; Neuroprotective Agents; Neutrophils; NF-kappa B; NFATC Transcription Factors; Nicotiana; Nicotine; Nitrates; Nitrification; Nitrites; Nitro Compounds; Nitrogen; Nitrogen Dioxide; North Carolina; Nuclear Magnetic Resonance, Biomolecular; Nuclear Proteins; Nucleic Acid Hybridization; Nucleosomes; Nutrients; Obesity; Obesity, Morbid; Oceans and Seas; Oncogene Protein v-akt; Oncogenes; Oocytes; Open Reading Frames; Osteoclasts; Osteogenesis; Osteoporosis; Osteoporosis, Postmenopausal; Outpatients; Ovarian Neoplasms; Ovariectomy; Overweight; Oxazines; Oxidants; Oxidation-Reduction; Oxidative Stress; Oxides; Oxidoreductases; Oxygen; Oxygen Inhalation Therapy; Oxygenators, Membrane; Ozone; Paclitaxel; Paenibacillus; Pain Measurement; Palliative Care; Pancreatic Neoplasms; Pandemics; Parasympathetic Nervous System; Particulate Matter; Pasteurization; Patient Preference; Patient Satisfaction; Pediatric Obesity; Permeability; Peroxiredoxins; Peroxynitrous Acid; Pharmaceutical Services; Pharmacists; Pharmacy; Phaseolus; Phenotype; Phoeniceae; Phosphates; Phosphatidylinositol 3-Kinases; Phospholipid Transfer Proteins; Phospholipids; Phosphorus; Phosphorylation; Photoperiod; Photosynthesis; Phylogeny; Physical Endurance; Physicians; Pilot Projects; Piperidines; Pituitary Adenylate Cyclase-Activating Polypeptide; Plant Extracts; Plant Leaves; Plant Proteins; Plant Roots; Plaque, Atherosclerotic; Pneumonia; Pneumonia, Viral; Point-of-Care Testing; Polyethylene Glycols; Polymers; Polysorbates; Pore Forming Cytotoxic Proteins; Positron Emission Tomography Computed Tomography; Positron-Emission Tomography; Postprandial Period; Poverty; Pre-Exposure Prophylaxis; Prediabetic State; Predictive Value of Tests; Pregnancy; Pregnancy Trimester, First; Pregnancy, High-Risk; Prenatal Exposure Delayed Effects; Pressure; Prevalence; Primary Graft Dysfunction; Primary Health Care; Professional Role; Professionalism; Prognosis; Progression-Free Survival; Prolactin; Promoter Regions, Genetic; Proof of Concept Study; Proportional Hazards Models; Propylene Glycol; Prospective Studies; Prostate; Protein Binding; Protein Biosynthesis; Protein Isoforms; Protein Kinase Inhibitors; Protein Phosphatase 2; Protein Processing, Post-Translational; Protein Serine-Threonine Kinases; Protein Structure, Tertiary; Protein Transport; Proteoglycans; Proteome; Proto-Oncogene Proteins c-akt; Proto-Oncogene Proteins c-myc; Proto-Oncogene Proteins c-ret; Proto-Oncogene Proteins p21(ras); Proton Pumps; Protons; Protoporphyrins; Pseudomonas aeruginosa; Pseudomonas fluorescens; Pulmonary Artery; Pulmonary Disease, Chronic Obstructive; Pulmonary Gas Exchange; Pulmonary Veins; Pyrazoles; Pyridines; Pyrimidines; Qualitative Research; Quinoxalines; Rabbits; Random Allocation; Rats; Rats, Sprague-Dawley; Rats, Wistar; Receptors, Histamine H3; Receptors, Immunologic; Receptors, Transferrin; Recombinant Proteins; Recurrence; Reference Values; Referral and Consultation; Regional Blood Flow; Registries; Regulon; Renal Insufficiency, Chronic; Reperfusion Injury; Repressor Proteins; Reproducibility of Results; Republic of Korea; Research Design; Resistance Training; Respiration, Artificial; Respiratory Distress Syndrome; Respiratory Insufficiency; Resuscitation; Retinal Dehydrogenase; Retreatment; Retrospective Studies; Reverse Transcriptase Inhibitors; Rhinitis, Allergic; Ribosomal Proteins; Ribosomes; Risk Assessment; Risk Factors; Ritonavir; Rivers; RNA Interference; RNA-Seq; RNA, Messenger; RNA, Ribosomal, 16S; RNA, Small Interfering; Rosuvastatin Calcium; Rural Population; Saccharomyces cerevisiae; Saccharomyces cerevisiae Proteins; Salivary Ducts; Salivary Gland Neoplasms; San Francisco; SARS-CoV-2; Satiation; Satiety Response; Schools; Schools, Pharmacy; Seasons; Seawater; Selection, Genetic; Sequence Analysis, DNA; Serine-Threonine Kinase 3; Sewage; Sheep; Sheep, Domestic; Shock, Hemorrhagic; Signal Transduction; Silver; Silymarin; Single Photon Emission Computed Tomography Computed Tomography; Sirolimus; Sirtuin 1; Skin; Skin Neoplasms; Skin Physiological Phenomena; Sleep Initiation and Maintenance Disorders; Social Class; Social Participation; Social Support; Soil; Soil Microbiology; Solutions; Somatomedins; Soot; Specimen Handling; Spectrophotometry, Ultraviolet; Spectroscopy, Fourier Transform Infrared; Spectrum Analysis; Spinal Fractures; Spirometry; Staphylococcus aureus; STAT1 Transcription Factor; STAT3 Transcription Factor; Streptomyces coelicolor; Stress, Psychological; Stroke; Stroke Volume; Structure-Activity Relationship; Students, Medical; Students, Pharmacy; Substance Abuse Treatment Centers; Sulfur Dioxide; Surface Properties; Surface-Active Agents; Surveys and Questionnaires; Survival Analysis; Survival Rate; Survivin; Sweden; Swine; Swine, Miniature; Sympathetic Nervous System; T-Lymphocytes, Regulatory; Talaromyces; Tandem Mass Spectrometry; tau Proteins; Telemedicine; Telomerase; Telomere; Telomere Homeostasis; Temperature; Terminally Ill; Th1 Cells; Thiamethoxam; Thiazoles; Thiophenes; Thioredoxin Reductase 1; Thrombosis; Thulium; Thyroid Cancer, Papillary; Thyroid Carcinoma, Anaplastic; Thyroid Neoplasms; Time Factors; Titanium; Tomography, Emission-Computed, Single-Photon; Tomography, X-Ray Computed; TOR Serine-Threonine Kinases; Transcription Factor AP-1; Transcription Factors; Transcription, Genetic; Transcriptional Activation; Transcriptome; Transforming Growth Factor beta1; Transistors, Electronic; Translational Research, Biomedical; Transplantation Tolerance; Transplantation, Homologous; Transportation; Treatment Outcome; Tretinoin; Tuberculosis, Multidrug-Resistant; Tuberculosis, Pulmonary; Tubulin Modulators; Tumor Microenvironment; Tumor Necrosis Factor Inhibitors; Tumor Necrosis Factor-alpha; Twins; Ultrasonic Therapy; Ultrasonography; Ultraviolet Rays; United States; Up-Regulation; Uranium; Urethra; Urinary Bladder; Urodynamics; Uromodulin; Uveitis; Vasoconstrictor Agents; Ventricular Function, Left; Vero Cells; Vesicular Transport Proteins; Viral Nonstructural Proteins; Visual Acuity; Vital Capacity; Vitamin D; Vitamin D Deficiency; Vitamin K 2; Vitamins; Volatilization; Voriconazole; Waiting Lists; Waste Disposal, Fluid; Wastewater; Water Pollutants, Chemical; Whole Genome Sequencing; Wine; Wnt Signaling Pathway; Wound Healing; Wounds and Injuries; WW Domains; X-linked Nuclear Protein; X-Ray Diffraction; Xanthines; Xenograft Model Antitumor Assays; YAP-Signaling Proteins; Yogurt; Young Adult; Zebrafish; Zebrafish Proteins; Ziziphus

Topics: Adaptation, Physiological; Age Factors; Amines; Animals; Body Weight; Bronchi; DNA; Free Radicals; Glucose; Humans; Lipid Metabolism; Lung; Lung Diseases; Nitrogen Dioxide; Oxygen; Ozone; Protein Biosynthesis; Pulmonary Alveoli; Species Specificity; Sulfhydryl Compounds; Vitamin E

