ascorbic-acid and naphthalene

Naphthalene, a widely used industrial and household chemical, has rarely been an agent of poisoning worldwide. Severe haemolysis from naphthalene poisoning is rare and can be a challenge to clinicians. We report a 22-year-old female, who accidentally ingested naphthalene mixed coconut oil and got admitted with recurrent vomiting, headache and passage of dark urine. Severe intravascular haemolysis with hypotension and neutrophilic leukocytosis was detected. She was treated with red blood cell transfusions, intravenous saline infusion and ascorbic acid.

Topics: Administration, Oral; Anemia, Hemolytic; Ascorbic Acid; Coconut Oil; Erythrocyte Transfusion; Female; Glucose; Hemoglobinuria; Hemolysis; Humans; Hypotension; Infusions, Intravenous; Methemoglobinemia; Naphthalenes; Plant Oils; Poisoning; Severity of Illness Index; Treatment Outcome; Young Adult

Plant contamination by polycyclic aromatic hydrocarbons (PAHs) is crucial to food safety and human health. Enzyme inhibitors are commonly utilized in agriculture to control plant metabolism of organic components. This study revealed that the enzyme inhibitor ascorbic acid (AA) significantly reduced the activities of peroxidase (POD) and polyphenol oxidase (PPO), thus enhancing the potential risks of PAH contamination in tall fescue (Festuca arundinacea Schreb.). POD and PPO enzymes in vitro effectively decomposed naphthalene (NAP), phenanthrene (PHE) and anthracene (ANT). The presence of AA reduced POD and PPO activities in plants, and thus was likely responsible for enhanced PAH accumulation in tall fescue. This conclusion is supported by the significantly enhanced uptake of PHE in plants in the presence of AA, and the positive correlation between enzyme inhibition efficiencies and the rates of metabolism of PHE in tall fescue roots. This study provides a new perspective, that the common application of enzyme inhibitors in agricultural production could increase the accumulation of organic contaminants in plants, hence enhancing risks to food safety and quality.

Topics: Anthracenes; Ascorbic Acid; Biodegradation, Environmental; Biological Transport; Catechol Oxidase; Enzyme Assays; Enzyme Inhibitors; Festuca; Kinetics; Naphthalenes; Peroxidase; Phenanthrenes; Plant Proteins; Plant Roots; Polycyclic Aromatic Hydrocarbons; Soil Pollutants

Ingestional naphthalene mothball poisoning leading to prolonged haemolysis and methaemoglobinaemia can present with diagnostic and therapeutic challenges. A 19-year-old woman ingested 12 mothballs, and presented two days later with haemolysis and methaemoglobinaemia. She was treated with red blood cell transfusions, intravenous methylene blue, N-acetylcysteine and ascorbic acid. Continuous venovenous haemofiltration was conducted for 45 hours. Haemolysis with anaemia and methaemoglobinaemia persisted even after five days post-ingestion. Clinical and biochemical parameters improved. We describe a case of ingestional naphthalene poisoning with a good outcome after treatment.

Topics: Acetylcysteine; Adult; Anemia, Hemolytic; Ascorbic Acid; Erythrocyte Transfusion; Female; Hemolysis; Humans; Methemoglobinemia; Methylene Blue; Naphthalenes; Poisoning; Suicide, Attempted; Time Factors; Treatment Outcome

Alcoholic extract of the marine algae Chlorella vulgaris was examined for its free radical scavenging effect with reference to naphthalene-induced lipid peroxidation in serum, liver, and kidney of rats. Initially, upon naphthalene intoxication (435 mg/kg body weight, intraperitoneally), the lipid peroxidation activity increased significantly (P < 0.001), and in contrast, the enzymic antioxidants (superoxide dismutase, catalase, glutathione peroxidase) and non-enzymic antioxidants (glutathione, ascorbic acid, and alpha-tocopherol) levels decreased remarkably. When the naphthalene stressed rats were treated with Chlorella vulgaris extract (70 mg/kg body weight, orally), the lipid peroxidation activity reduced significantly (P < 0.001) and the activities of both the enzymic and non-enzymic antioxidants increased reaching near control values. The minimum concentration (70 mg/l) of the extract that exhibited maximum (85%) free radical scavenging activity was chosen for the experimental study. The present results suggest that Chlorella vulgaris extract exerts its chemo-preventive effect by modulating the antioxidants status and lipid peroxidation during naphthalene intoxication.