Middle East Respiratory Syndrome (MERS) is a novel respiratory illness firstly reported in Saudi Arabia in 2012. It is caused by a new corona virus, called MERS corona virus (MERS-CoV). Most people who have MERS-CoV infection developed severe acute respiratory illness.. This work is done to determine the clinical characteristics and the outcome of intensive care unit (ICU) admitted patients with confirmed MERS-CoV infection.. This study included 32 laboratory confirmed MERS corona virus infected patients who were admitted into ICU. It included 20 (62.50%) males and 12 (37.50%) females. The mean age was 43.99 ± 13.03 years. Diagnosis was done by real-time reverse transcription polymerase chain reaction (rRT-PCR) test for corona virus on throat swab, sputum, tracheal aspirate, or bronchoalveolar lavage specimens. Clinical characteristics, co-morbidities and outcome were reported for all subjects.. Most MERS corona patients present with fever, cough, dyspnea, sore throat, runny nose and sputum. The presence of abdominal symptoms may indicate bad prognosis. Prolonged duration of symptoms before patients' hospitalization, prolonged duration of mechanical ventilation and hospital stay, bilateral radiological pulmonary infiltrates, and hypoxemic respiratory failure were found to be strong predictors of mortality in such patients. Also, old age, current smoking, smoking severity, presence of associated co-morbidities like obesity, diabetes mellitus, chronic heart diseases, COPD, malignancy, renal failure, renal transplantation and liver cirrhosis are associated with a poor outcome of ICU admitted MERS corona virus infected patients.. Plasma HO-1, ferritin, p21, and NQO1 were all elevated at baseline in CKD participants. Plasma HO-1 and urine NQO1 levels each inversely correlated with eGFR (. SnPP can be safely administered and, after its injection, the resulting changes in plasma HO-1, NQO1, ferritin, and p21 concentrations can provide information as to antioxidant gene responsiveness/reserves in subjects with and without kidney disease.. A Study with RBT-1, in Healthy Volunteers and Subjects with Stage 3-4 Chronic Kidney Disease, NCT0363002 and NCT03893799.. HFNC did not significantly modify work of breathing in healthy subjects. However, a significant reduction in the minute volume was achieved, capillary [Formula: see text] remaining constant, which suggests a reduction in dead-space ventilation with flows > 20 L/min. (ClinicalTrials.gov registration NCT02495675).. 3 组患者手术时间、术中显性失血量及术后 1 周血红蛋白下降量比较差异均无统计学意义（. 对于肥胖和超重的膝关节单间室骨关节炎患者，采用 UKA 术后可获满意短中期疗效，远期疗效尚需进一步随访观察。.. Decreased muscle strength was identified at both time points in patients with hEDS/HSD. The evolution of most muscle strength parameters over time did not significantly differ between groups. Future studies should focus on the effectiveness of different types of muscle training strategies in hEDS/HSD patients.. These findings support previous adverse findings of e-cigarette exposure on neurodevelopment in a mouse model and provide substantial evidence of persistent adverse behavioral and neuroimmunological consequences to adult offspring following maternal e-cigarette exposure during pregnancy. https://doi.org/10.1289/EHP6067.. This RCT directly compares a neoadjuvant chemotherapy regimen with a standard CROSS regimen in terms of overall survival for patients with locally advanced ESCC. The results of this RCT will provide an answer for the controversy regarding the survival benefits between the two treatment strategies.. NCT04138212, date of registration: October 24, 2019.. Results of current investigation indicated that milk type and post fermentation cooling patterns had a pronounced effect on antioxidant characteristics, fatty acid profile, lipid oxidation and textural characteristics of yoghurt. Buffalo milk based yoghurt had more fat, protein, higher antioxidant capacity and vitamin content. Antioxidant and sensory characteristics of T. If milk is exposed to excessive amounts of light, Vitamins B. The two concentration of ZnO nanoparticles in the ambient air produced two different outcomes. The lower concentration resulted in significant increases in Zn content of the liver while the higher concentration significantly increased Zn in the lungs (p < 0.05). Additionally, at the lower concentration, Zn content was found to be lower in brain tissue (p < 0.05). Using TEM/EDX we detected ZnO nanoparticles inside the cells in the lungs, kidney and liver. Inhaling ZnO NP at the higher concentration increased the levels of mRNA of the following genes in the lungs: Mt2 (2.56 fold), Slc30a1 (1.52 fold) and Slc30a5 (2.34 fold). At the lower ZnO nanoparticle concentration, only Slc30a7 mRNA levels in the lungs were up (1.74 fold). Thus the two air concentrations of ZnO nanoparticles produced distinct effects on the expression of the Zn-homeostasis related genes.. Until adverse health effects of ZnO nanoparticles deposited in organs such as lungs are further investigated and/or ruled out, the exposure to ZnO nanoparticles in aerosols should be avoided or minimised.

Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor Proteins, Signal Transducing; Adenine; Adenocarcinoma; Adipogenesis; Administration, Cutaneous; Administration, Ophthalmic; Adolescent; Adsorption; Adult; Aeromonas hydrophila; Aerosols; Aged; Aged, 80 and over; Aging; Agriculture; Air Pollutants; Air Pollution; Airway Remodeling; Alanine Transaminase; Albuminuria; Aldehyde Dehydrogenase 1 Family; Algorithms; AlkB Homolog 2, Alpha-Ketoglutarate-Dependent Dioxygenase; Alzheimer Disease; Amino Acid Sequence; Ammonia; Ammonium Compounds; Anaerobiosis; Anesthetics, Dissociative; Anesthetics, Inhalation; Animals; Anti-Bacterial Agents; Anti-HIV Agents; Anti-Infective Agents; Anti-Inflammatory Agents; Antibiotics, Antineoplastic; Antibodies, Antineutrophil Cytoplasmic; Antibodies, Monoclonal, Humanized; Antifungal Agents; Antigens, Bacterial; Antigens, CD; Antigens, Differentiation, Myelomonocytic; Antimetabolites, Antineoplastic; Antineoplastic Agents; Antineoplastic Combined Chemotherapy Protocols; Antioxidants; Antitubercular Agents; Antiviral Agents; Apolipoproteins E; Apoptosis; Arabidopsis; Arabidopsis Proteins; Arsenic; Arthritis, Rheumatoid; Asthma; Atherosclerosis; ATP-Dependent Proteases; Attitude of Health Personnel; Australia; Austria; Autophagy; Axitinib; Bacteria; Bacterial Outer Membrane Proteins; Bacterial Proteins; Bacterial Toxins; Bacterial Typing Techniques; Bariatric Surgery; Base Composition; Bayes Theorem; Benzoxazoles; Benzylamines; beta Catenin; Betacoronavirus; Betula; Binding Sites; Biological Availability; Biological Oxygen Demand Analysis; Biomarkers; Biomarkers, Tumor; Biopsy; Bioreactors; Biosensing Techniques; Birth Weight; Blindness; Blood Chemical Analysis; Blood Gas Analysis; Blood Glucose; Blood Pressure; Blood Pressure Monitoring, Ambulatory; Blood-Brain Barrier; Blotting, Western; Body Mass Index; Body Weight; Bone and Bones; Bone Density; Bone Resorption; Borates; Brain; Brain Infarction; Brain Injuries, Traumatic; Brain Neoplasms; Breakfast; Breast Milk Expression; Breast Neoplasms; Bronchi; Bronchoalveolar Lavage Fluid; Buffaloes; Cadherins; Calcification, Physiologic; Calcium Compounds; Calcium, Dietary; Cannula; Caprolactam; Carbon; Carbon Dioxide; Carboplatin; Carcinogenesis; Carcinoma, Ductal; Carcinoma, Ehrlich Tumor; Carcinoma, Hepatocellular; Carcinoma, Non-Small-Cell Lung; Carcinoma, Pancreatic Ductal; Carcinoma, Renal Cell; Cardiovascular Diseases; Carps; Carrageenan; Case-Control Studies; Catalysis; Catalytic Domain; Cattle; CD8-Positive T-Lymphocytes; Cell Adhesion; Cell Cycle Proteins; Cell Death; Cell Differentiation; Cell Line; Cell Line, Tumor; Cell Movement; Cell Nucleus; Cell Phone Use; Cell Proliferation; Cell Survival; Cell Transformation, Neoplastic; Cell Transformation, Viral; Cells, Cultured; Cellulose; Chemical Phenomena; Chemoradiotherapy; Child; Child Development; Child, Preschool; China; Chitosan; Chlorocebus aethiops; Cholecalciferol; Chromatography, Liquid; Circadian Clocks; 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Little is known about the association between air pollution and hypertension among children, and no studies report whether breastfeeding modifies this association in children.. Nine thousand three hundred fifty-four Chinese children, ages 5-17 years old, from 24 elementary schools and 24 middle schools in the Seven Northeastern Cities during 2012-2013 were evaluated. The weight, height, and BP were measured. Four-year average concentrations of particles with an aerodynamic diameter of ≤10 μm (PM10), sulfur dioxide (SO2), nitrogen dioxides (NO2), ozone (O3), and carbon monoxide (CO) were calculated from monitoring stations. Two-level regression analysis was used to examine the effects, controlling for covariates.. The results showed that associations existed between hypertension and pollutants. The odds ratios for hypertension ranged from 1.12 per 46.3 μg/m3 increase for O3 (95% confidence interval [CI], 1.10-1.13) to 1.68 per 30.6 μg/m3 increase for PM10 (95% CI, 1.53-1.86). The increases in mean diastolic BP ranged from 0.58 mm Hg per 46.3 μg/m3 increase for O3 (95% CI, 0.52-0.63 mm Hg) to 2.89 mm Hg per 563.4 μg/m3 increase for CO (95% CI: 2.53-3.24 mm Hg). The increase in systolic BP ranged from 0.50 mm Hg per 46.3 μg/m3 increase for O3 (95% CI: 0.43-0.57 mm Hg) to 2.10 mm Hg per 30.6 μg/m3 increase for PM10 (95% CI, 1.73-2.47 mm Hg). Compared with children who had been breastfed, non-breastfed children exhibited consistently stronger effects.. Study findings indicate that high levels of PM10, SO2, NO2, O3, and CO are associated with increased arterial BP and hypertension among the children. Breastfeeding may reduce the risk.

Topics: Adolescent; Air Pollutants; Air Pollution; Blood Pressure; Body Height; Body Weight; Breast Feeding; Carbon Monoxide; Child; Child, Preschool; China; Cities; Cross-Sectional Studies; Female; Humans; Hypertension; Male; Nitrogen Dioxide; Ozone; Prevalence; Sulfur Dioxide

A new series of diazadioxa oxovanadium(IV) macrocyclic complexes of type [VO(mac)]SO(4) have been synthesized via the condensation reaction of a 3-(phenyl/substituted phenyl)-4-amino-5-hydrazino-1,2,4-triazole (H(2)L) with salicylaldehyde/2-hydroxyacetophenone and 1,4-dibromobutane in the presence of oxovanadium(IV) sulfate in ethanol. All the newly synthesized compounds were characterized on the basis of elemental analyses, conductance measurements, magnetic properties, spectral (UV-Vis, IR, EPR) and XRD studies. The particle size of the complexes has been calculated from XRD spectra using Debye-Scherrer formula and these are found to be in 31-32 nm range. The efficacy of two macrocyclic complexes was also studied in streptozotocin-induced diabetic rats over a period of 30 days. The administration of these complexes in diabetic rats reversed the diabetic effect due to their insulin-mimetic effects.

Topics: Animals; Blood Glucose; Blood Proteins; Body Weight; Cholesterol; Coordination Complexes; Creatinine; Dioxanes; Electron Spin Resonance Spectroscopy; Electrons; Glucose Tolerance Test; Hemoglobins; Insulin; Macrocyclic Compounds; Male; Nitrogen Dioxide; Rats; Rats, Wistar; Spectrophotometry, Infrared; Urea; Vanadates; X-Ray Diffraction

Recombinant human erythropoietin (rHuEPO), used clinically for renal anemia, reportedly exhibits pleiotropic properties in various tissues. To test whether it ameliorates vascular injury, rHuEPO (75U/kg) was administered subcutaneously every 3days for 10days to 5/6 nephrectomized hypertensive rats (5/6Nx) treated with 1% NaCl. rHuEPO had no effect on increased systolic blood pressure or decreased hematocrit values, but normalized levels of proteinuria and creatinine clearance. Vasodilation in response to acetylcholine in the aortic ring was impaired in the 5/6Nx, and improved by treatment with rHuEPO. Immunohistochemical analysis revealed that the infiltration of adventitial areas by macrophages and expression of osteopontin were enhanced in the 5/6Nx aorta and the overexpression was suppressed by rHuEPO. rHuEPO also attenuated medial hyperplasia. Akt signaling was activated by the increased expression of phosphorylated Akt and GSK-3β in aorta from rHuEPO-treated 5/6Nx. rHuEPO restored plasma NOx (NO(2)(-)+NO(3)(-)) levels and endothelial nitric oxide synthase (eNOS) content in the 5/6Nx aorta. Treatment with an eNOS substrate, l-arginine, which caused a similar increase in plasma NOx levels as the rHuEPO treatment, resulted in a normalization of endothelial dysfunction and vascular inflammation. These results suggest that a low dose of rHuEPO exerted vasoprotective effects in rats with hypertensive renal failure.

Topics: Acetylcholine; Animals; Aorta; Aorta, Thoracic; Blood Pressure; Body Weight; Connective Tissue; Dose-Response Relationship, Drug; Endothelium, Vascular; Erythropoietin; Gene Expression Regulation, Enzymologic; Hematocrit; Hematopoiesis; Humans; Hypertension; Macrophages; Male; Nephrectomy; Nitric Oxide; Nitric Oxide Synthase Type III; Nitrogen Dioxide; Nitrogen Oxides; Nitroprusside; Osteopontin; Phosphoproteins; Rats; Rats, Wistar; Recombinant Proteins

An association between exposure to traffic-related air pollution and reduced birth weight has been suggested. However, previous studies have failed to adjust for maternal size, which is an indicator of individual genetic growth potential. Therefore, we evaluated the association of air pollution with birth weight, term low birth weight (term-LBW), and small for gestational age (SGA), with adjustment for maternal size. Individual data were extracted from a database that is maintained by a maternal and perinatal care center in Shizuoka, Japan. We identified liveborn singleton births (n=14,204). Using geocoded residential information, each birth was assigned a number of traffic-based exposure indicators: distance to a major road; distance-weighted traffic density; and estimated concentration of nitrogen dioxide by land use regression. The multivariate adjusted odds ratios and their 95% confidence intervals (CIs) for the associations between exposure indicators and outcomes were then estimated using logistic regression models. Overall, exposure indicators of air pollution showed no clear pattern of association. Although there are many limitations, we did not find clear associations between birth-weight-related outcomes and the three markers of traffic-related air pollution.

Topics: Air Pollutants; Birth Weight; Body Weight; Environmental Exposure; Female; Humans; Infant, Newborn; Japan; Logistic Models; Male; Nitrogen Dioxide; Pregnancy; Retrospective Studies; Seasons; Socioeconomic Factors; Vehicle Emissions

Although a number of animal studies have been conducted to investigate the toxic effects of gaseous pollutants on human airways, the anatomical and physiological differences between animals and humans represent a challenge in extrapolating the animal data to humans. The aim of this study was to examine how interspecies anatomical and physiological differences influence the transport of the inhaled gases throughout the airways and alveoli. We designed mathematical airway models of three mammalian species, rats, dogs, and humans, in which interspecies differences in airway dimensions and respiratory patterns were taken into account. We then simulated the bulk flow of three gases (ozone [O(3)], nitrogen dioxide [NO(2)], and sulfur dioxide [SO(2)]) and obtained the intra-airway concentrations of the gases and the amount absorbed using these models. For all three gases, both real-time and mean concentrations in the upper and lower airways were higher in humans when compared with rats and dogs. For example, the mean concentration of O(3) in the 5th bronchi of humans was 3 and 12 times higher than in rats and dogs, respectively. Similarly, the amount of absorbed gases corrected for airway surface area was again higher in the upper and lower airways of humans than the other two species. Sensitivity analysis indicated that tidal volume, respiratory rate, and surface area of the upper and lower airways had significant impact on the results. In conclusion, kinetics of inhaled gaseous substances vary substantially among animals and humans, and such variations are, at least partially, the result of anatomical and physiological differences in their airways.

Topics: Air Pollutants; Algorithms; Animals; Body Surface Area; Body Weight; Computer Simulation; Dogs; Humans; Models, Anatomic; Models, Statistical; Nitrogen Dioxide; Oxidants, Photochemical; Ozone; Pulmonary Alveoli; Rats; Respiratory Mechanics; Respiratory System; Species Specificity; Sulfur Dioxide

Ambient exposure to nitrogen dioxide, a critical air pollutant in developed countries, is positively associated with cardiovascular mortality and morbidity. Although its cardiovascular effects are predominantly shown in patients with high risk of atherogenesis, no studies have elucidated whether daily exposure to nitrogen dioxide air pollution enhances atherogenic metabolisms, primarily in obese subjects who are susceptible to atherogenesis and subsequent cardiovascular diseases. We used male Otsuka Long-Evans Tokushima Fatty (OLETF) rats as obese subjects and Long-Evans Tokushima (LETO) rats as nonobese controls. The animals were continuously exposed to nitrogen dioxide at a concentration of 0, 0.16, 0.8, or 4.0 ppm from 8 weeks of age through 32 weeks. At 40 weeks of age, levels of body weight, triglyceride, and total cholesterol were significantly greater in the OLETF rats than in the LETO rats. A ratio of high-density lipoprotein (HDL) to total cholesterol was significantly smaller in the former than in the latter. In the LETO rats, nitrogen dioxide exposure significantly decreased only the levels of HDL as compared with clean air exposure. In the OLETF rats, however, nitrogen dioxide exposure at a concentration of 0.16 ppm significantly elevated triglyceride concentration and decreased the ratio of HDL to total cholesterol as well as the levels of HDL. Nitrogen dioxide air pollution near ambient levels is an atherogenic risk primarily in obese subjects.