Topics: Animals; Antioxidants; Ascorbic Acid; Catalase; Chlorella vulgaris; Free Radical Scavengers; Glutathione; Glutathione Peroxidase; Lipid Peroxidation; Male; Naphthalenes; Oxidative Stress; Plant Extracts; Rats; Rats, Wistar; Reactive Oxygen Species; Superoxide Dismutase; Thiobarbituric Acid Reactive Substances; Vitamin E

1,4-Dihydropyridines (DHPs) used in the treatment of cardiovascular diseases, are calcium channel antagonists and also antioxidant agents. These drugs are metabolized through cytochrome P(450) oxidative system, majority localized in the hepatic endoplasmic reticulum. Several lipophilic drugs generate oxidative stress to be metabolized by this cellular system. Thus, DHP antioxidant properties may prevent the oxidative stress associated with hepatic biotransformation of drugs. In this work, we tested the antioxidant capacity of several synthetic nitro-phenyl-DHPs. These compounds (I-IV) inhibited the microsomal lipid peroxidation, UDPGT oxidative activation and microsomal thiols oxidation; all phenomena induced by Fe(3+)/ascorbate, a generator system of oxygen free radicals. As the same manner, these compounds inhibited the oxygen consumption induced by Cu(2+)/ascorbate in the absence of microsomes. Furthermore, compound III (2,6-dimethyl-4-(4-nitrophenyl)-1,4-dihydropyridin-3,5-ethyl-dicarboxylate) and compound V (N-ethyl-2,6-dimethyl-4-(4-nitrophenyl)-1,4-dihydropyridin-3,5-methyl-dicarboxylate) inhibited the microsomal lipid peroxidation induced by Nitrofurantoin and naphthalene in the presence of NADPH. Oxidative stress induced on endoplasmic reticulum may alter the biotransformation of drugs, so, modifying their plasmatic concentrations and therapeutic effects. When drugs which are activated by biotransformation are administered together with antioxidant drugs, such as DHPs, oxidative stress induced in situ may be prevented.

Topics: Animals; Antioxidants; Ascorbic Acid; Dihydropyridines; Enzyme Activation; Glucuronosyltransferase; Lipid Peroxidation; Microsomes, Liver; Molecular Structure; NADP; Naphthalenes; Nitrofurantoin; Oxidation-Reduction; Oxygen Consumption; Rats; Sulfhydryl Compounds; UDP-Glucuronosyltransferase 1A9

The kinetics of reduction of the radical R*, 5-dimethylaminonaphthalene-1-sulfonyl-4-amino-2,2,6,6-tetramethyl-1-piperidine-oxyl by blood and its components were studied using the EPR technique. The results demonstrate that R* is adsorbed to the outer surface of the membrane and does not penetrate into the erythrocytes. A series of control experiments in PBS demonstrate that ascorbate is the only natural reducing agent that reacts with R*. The observed first order rate of disappearance of the nitroxide radical k, is: k(blood) > k(eryth) > k(plasma) and k(blood) approximately = k(eryth) + k(plasma). The results demonstrate that: a. The erythrocytes catalyze the reduction of R* by ascorbate. b. The rate of reduction of the radical is high though it does not penetrate the cells. c. In human erythrocytes there is an efficient electron transfer route through the cell membrane. d. The study points out that R* is a suitable spin label for measuring the reduction kinetics and antioxidant capacity in blood as expressed by reduction by ascorbate.