Topics: Air Pollution; Animals; Arteriosclerosis; Blood Glucose; Body Weight; Cholesterol; Cholesterol, HDL; Humans; Inhalation Exposure; Male; Nitrogen Dioxide; Obesity; Oxidants, Photochemical; Rats; Rats, Long-Evans; Risk Factors; Triglycerides

Brief, high-level nitrogen dioxide (NO(2)) exposures are major hazards during fires and heat-generating explosions. To characterize the lung response to a brief high-level NO(2) exposure, we exposed two groups (n = 5) of 325-375 g, male, Sprague-Dawley rats to either 200 +/- 5 ppm (376 +/- 9 mg/m(3)) NO(2) or room air for 15 min. The rats were nose-only exposed in a multiport exposure chamber fitted with pressure transducers to monitor their respiration during exposure. One hour after exposure, we euthanized the rats, collected blood samples, lavaged the lungs with warm saline, and then excised them. One lung lobe was cooled to -196 degrees C and used for low-temperature electron paramagentic resonance (EPR) analysis. The remainder was homogenized and used for biochemical analyses. Inspired minute ventilation (V(i)) during exposure decreased 59% (p < 0.05). Calculated total inspired dose was 0.880 mg NO(2). In lung lavage, both total and alveolar macrophage cell counts declined (approximately 75%, p < 0.05), but epithelial cell count increased 8.5-fold. Lung weight increased 40% (p < 0.05) after exposure. In the blood, potassium and methemoglobin increased 45 and 18% (p < 0.05), respectively; glucose, lactate, and total hemoglobin were not altered significantly. EPR analysis of lung tissue revealed hemoglobin oxidation and carbon-centered radical formation. Vitamins E and C and uric acid were depleted, and lipid peroxidation measured by three different methods (TBARS, conjugated dienes, and fluorescent peroxidation end products) was elevated, but total protein, DNA, and lipid contents were unchanged. These observations combined demonstrate that a brief (15 min) high-level (200 ppm) NO(2) exposure of rats was sufficient to cause significant damage. However, comparison of the exposure dose normalized to rat body weight with previously reported sheep and estimated human values revealed significant differences. This raises a question about interspecies dosimetry and species-specific responses when animal data are extrapolated to humans and used for safety standard setting, particularly with high-level brief exposures.

Topics: Administration, Inhalation; Air; Animals; Antioxidants; Blood Chemical Analysis; Body Weight; Bronchoalveolar Lavage Fluid; Dose-Response Relationship, Drug; Electron Spin Resonance Spectroscopy; Lung; Male; Nitrogen Dioxide; Nose; Organ Size; Rats; Rats, Sprague-Dawley; Species Specificity

To evaluate the early molecular events of oxidant-induced pulmonary fibrosis, rats were continuously exposed to 0.4 ppm ozone and 7 ppm nitrogen dioxide. The early responses to the combined gases could be divided into three phases. Acute pulmonary inflammation indicated by an increase in pulmonary edema as well as an influx of neutrophils into the airspaces first occurred on days 1 to 3 of the exposure. The pulmonary inflammation was reversed by day 8, and no biochemical or morphologic aspects of tissue responses were detected from days 15 to 45, suggesting that rats adapted to the stimuli during that period. Pulmonary fibrosis could be detected by an increase in the biomarker of lung collagen content at day 60 and by histopathologic evaluation by day 90. Enhanced expression of macrophage inflammatory protein-2 was observed only at day 1, whereas the pulmonary expression of transforming growth factor-beta was upregulated on days 60 and 90 of the exposure. Macrophage expressions of interleukin-1beta and interleukin-6 were enhanced during acute pulmonary inflammation; however, macrophage expression of tumor necrosis factor-alpha was elevated at both day 1 and days 60-90. Activation of nuclear factor-kappa B and increased expression of thioredoxin in the lungs was also observed at day 1 and days 60-90. The expression of antioxidant enzymes, such as manganeous superoxide dismutase and glutathione peroxidase, was not altered during exposure. These results indicate that macrophage activation and the expression of macrophage-derived cytokines may play an important role in the early pulmonary responses against the combined gases.

Topics: Administration, Inhalation; Albumins; Animals; Blotting, Northern; Body Weight; Bronchoalveolar Lavage Fluid; Collagen; Cytokines; DNA Primers; Glutathione Peroxidase; Hydroxyproline; Immunoenzyme Techniques; Interleukins; Lung; Male; Nitrogen Dioxide; Oxidants, Photochemical; Ozone; Pulmonary Fibrosis; Rats; Rats, Sprague-Dawley; RNA, Messenger; Superoxide Dismutase

1. In previous studies a rat inhalation model was developed to investigate the effects of intervention after acute NO2 exposure. The object of the present study was to investigate whether acute NO2 intoxication induced comparable effects in rabbits as it does in rats. Where the effects of intervention in both species are similar, then the conclusions drawn from these studies may have more relevance for the treatment of man. 2. Biochemical variables in bronchoalveolar lavage and supernatant from lung homogenate, which may be relevant for the evaluation of lung injury and repair, were investigated and compared with histology. 3. After NO2 exposure for 10 min, the pulmonary effects observed became more pronounced with increasing NO2 concentrations (0, 125, 175, 250, 400, 600 or 800 ppm) [1 ppm NO2 is 1.88 mg m-3]. The effects in rabbits were found to be broadly comparable with those in rats. 4. To achieve severe lung injury in rabbits without mortality, enabling investigations of the effects of intervention over several days, exposure to a NO2 concentration of 600 ppm for 10 min was most appropriate, while a concentration of 175 ppm NO2 was needed to attain comparable effects in rats. 5. The repair phase starts later, namely at 3 days after exposure in rats, compared to 5 days in rabbits.

Topics: Animals; Atmosphere Exposure Chambers; Blood Cell Count; Body Weight; Bronchoalveolar Lavage Fluid; Disease Models, Animal; Dose-Response Relationship, Drug; Female; Lung; Male; Nitrogen Dioxide; Organ Size; Rabbits; Rats; Species Specificity

1. In previous studies a rat inhalation model was developed to investigate the efficacy of treatment in acute NO2 intoxication. 2. Desferrioxamine was administered intravenously to study its effect on histological alterations in lung tissue in rats after acute NO2 exposure. 3. Twenty four hours after exposure to 175 ppm NO2 for 10 minutes the lung injury observed by light microscopy in the desferrioxamine treated rats was less pronounced than in the saline treated rats. 4. Desferrioxamine appeared to provide more protection with a dose of 100 mg kg-1 24 h-1 than with 200 mg kg-1 24 h-1.

Topics: Administration, Inhalation; Animals; Body Weight; Deferoxamine; Female; Injections, Intravenous; Lung; Lung Diseases; Nitrogen Dioxide; Organ Size; Rats; Rats, Wistar

Male ICR mice were exposed continuously to ozone (O3) and nitrogen dioxide (NO2) for 7 days to examine the effects on drinking and eating behaviors. Ozone at 0.1 ppm did not affect drinking and eating activities, whereas drinking activity decreased in a concentration-dependent manner to 47.7, 12.8, and 3.0% of the control value with 2-day exposures to 0.2, 0.4, and 0.8 ppm O3, respectively, and eating activity decreased to 35.2 and 8.7% of the control value at 0.4 and 0.8 ppm O3, respectively. Body weight also decreased markedly by 2.0, 4.6, and 7.5 g at 0.2, 0.4, and 0.8 ppm O3, respectively. These decrements reached a maximum on the second day of exposure. However, alterations in drinking and eating activities and body weight were transient, leading to recovery during the continuous O3 exposures. The recovery processes were dependent on the concentrations of O3. Nitrogen dioxide at 4 ppm did not affect drinking and eating activities, whereas drinking activity decreased in a concentration-dependent manner to 56.8, 8.3, and 18.7% of the control value with 2-day exposures to 6, 8, and 12 ppm NO2, respectively, and eating activity decreased markedly to 21.8 and 16.4% at 8 and 12 ppm NO2, respectively. Body weight also decreased by 2.5, 5.5, and 6.1 g at 6, 8, and 12 ppm NO2, respectively. These decrements reached a maximum on the second day of exposure. As in the O3 exposures, the decrements in drinking and eating activities and body weight were transient and recovered during the continuous exposures to NO2 depending on the concentrations of NO2. Drinking and eating activities and body weights of mice that had been previously exposed to 12 ppm NO2 for 7 days did not show changes when the mice were exposed to 0.4 ppm O3 9 days after NO2 exposure. The present study demonstrates that photochemical oxidants suppress drinking and eating behaviors in mice and that they recover thereafter under the continuous exposure conditions.

Topics: Animals; Behavior, Animal; Body Weight; Drinking Behavior; Feeding Behavior; Male; Mice; Mice, Inbred ICR; Nitrogen Dioxide; Ozone; Rats

1. The pulmonary toxic events induced by acute nitrogen dioxide (NO)2 exposure were studied in the rat to develop an inhalation model to investigate therapeutic measures. 2. A good correlation was observed between the lung weights and severity of the atypical pneumonitis. The pulmonary effects observed, became more pronounced with increasing NO2 concentrations (0, 25, 75, 125, 175 or 200 ppm, 1 ppm NO2 = 1.88 mg m-3 NO2) and exposure times (5, 10, 20 or 30 min). 3. An adequate NO2 concentration is 175 ppm, because it can induce a severe lung injury without mortality. This makes it possible to investigate suitable therapeutic interventions for several days. 4. Following acute inhalatory NO2 intoxication, transformation of NO2 to nitrate is presumably more notable than transformation to nitrite. 5. The transformation of NO2 to nitrate in lung tissue causes a slight increase in the serum nitrite concentration, which does not induce measurable formation of methaemoglobin. 6. Presumably, methaemoglobin does not contribute to the toxicity of NO2 intoxication.

Topics: Administration, Inhalation; Animals; Atmosphere Exposure Chambers; Biotransformation; Body Weight; Female; Lung; Models, Biological; Nitrogen Dioxide; Organ Size; Pneumonia; Pulmonary Alveoli; Rats; Rats, Inbred Strains

1. In previous studies a rat inhalation model was developed to investigate the treatment of acute nitrogen dioxide (NO2) intoxication. 2. Biochemical parameters, which may be important for the evaluation of lung injury and repair, were reviewed and compared with the histology. 3. After exposure to high NO2 concentrations (75 ppm, 125 ppm or 175 for 10 min) the lung injury observed by light microscope was most pronounced after 24 h and became worse with increasing concentration. 4. The most sensitive indicators for lung injury in the broncho-alveolar lavage fluid (BAL) were protein and albumin concentrations, angiotensin converting enzyme activity, beta-glucuronidase activity and the presence of neutrophil leucocytes. The changes observed in these variables were dose-dependent. Following exposure to 175 ppm the protein and albumin concentrations and the angiotensin converting enzyme activity showed a 100-fold increase, while the beta-glucuronidase activity showed a 10-fold increase. 5. Glucose-6-phosphate dehydrogenase and glutathione peroxidase in the supernatant of lung homogenate and gamma-glutamyl transferase activity in BAL are likely to be the most practical parameters for monitoring the phase of repair because their activities were maximal at the moment histological changes were reduced in intensity. 6. Repair was almost complete 7 d following exposure.

Topics: Administration, Inhalation; Alkaline Phosphatase; Animals; Atmosphere Exposure Chambers; Body Weight; Bronchoalveolar Lavage Fluid; Female; Lung; Nitrogen Dioxide; Organ Size; Oxidoreductases; Rats; Rats, Inbred Strains

The effect of chronic exposure to low (0.5 ppm) and high (10 ppm) concentrations of NO2 on the development of the ferret lung was studied in animals exposed 4 h/day, 5 days/week from age 6 weeks through 20 weeks. Morphometric analysis showed significant changes in alveolar dimensions at both concentrations, compared to air-exposed controls. Thickened alveolar walls, increased cellularity and collagen deposition, increased lung size and the appearance of lesions indicative of oxidant damage indicate that even low concentrations of this gas during lung development may have adverse consequences for adult lung function.

Topics: Animals; Body Weight; Collagen; Dose-Response Relationship, Drug; Female; Ferrets; Lung; Lung Volume Measurements; Male; Nitrogen Dioxide

To examine the pulmonary effects of relatively low levels of NO2 and O3, and test for any possible interaction in their effects, we exposed 3-mo-old male Sprague-Dawley rats, free of specific pathogens, to either filtered room air (control) or 1.20 ppm (2256 micrograms/m3) NO2, 0.30 ppm (588 micrograms/m3) O3, or a combination of the two oxidants continuously for 3 d. We studied a series of parameters in the lung, including lung weight, and enzyme activities related to NADPH generation, sulfhydryl metabolism, and cellular detoxification. The results showed that relative to control, exposure to NO2 caused small but nonsignificant changes in all the parameters; O3 caused significant increases in all the parameters except for superoxide dismutase; and a combination of NO2 and O3 caused increases in all the parameters, and the increases were greater than those caused by NO2 or O3 alone. Statistical analysis of the data showed that the effects of combined exposure were synergistic for 6-phosphogluconate dehydrogenase, isocitrate dehydrogenase, glutathione reductase, and superoxide dismutase activities, and additive for glutathione peroxidase and disulfide reductase activities, but indifferent from those of O3 exposure for other enzyme activities.

Topics: Animals; Body Weight; Dose-Response Relationship, Drug; Drug Synergism; Lung; Male; NADP; Nitrogen Dioxide; Organ Size; Ozone; Rats; Rats, Inbred Strains; Regression Analysis; Sulfhydryl Compounds; Superoxide Dismutase

The effect of acute exposure to nitrogen dioxide (NO2) on splenic T lymphocyte subpopulations was studied in C57BL/6cum mice. The mice were exposed to 4 ppm NO2 for 8 hr. Monoclonal antibodies to T lymphocyte differentiation antigens and fluorescence-activated cell sorter (FACS) analysis were used to detect changes in T lymphocyte subpopulations. Percentages of total T lymphocytes (Thy-1.2-positive), T-helper/inducer lymphocytes (L3T4-positive), and T-cytotoxic/suppressor lymphocytes (Lyt-2-positive) were significantly lower in NO2-exposed animals than in filtered-air-breathing controls. Large T-cytotoxic/suppressor cells were found to be the most susceptible subpopulation. Spleen and body weights of the mice were also determined. There were no differences between body weights of control and exposed animals; however, exposed mice had significantly lower spleen weights. This is the first report providing evidence linking alterations in T lymphocyte subpopulations to acute NO2 exposure at occupational levels. T lymphocytes play a central role in regulatory and effector immunological functions such as mediating delayed hypersensitivity, regulating immunoglobulin production, and lysing virus-infected and neoplastic cells. The biological significance of these findings remains to be established, but it is very likely that functional impairment occurs since an optimal immune response depends upon a proper balance of the T lymphocyte subpopulations. Detection of alterations in T lymphocyte subpopulations using monoclonal antibodies and FACS analysis may provide an extremely sensitive means of demonstrating NO2-induced changes in the immune system.

Topics: Animals; Body Weight; Female; Flow Cytometry; Fluorescent Antibody Technique; Mice; Mice, Inbred C57BL; Nitrogen Dioxide; Organ Size; Reference Values; Spleen; T-Lymphocytes

The sensitivity of different parameters for the determination of lung injury caused by nitrogen dioxide (NO2) was investigated. Male rats were exposed to concentrations of 0, 4, 10 or 25 ppm NO2 for 6 h/day, for 7, 14 or 21 days. Histopathology of the nasal cavity, larynx, trachea and lungs was compared with the changes in macrophage function and morphology. In addition several biochemical parameters were determined in lung lavages. Cytotoxic effects were investigated in primary cultures of rat and bovine alveolar macrophages, exposed to the same NO2-levels as in the in vivo exposure. Treatment-related histopathological changes were observed in the lungs. No differences between exposed and control animals were observed in the nasal cavity, larynx or trachea. The morphology of the lavaged alveolar macrophages was changed at all exposure concentrations on day 7, 14 and 21. An increase in the number of macrophages was found after exposure to 10 and 25 ppm NO2 on days 7, 14 and 21. The phagocytic capacity was diminished after 14 and 21 days exposure to 25 ppm and at both times exposure to 10 and 25 ppm increased the level of gamma-glutamyl transferase (GGT) in lavage fluids. Morphology of the macrophages and levels of GGT were found to be sensitive parameters of nitrogen dioxide toxicity. In vitro exposure of rat and bovine alveolar macrophages to comparable NO2-concentrations induced effects on phagocytosis similar to those observed for macrophages from exposed rats.

Topics: Administration, Inhalation; Alkaline Phosphatase; Animals; Body Weight; Bronchoalveolar Lavage Fluid; Cell Survival; gamma-Glutamyltransferase; L-Lactate Dehydrogenase; Lung Diseases; Macrophages; Male; Nitrogen Dioxide; Phagocytosis; Proteins; Rats; Rats, Inbred Strains

Pulmonary function was examined for juvenile and young adult Fischer 344 rats that were continuously exposed to NO2 (0.5, 1.0, or 2.0 ppm) for up to 6 wk. The exposure included twice daily 1-h spikes equal to 3 times the baseline concentration. This spike-to-baseline ratio was chosen to simulate morning and evening urban rush-hour conditions. Juvenile rats were examined after 3 and 6 wk of NO2 exposure, whereas young adult rats were examined after 1-, 3-, and 6-wk intervals. Lung volumes, compliance, and efficiency of ventilation distribution were evaluated. Lung volumes increased in the juvenile rats after 3- and 6-wk exposures to 1.0 and 2.0 ppm NO2, but were unchanged in young adult rats. Lung compliance increased in juvenile rats exposed to 1.0 or 2.0 ppm NO2 for 3 wk. However, it was unchanged in juvenile rats exposed for 6 wk or in young adult rats exposed for 1 or 3 wk. Compliance decreased in young adult rats exposed to 2.0 ppm NO2 for 6 wk and was correlated to an overall thickening of alveolar interstitium and septal tissue. However, the observed changes in pulmonary function were marginal and reversible, since lung-function measurements were not different from controls after a 3-wk recovery period.