Topics: Antioxidants; Ascorbic Acid; Blood Chemical Analysis; Cell Membrane; Cyclic N-Oxides; Dansyl Compounds; Dose-Response Relationship, Drug; Electron Spin Resonance Spectroscopy; Erythrocytes; Ferrocyanides; Hematocrit; Humans; Kinetics; Magnetics; Naphthalenes; Nitric Oxide; Piperidines; Spin Labels; Time Factors

Chemically reactive epoxide metabolites have been implicated in various forms of drug and chemical toxicity. Naphthalene, which is metabolized to a 1,2-epoxide, has been used as a model compound in this study in order to investigate the effects of perturbation of detoxication mechanisms on the in vitro toxicity of epoxides in the presence of human liver microsomes. Naphthalene (100 microM) was metabolized to cytotoxic, protein-reactive and stable, but not genotoxic, metabolites by human liver microsomes. The metabolism-dependent cytotoxicity and covalent binding to protein of naphthalene were significantly higher in the presence of phenobarbitone-induced mouse liver microsomes than with human liver microsomes. The ratio of trans-1,2-dihydrodiol to 1-naphthol was 8.6 and 0.4 with the human and the induced mouse microsomes, respectively. The metabolism-dependent toxicity of naphthalene toward human peripheral mononuclear leucocytes was not affected by the glutathione transferase mu status of the co-incubated cells. Trichloropropene oxide (TCPO; 30 microM), an epoxide hydrolase inhibitor, increased the human liver microsomal-dependent cytotoxicity (19.6 +/- 0.9% vs 28.7 +/- 1.0%; P = 0.02) and covalent binding to protein (1.4 +/- 0.3% vs 2.8 +/- 0.2%; P = 0.03) of naphthalene (100 microM), and reversed the 1,2-dihydrodiol to 1-naphthol ratio from 6.6 (without TCPO) to 2.6, 0.6 and 0.1 at TCPO concentrations of 30, 100 and 500 microM, respectively. Increasing the human liver microsomal protein concentration reduced the cytotoxicity of naphthalene, while increasing its covalent binding to protein and the formation of the 1,2-dihydrodiol metabolite. Co-incubation with glutathione (5 mM) reduced the cytotoxicity and covalent binding to protein of naphthalene by 68 and 64%, respectively. Covalent binding to protein was also inhibited by gestodene, while stable metabolite formation was reduced by gestodene (250 microM) and enoxacin (250 microM). The study demonstrates that human liver cytochrome P450 enzymes metabolize naphthalene to a cytotoxic and protein-reactive, but not genotoxic, metabolite which is probably an epoxide. This is rapidly detoxified by microsomal epoxide hydrolase, the efficiency of which can be readily determined by measurement of the ratio of the stable metabolites, naphthalene 1,2-dihydrodiol and 1-naphthol.

Topics: Adult; Animals; Ascorbic Acid; Base Sequence; Biotransformation; Cytochrome P-450 Enzyme Inhibitors; Glutathione; Humans; Male; Mice; Microsomes, Liver; Mitotic Index; Molecular Sequence Data; Monocytes; NADP; Naphthalenes; Phenobarbital; Polymerase Chain Reaction; Sister Chromatid Exchange; Trichloroepoxypropane

Topics: Animals; Ascorbic Acid; Carbohydrate Metabolism; Naphthalenes; Rats; Vitamins

Topics: Animals; Ascorbic Acid; Hexoses; Naphthalenes; Pentoses; Rats

Topics: Ascorbic Acid; Flavonoids; Hemostatics; Naphthalenes; Sulfonic Acids; Vitamins

Topics: Ascorbic Acid; Blood Coagulation; Flavonoids; Hemostatics; Hydrocarbons, Aromatic; Naphthalenes; Thrombelastography; Vitamins

Topics: Animals; Ascorbic Acid; Blood; Cattle; Cattle Diseases; Collagen; Naphthalenes; Poisoning; Skin; Vitamin A

Topics: Ascorbic Acid; Flavonoids; Hemoptysis; Humans; Naphthalenes; Vitamins

Topics: Ascorbic Acid; Flavonoids; Hemostasis; Hemostatics; Humans; Naphthalenes; Vitamins