Topics: Animals; Body Weight; Lung; Lung Compliance; Male; Nitrogen Dioxide; Rats; Rats, Inbred F344

Topics: Animals; Body Weight; Kynurenic Acid; Liver; Male; NAD; NADP; Nitrogen Dioxide; Pyridoxal Phosphate; Rats; Rats, Inbred F344; Tryptophan; Xanthurenates

The effects of the cytochrome P450 inducer beta-naphthoflavone (BNF) on NO2 toxicity were studied in two strains of mice. In one strain (C57B1/6J), cytochrome P450 could be induced by the aromatic hydrocarbon, while in the other strain (DBA/2J) cytochrome P450 was not inducible by this compound. Mice were treated with BNF before and during 4 days of exposure to 20 ppm NO2. The body growth of NO2-exposed mice improved only in BNF-treated C57B1/6J mice. In this strain, BNF reduced both pulmonary edema (as measured by wet and dry lung weights or as assessed by histological studies) and lung peroxidation (as measured by malondialdehyde). This protective effect of BNF on NO2 toxicity in C57B1/6J mice was associated with an increase in the components of the cytochrome P450 system (cytochrome P450 and cytochrome b5), whereas the activities of pulmonary antioxidant enzymes (superoxide dismutase, glutathione peroxidase, and glutathione reductase) were not significantly increased. These data suggest that the induction of the cytochrome P450 system may be important in promoting NO2 tolerance in those strains of mice in which the cytochrome P450 system is genetically inducible.

Topics: Animals; Antioxidants; Benzoflavones; beta-Naphthoflavone; Body Weight; Cytochrome P-450 Enzyme System; Enzyme Induction; Female; Flavonoids; Lipid Peroxides; Lung; Malondialdehyde; Mice; Mice, Inbred C57BL; Mice, Inbred DBA; Nitrogen Dioxide; Pulmonary Edema; Species Specificity

The effects of food restriction or 20 ppm NO2 exposure on humoral immunity were investigated in normal and adrenalectomized C57Bl/6 mice. The thymic and splenic weights of sham-operated mice were similarly diminished after 4 days of NO2 exposure or 4 days of food depletion. The responses of corresponding adrenalectomized mice were less depressed. Undernutrition induced lymphoid organ involution and corticosteroids were partly involved. Plaque-forming cells (PFC) per spleen and per 10(6) cells were markedly depressed after 4 days of NO2 exposure, but less so after food deprivation. The same significant suppression of PFC was observed in adrenalectomized groups. Depression of humoral immunity was independent of stress-induced endogenous steroids. Moreover, NO2 had a specific effect on humoral immunodepression, food restriction being an associated factor.

Topics: Animals; Antibody Formation; Body Weight; Corticosterone; Female; Food Deprivation; Mice; Mice, Inbred C57BL; Nitrogen Dioxide; Organ Size; Spleen; Stress, Physiological; Thymus Gland

Chlorphentermine HCl (CP) was used to induce preexisting alveolar alterations resembling a pulmonary lipidosis in mice to study these effects on the severity and duration of nitrogen dioxide (NO2) toxicity. Results indicated that a daily dose of 120 mg/kg for 14 days produced consistent histopathologic changes characterized by an accumulation of large foamy macrophages. Male Swiss-Webster mice were divided into a control and three treatment groups. Group 1 received 120 mg/kg CP po daily for 2 weeks followed by exposure to air for 48 hr. Group 2 received 20 ppm NO2 for 48 hr via whole-body inhalation, and group 3 received 120 mg/kg CP daily for 2 weeks followed by 20 ppm NO2 for 48 hr. The fourth group served as a nontreated control and received water in place of CP and air in place of NO2. All groups were compared by morphologic evaluation of pulmonary tissues at the light and electron microscopic levels at Days 0, 1, 3, 5, and 7 after the 48-hr exposure to air or NO2. In a second experiment using the same treatment groups, thin-section light microscopy was used to count the number of type I and type II cells and macrophages. NO2 exposure alone caused deaths in 20.8 and 18.5% of the mice in the two studies, but no deaths were seen in the combination groups from both experiments. Histopathologic evaluation showed a typical cellular response to the NO2 exposure, but differences were noted between the two groups receiving NO2 on this treatment. There was increased type II cell hyperplasia and terminal bronchiolitis on Days 0 and 1 but less on Days 3 to 7 in the combination group compared to the NO2 alone group. CP treatment prior to NO2 exposure caused less terminal bronchiolar epithelial hyperplasia and less pulmonary edema than was seen in the NO2 along group. The CP treatment appeared to protect against the lethal effects of NO2 at the concentration and time of exposure used and altered the cellular repair mechanism that occurs in response to NO2 toxicity. CP treatment prior to NO2 exposure caused significantly less loss of type I cells and less increase in type II cells due to NO2 damage. The combination treatment also caused an increase in macrophages greater than that seen in either individual treatment, and this number remained increased through 5 days post-NO2 exposure, whereas the NO2 alone caused a steady increase in macrophages following the exposure until Day 3.(ABSTRACT TRUNCATED AT 400 WORDS)

Topics: Animals; Body Weight; Cell Count; Chlorphentermine; Hyperplasia; Lipidoses; Lung; Macrophages; Male; Mice; Microscopy, Electron; Nitrogen Dioxide; Phentermine

The natural resistance of nonimmunized C57Bl/6 mice to an intraperitoneal Klebsiella pneumoniae challenge was not significantly affected by prior continuous exposure to 20 ppm NO2 for 4 days. In contrast, the acquired resistance of mice immunized just before and infected just after NO2 exposure was seriously impaired. This could not be explained by the loss of appetite (about 30%) observed in NO2 treated mice, for neither the natural nor acquired resistance of control air exposed mice given approximately 70% ad libitum food and water were significantly modified.

Topics: Animals; Body Weight; Drinking; Eating; Female; Immune Tolerance; Immunization; Klebsiella Infections; Klebsiella pneumoniae; Mice; Mice, Inbred C57BL; Nitrogen Dioxide

This study assessed the relationship between nitrogen dioxide inhalation and the development of pulmonary emphysema and investigated how the severity of preexisting emphysema brought about by protease (elastase) instillation into the lung may be augmented by a subchronic exposure to a relatively high concentration of nitrogen dioxide. Lungs of adult Fischer-344 rats were evaluated for emphysematous changes after (1) a single intratracheal instillation of elastase (E), (2) a 25-d exposure to 35 ppm nitrogen dioxide (NO2), and (3) elastase instillation followed by 25-d exposure to 35 ppm NO2 (E + NO2). Rats instilled with sterile normal saline and subsequently exposed to filtered air served as a control group (NS). Residual volumes (RV) of the NO2 and NS groups were virtually identical, whereas the RV of the E and E + NO2 lungs (2.3 and 2.3 ml, respectively) were significantly greater than those of the NS and NO2 lungs (1.3 and 1.4 ml, respectively). Directionally similar changes in the excised lung volumes and total lung capacities were obtained with the E and E + NO2 groups; NO2 alone, however, did not alter these volumetric parameters. No differences in arterial blood gases and pH values, minute ventilation, or breathing frequencies were found among the experimental groups. The mean linear intercept values (MLI) obtained with the NS and NO2 exposed lungs were essentially identical with average values of approximately 62 micron. This morphometric parameter was substantially increased in the E- and E + NO2-exposed lungs; no significant differences, however, were found between the MLI values obtained with the E and E + NO2 lungs (approximately 95 and approximately 97 micron, respectively). From these data, as well as histologic examinations of lung sections for evidence of emphysema, we conclude that (1) a subchronic, moderately high level of NO2 exposure does not produce an irreversible emphysematous lesion in the rat model and (2) exposure of rats to 35 ppm for 25 d after elastase instillation into the lungs does not potentiate protease-induced emphysema or bring about a progression in preexisting emphysema.

Topics: Animals; Blood Gas Analysis; Body Weight; Lung; Male; Nitrogen Dioxide; Organ Size; Pancreatic Elastase; Pulmonary Emphysema; Rats; Rats, Inbred F344; Respiratory Function Tests

The effects following 20 ppm NO2 exposure on humoral immunity were investigated in C57Bl/6 mice after 48, 72, and 96 h exposure. Both spleen plaque-forming cell (PFC) responses and serum hemagglutinins (HA) using sheep red blood cells (SRBC) as antigen were studied. Splenic and thymic weight and cellularity decreased on acute exposure to NO2. PFC were markedly depressed after 48 h exposure and continued to decrease as exposure time was lengthened. HA titers were also depressed. The same significant suppression of PFC and HA titers was observed in adrenalectomized mice after 96 h NO2 exposure. The depression of humoral immunity in NO2-exposed mice was independent of stress-induced endogenous steroids.

Topics: Adrenal Glands; Animals; Antibody Formation; Atmosphere Exposure Chambers; Body Weight; Female; Hemagglutination Tests; Immunity, Cellular; Mice; Mice, Inbred C57BL; Nitrogen Dioxide; Organ Size; Spleen; Thymus Gland; Viral Plaque Assay

Male Wistar rats were exposed continuously for 1 or 2 months to 3.5 ppm NO2. Levels of histamine and serotonin in lung, noradrenaline in hypothalamus, corticosterone and thyroxine in serum and catecholamines in the adrenals were estimated. No significant changes were observed in lung histamine and serotonin, serum corticosterone, or adrenal catecholamine levels; or in the weights of lung, spleen, adrenal glands, hypothalamus, liver and the whole body. The only significant change was a decrease in the concentration of hypothalamic noradrenaline after 2 months of exposure. The results suggest that prolonged exposure to 3.5 ppm NO2 does not result in changes in hormone levels, organ and body weights, and therefore does not precipitate pulmonary defensive reactions or non-specific stress response.

Topics: Adrenal Glands; Air Pollutants; Animals; Body Weight; Brain Chemistry; Hormones; Lung; Male; Nitrogen Dioxide; Organ Size; Rats; Rats, Inbred Strains; Time Factors

Topics: Administration, Inhalation; Adrenocorticotropic Hormone; Animals; Body Weight; Corticosterone; Histamine; Lung; Male; Nitrogen Dioxide; Organ Size; Rats; Rats, Inbred Strains; Time Factors

The effect of short-term intake of LiCl in drinking fluid on NO2 toxicity was studied in mice as a function of mortality and of specific activities of mouse liver alcohol dehydrogenase (L-ADH) and aldehyde dehydrogenases (L-ALDH). Pretreatment with LiCl for 10 days decreased mortality in mice exposed to 60 to 70 PPM NO2 for 6 hr compared to controls. Pretreatment with LiCl for 10 days under continued exposure to 5 PPM NO2 resulted in a decrease in liver weight compared to control. Lithium treated mice exposed to NO2 showed less gain in body weight than the controls treated with LiCl and exposed to air. The latter group showed an induction of mitochondrial but not cytoplasmic L-ALDH and the NO2 exposure did not alter endogenous L-ALDH from corresponding controls. This induction of mitochondrial ALDH was associated with an increase in both Vmax and the apparent Km. Exposure to NO2 for 10 consecutive days resulted in inhibition of cytoplasmic L-ALDH. The data suggest that Li+ antagonized NO2 toxicity. A possible mechanism for reduction of NO2 toxicity by LiCl may be due to Li+ action on stabilizing cell membranes and/or modifying intercellular pulmonary response to NO2 injury.

Topics: Acetaldehyde; Alcohol Dehydrogenase; Alcohol Oxidoreductases; Aldehyde Dehydrogenase; Animals; Body Weight; Ethanol; Female; Lithium; Liver; Male; Mice; Mitochondria, Liver; Nitrogen Dioxide; Organ Size; Rats; Rats, Inbred Strains

This study examined the relation between lipid peroxidation and the antioxidative protective system in lungs of rats exposed to low levels of nitrogen dioxide (NO2). JCL:male Wistar rats were exposed to 0, 0.04, 0.4, and 4 ppm NO2 for 9, 18, and 27 months. Lipid peroxidation measured by TBA method, increased significantly in the 4 ppm NO2 group of the 9-month exposure and in the 0.4 and 4 ppm NO2 groups of the 18-month exposure. The activity of glutathione peroxidase measured with hydrogen peroxide as substrate decreased significantly in the 4 ppm NO2 group of the 9-month exposure and in the 0.4 and 4 ppm NO2 groups of the 18-month exposure. Furthermore, the activities of two glutathione S-transferases, aryl and aralkyl S-transferase, also decreased in the 0.4 and 4 ppm NO2 groups of the 18-month exposure, but not in any groups of the 9-month exposure. The activity of glutathione peroxidase measured with cumene hydroperoxide as substrate did not show any significant changes in any NO2 group. The activities of glucose-6-phosphate dehydrogenase and glutathione reductase were significantly higher than those in the control group for the 9-month exposure. In the 18-month exposure, however, they showed a tendency to return to control level. The activities of superoxide dismutase and disulfide reductase upon NO2 exposure for 9 and 18 months were not different from control values. To confirm that lipid peroxidation was increased with greater NO2 concentrations and exposure times, ethane and pentane exhalation in breath as an index of lipid peroxidation was examined. Ethane exhalation increased significantly following 0.04, 0.4, and 4 ppm NO2 exposure for 9 and 18 months. Furthermore, ethane formation of rats exposed to 0.04 and 0.4 ppm NO2 for 27 months also increased to twice the control level. On the other hand, after exposure to 4 ppm NO2 for 27 months, ethane levels returned to control level. Pentane formation increased significantly only in the 0.04 and 0.4 ppm groups in the 18-month exposure. Ethane exhalation in rats exposed to 0.04, 0.12, and 0.4 ppm NO2 for 9 and 18 months was similar. These results suggested that the antioxidative protective ability was decreased with prolonged exposure, while formation of cytotoxic lipid peroxides was increased.(ABSTRACT TRUNCATED AT 400 WORDS)

Topics: Animals; Body Weight; Lipid Peroxides; Lung; Male; Nitrogen Dioxide; Organ Size; Oxidation-Reduction; Rats; Rats, Inbred Strains; Time Factors

Morphometric and morphologic methods have been used to evaluate changes in rat lungs caused by the inhalation of a variety of oxidants. Exposure to 100% oxygen causes diffuse pulmonary injury and leads to death after 66-72 h of exposure. The primary insult leading to death in rats exposed to hyperoxia is injury to pulmonary capillary endothelium. Sublethal exposure to hyperoxia was found to cause diffuse injury to all major components of the alveolar septum and was associated with destruction of approximately 50% of the pulmonary capillary endothelial cells. A corresponding decrease in pulmonary capillary surface area and capillary lumen volume also occurred. Exposure to ozone and to nitrogen dioxide in low concentrations did not cause a diffuse injury throughout the alveolar region of the lung, but rather led predominantly to structural alterations in terminal bronchioles and in their adjacent alveoli. Morphometric evaluation of animals exposed to 0.25 ppm ozone and to 2 ppm NO2 demonstrated quantitatively and qualitatively similar lesions. These lesions primarily involve injury and remodelling of the alveolar epithelium. These changes in the alveolar epithelium were also associated with the recruitment of increased numbers of alveolar macrophages to the proximal alveolar region. The different types of lung injury caused by various oxidants are most likely to be related to differences in their reactivity with tissue components and to differences in concentration, distribution, and diffusion characteristics of the oxidant gases.

Topics: Animals; Atmosphere Exposure Chambers; Body Weight; Lung; Male; Nitrogen Dioxide; Oxygen; Ozone; Pulmonary Alveoli; Rats; Rats, Inbred F344

In vivo exposure of rats to 10 ppm nitrogen dioxide (NO2) for 6 h caused approx. 5-fold increase in the content of cyclic GMP in lung tissue. This increased cyclic GMP level lasted up to 24 h but returned to the normal level within 2 days, even when the NO2 exposure continued. This increase in the content of cyclic GMP of lung tissue by NO2 exposure was observed in both young and aged rats. There were no statistically significant changes in the content of cyclic AMP in lung tissue.

Topics: Animals; Body Weight; Cyclic GMP; Lung; Male; Nitrogen Dioxide; Organ Size; Rats; Rats, Inbred Strains; Time Factors

Topics: Animals; Antioxidants; Body Weight; Glutathione Peroxidase; Glutathione Transferase; Lipid Peroxides; Lung; Male; Nitrogen Dioxide; Rats; Rats, Inbred Strains; Superoxide Dismutase; Time Factors

Topics: Animals; Antioxidants; Body Weight; Diet; DNA; Lipid Metabolism; Lung; Lung Diseases; Nitrogen Dioxide; Organ Size; Proteins; Rats; Rats, Inbred Strains; Vitamin E

In order to examine the effects of NO2 on the fatty acid content of the lung and liver phospholipids, the phospholipid fractions of rats exposed to 20 ppm NO2 for 20 and 40 h were extracted and analyzed using gas chromatography. Among the ftty acid species in the lung, the relative amount of palmitic acid, palmitoleic acid and linoleic acid increased significantly, whereas myristic acid, stearic acid and oleic acid decresed significantly after exposure to NO2. These changes in the composition of fatty acids are discussed in comparison with the results of acute, subacute and chronic exposure to NO2 reported by other workers. In the case of the fatty acid species in the liver, a significant increase for stearic acid and arachidonic acid and a decrease in oleic acid were observed.

Topics: Animals; Body Weight; Fatty Acids; Female; Liver; Lung; Nitrogen Dioxide; Organ Size; Phospholipids; Rats

Rats of similar age and size were exposed continuously to nitrogen dioxide (NO2) at a concentration of about 15 ppm in air for 1, 2, 3, and 4 wk and 2, 3, 4, 5, 7, 13, 15, and 17 months. Large increases in lung volume and lesions of the small airways and their epithelium and that of adjacent alveoli developed. The lesions in the terminal bronchioles involved hypersecretion and asggregation of cellular debris and free cells in their lumena. A calibrated grid fitted to an eyepiece was used to measure the diameters of all patent bronchioles at the proximal point of the first alveolar "break" in the respiratory bronchiole. The terminal bronchioles and their short respiratory bronchioles inthe NO2-exposed animals developed stenosis, which increased with time. The maximum change, occurring after 17 months of exposure, was a 45.6% reduction in bronchiolar diameter. Over-all constriction was underestimated because nonpatent sections of bronchioles were excluded The ratio of lung volume to bronchiolar diameter in exposed animals also increased with time as a result of the rising volume and the falling bronchiolar diameter. Probable are discussed.

Topics: Animals; Body Weight; Bronchi; Constriction, Pathologic; Lung; Lung Volume Measurements; Male; Nitrogen Dioxide; Organ Size; Pulmonary Emphysema; Pulmonary Ventilation; Rats

Dietary vitamin E affects the susceptibility of mice and rats to ozone and nitrogen dioxide, suggesting a free radical mechanism of toxicity. Conventional peroxidation does not completely explain the effects of alterations of lung fatty acid composition on both nitrogen dioxide and ozone toxicity. A new scheme is proposed based on the cyclization of beta, gamma-allylic peroxyl free radicals to monocyclic and bicyclic peroxides to explain the relationship between diet and toxicity. Similar results are likely with other toxicants producing peroxidation as a mechanism of toxicity. Such cyclic peroxides may mimic or interfere with the prostaglandin system. Several chronic diseases may be exacerbated through such a subtle toxic mechanism. The level of vitamin E needed for protection against peroxidation toxicity may be much greater than the present U. S. dietary intake.

Topics: Air Pollutants; Animals; Body Weight; Environmental Pollutants; Fatty Acids; Free Radicals; Lung; Mice; Nitrogen Dioxide; Nutritional Physiological Phenomena; Ozone; Rats; Vitamin E

The effect of dietary vitamin A and NO2 exposure on the hamster lung was evaluated by histopathology, electron microscopy, and thymidine uptake studies. Hamsters were maintained on deficient (0 micrograms), adequate (100 micrograms), and high (200 micrograms) dose levels of vitamin A while being exposed repeatedly to 10 ppm of NO2 for 5 hours once a week over an 8-week period. Hamsters of the deficient group exhibited clinical and morphologic changes characteristic of vitamin A deficiency. Animals maintained on adequate and high dose levels of vitamin A were not affected by vitamin A deficiency. Hypertrophy and hyperplasia of the epithelial cells of the terminal bronchiolar alveolar region of lungs of adequately and highly dosed animals were greater than those observed in the deficient animals, when NO2 exposure was given. However, the extent of the lesions observed in all three groups was less than that seen in normal hamsters given a single, 5-hour NO2 exposure. Ultrastructural changes observed in vitamin A-deficient hamsters exposed to NO2 were hypertrophy and hyperplasia of bronchiolar epithelial cells, diffuse loss of cilia, membrane damage, and mitochondrial damage manifested by calcium deposition. Tritiated thymidine uptake studies of lungs of animals exposed repeatedly revealed a rather erratic cell renewal pattern following NO2 exposure in comparison to the group of animals exposed singly.

Topics: Animals; Blood Cell Count; Body Weight; Cricetinae; Diet; Dose-Response Relationship, Drug; Environmental Exposure; Female; Hypertrophy; Lung; Nitrogen Dioxide; Organ Specificity; Pregnancy; Vitamin A; Vitamin A Deficiency

Male Wistar rats were continuously exposed to NO2 (14.4 ppm), SO2 (46.5 ppm) and to a mixture of both gases and their effect on lung microsomal aryl hydrocarbon (benzo(a)pyrene) hydroxylase (AHH) activity was determined. The pre-exposed animals were administered methylcholanthrene (MC) to investigate the exposure effect on enzyme inducibility and pattern of B(a)P metabolites. NO2 significantly increased AHH activity but no marked change was noted with SO2. Induction of AHH by MC was markedly inhibited by SO2, only slightly by mixture of NO2-SO2 but not with NO2 alone.

Topics: Animals; Aryl Hydrocarbon Hydroxylases; Benzopyrene Hydroxylase; Body Weight; Lung; Male; Microsomes; Nitrogen Dioxide; Rats; Sulfur Dioxide; Time Factors

Hamsters exposed to 10 ppm NO2 for 5 hr once a week for 4 weeks while undergoing acute vitamin A deficiency showed much reduced epithelial cell regeneration in the terminal bronchioles. Quantitative analysis done by autoradiography and scintillation counting from lung tissues indicates much reduced cell kinetics occurring in terminal bronchiolar alveolar region. Alveolar necrosis was often observed and no type II cell reversion occurred. Virus particles were found within the alveolar epithelial plasma membrane.

Topics: Animals; Body Weight; Cricetinae; DNA; Nitrogen Dioxide; Pulmonary Alveoli; Viruses; Vitamin A Deficiency

Groups of rats were fed diets containing supplemented adequate, or deficient amounts of alpha-tocopherol. Some rats from each group were exposed for 2 h to high-level concentrations of nitrogen dioxide in their breathing air. A comparison of wet and dry lung weights did not indicate that exposure of the gas was a cause of edema. Proportion of lung weight to total body weight was increased in all animals with the lipid content diminishing according to the amount of dietary apha-tocopherol available. Dietary intake of the vitamin did not seem to protect the lipid content of lungs of the supplemented dietary group from oxidation. No difference in total peroxides was noted between any of the groups. Inflation and deflation compliance measurements were greater for both exposed and non-exposed supplemented animals when compared to the adequate and deficient groups.

Topics: Animals; Body Weight; Diet; Environmental Exposure; Lipid Metabolism; Lung; Lung Compliance; Male; Nitrogen Dioxide; Organ Size; Oxidation-Reduction; Rats; Vitamin E

Topics: Age Factors; Animals; Animals, Newborn; Body Weight; Environment, Controlled; Environmental Exposure; Environmental Pollutants; Female; Lung; Maternal-Fetal Exchange; Nitrogen Dioxide; Pregnancy; Pregnancy, Animal; Pulmonary Alveoli; Rats; Time Factors

Topics: Animals; Blood Cell Count; Body Weight; Carbon Monoxide; Dogs; Drug Synergism; Environmental Exposure; Female; Heart; Hemoglobinometry; Kidney; Lung; Lung Diseases; Nitrogen Dioxide; Organ Size; Pulmonary Diffusing Capacity; Respiratory Function Tests; Sulfur Dioxide; Sulfuric Acids; Time Factors

Topics: Air Pollution; Animals; Body Weight; Environmental Exposure; Female; Gases; Lung; Mice; Nitrogen Dioxide; Orthomyxoviridae Infections; Time Factors

Topics: Air Pollution; Airway Resistance; Analysis of Variance; Animals; Body Weight; Computers; Female; Lung Compliance; Macaca; Male; Methods; Nitrogen Dioxide; Respiration; Respiratory Function Tests; Spirometry; Statistics as Topic; Sulfur Dioxide; Time Factors

Topics: Agricultural Workers' Diseases; Animal Diseases; Animals; Body Weight; Carbon Dioxide; Diagnosis, Differential; Gases; Heart; Housing; Humans; Intestines; Kidney; Liver; Lung; Nitric Oxide; Nitrogen Dioxide; Organ Size; Pathology; Poisoning; Species Specificity; Spectrum Analysis; Spleen; Swine; Swine Diseases

Topics: Air Pollution; Animals; Body Weight; Carbon Monoxide; Diffusion; Dogs; Environmental Exposure; Lung Compliance; Methods; Nitric Oxide; Nitrogen Dioxide; Ozone; Respiration; Respiratory Function Tests; Sulfur Dioxide; Time Factors; Vehicle Emissions

Topics: Aging; Animals; Body Weight; Bronchi; Elastic Tissue; Lung Diseases; Nitrogen Dioxide; Organ Size; Pulmonary Alveoli; Pulmonary Fibrosis; Rats; Staining and Labeling; Time Factors

Topics: Animals; Animals, Newborn; Body Weight; Injections, Intraperitoneal; Mice; Nitrogen Dioxide; Organ Size; Pulmonary Edema; Rats; Thiourea

Topics: Animals; Body Weight; Bronchi; Environmental Exposure; Lung; Lung Diseases; Microscopy, Electron; Nitrogen Dioxide; Organ Size; Rats; Respiration

Topics: Animals; Antibody Formation; Body Weight; Environmental Exposure; Female; Hematocrit; Isoenzymes; Klebsiella Infections; L-Lactate Dehydrogenase; Leukocyte Count; Mice; Nitrogen Dioxide; Phagocytosis; Pneumonia; Time Factors

Topics: Animals; Body Weight; Corneal Opacity; Dogs; Guinea Pigs; Haplorhini; Nitrogen Dioxide; Pulmonary Edema; Rabbits; Rats; Respiratory System; Species Specificity

Topics: Biochemical Phenomena; Biochemistry; Blood Chemical Analysis; Body Weight; Cricetinae; Dogs; Guinea Pigs; Lung Neoplasms; Mice; Neoplasms; Neoplasms, Experimental; Nitrogen Dioxide; Rabbits; Rats; Research; Respiratory Function Tests; Toxicology