ascorbic-acid and Poisoning

Ethyl alcohol (ethanol) is readily absorbed from all parts of the gastrointestinal tract due to its hydrophilic potential. The biological effects in humans refer to practically every organ and system. The basic enzyme involved in its oxidation is alcohol dehydrogenase. Another important metabolic pathway is the Microsomal Ethanol-Oxidizing System (MEOS). Toxic effect on basic cell functions is produced both by ethanol and acetic aldehyde, its oxidation product which accounts for most of the acute and delayed effects of ethanol toxicity. In acute ethanol intoxication's the CNS symptoms are the first to manifest. Ethanol affects the CNS functions mainly through stimulating opiate and benzodiazepine receptors and a number of neurotransmitters. However, the attempts to diminish the toxic effects of ethanol on CNS by blocking the affected receptors have proved to be ineffective. In acute poisoning a basic essential is to sustain vital functions by following the principles of intensive care. Each case of acute ethanol intoxication must be subject to neurological examination for possible cerebro-cranial traumas. The diagnostics and treatment procedures should take account of the possible symptoms: convulsions, respiratory and cardiac failure, hypoglycemia, hypothermia, and severe gastric dysfunction. Vital signs monitoring and control of acid-base and water-electrolyte balance are a must. The toxic properties of ethanol metabolites can be particularly hazardous to patients treated with disulfiram. The patients who develop "antabuse response" should be given immediately iron and vitamin C intravenously.

Topics: Acute Disease; Ascorbic Acid; Ethanol; Humans; Injections, Intravenous; Iron; Poisoning

Topics: Animal Feed; Animals; Anticholesteremic Agents; Antitoxins; Ascorbic Acid; Azo Compounds; Carbohydrates; Cellulose; Cyclamates; Diet; Dietary Carbohydrates; Heptoses; Humans; Medicago sativa; Methyl Ethers; Mice; Pectins; Plants; Poaceae; Poisoning; Polysaccharides; Polysorbates; Rats; Sodium; Surface-Active Agents; Triazines

To investigate whether acute dipterex poisoning (ADP) may cause oxidative stress and free radical damage in the bodies of acute dipterex poisoning patients (ADPPs), and to explore the mechanisms by which ADP may cause oxidative stress and free radical damage.. Fifty ADPPs and fifty healthy adult volunteers (HAVs) whose ages, gender and others were matched with the ADPPs were enrolled in a randomized controlled study, in which concentrations of nitric oxide (NO), vitamin C (VC), vitamin E (VE) and beta-carotene (beta-CAR) in plasma as well as concentration of lipoperoxide (LPO), and activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX) and acetylcholinesterase (AChE) in erythrocytes were determined by spectrophotometric analytical methods.. Compared with the average values of experimental parameters in the HAVs group, the average values of plasma NO and erythrocyte LPO in the ADPPs group were significantly increased (P<0.0001), while those of plasma VC, VE and beta-CAR as well as erythrocyte SOD, CAT, GPX and AChE in the ADPPs group were significantly decreased (P<0.0001). Bivariate correlation analysis and partial correlation analysis suggested that when NO and LPO values were increased, and VC, VE, beta-CAR, SOD, CAT and GPX values were decreased in the ADPPs, AChE value was decreased gradually in the ADPPs (P<0.001-0.0001). Reliability analysis of experimental parameters reflecting oxidative stress and free radical damage in the ADPPs showed that the reliability coefficient (8 items) alpha=0.6909, and the standardized item alpha=0.8574.. The findings in the present study suggest that ADP can cause oxidative stress and free radical damage, and inhibit markedly erythrocyte acetylcholinesterase activity in ADPPs.

Topics: Acetylcholinesterase; Adolescent; Adult; Ascorbic Acid; beta Carotene; Case-Control Studies; Catalase; China; Cholinesterase Inhibitors; Erythrocytes; Female; Free Radicals; Glutathione Peroxidase; Humans; Insecticides; Lipid Peroxides; Male; Nitric Oxide; Oxidative Stress; Poisoning; Random Allocation; Superoxide Dismutase; Trichlorfon; Vitamin E

To study relationship between acute dipterex poisoning and oxidative stress and free radical damage.. Eighty-two patients with acute dipterex poisoning (ADPP) and ninety-two healthy adult volunteers (HAV) were enrolled in the study with randomized controlled trial design. Plasma levels of vitamin C (VC) and vitamin E (VE), as well as level of lipoperoxide (LPO) and activities of superoxide dismutase (SOD) and acetylcholinesterase (AChE) in the red blood cells (RBC), were determined by spectrophotometry.. Levels of VC and VE, and activities of SOD and AChE were (37.35 +/- 9.98) micromol/L, (16.57 +/- 4.54) micromol/L, (1 785 +/- 154) U/g Hb and (213.1 +/- 57.6) U/g Hb, respectively, in the ADPP group, significantly lower than those in the HAV group, (55.34 +/- 15.98) micromol/L, (25.66 +/- 7.24) micromol/L, (2 124 +/- 185) U/g Hb and (305.3 +/- 83.6) U/g Hb, respectively. Plasma level of LPO was (35.20 +/- 5.29) nmol/g Hb in the ADPP group, significantly higher than that in the HAV group, (27.87 +/- 4.66) nmol/g Hb. Partial correlation analysis suggested that there existed negative correlation between activity of AChE in the RBC and plasma level of LPO (r = -0.274, P = 0.013) and positive correlation between activity of AChE in the RBC and plasma levels of VC and VE, and activity of SOD in the RBC (r = 0.333, P = 0.002, r = 0.269, P = 0.015 and r = 0.248, P = 0.026, respectively) in the ADPP, adjusted for age. Coefficient of reliability alpha was 0.682 (P < 0.001), with a standardized alpha of 0.868 (P < 0.001).. There exist severe oxidative stress and free radical damage in patients with acute dipterex poisoning.

Topics: Acetylcholinesterase; Adolescent; Adult; Ascorbic Acid; Erythrocytes; Female; Free Radicals; Humans; Lipid Peroxidation; Male; Oxidative Stress; Oxygen; Poisoning; Superoxide Dismutase; Trichlorfon; Vitamin E

This study was conducted to evaluate whether vitamin C (VC) was associated with total antioxidant status (TAS) in human plasma and to determine the usefulness of VC on TAS in the treatment of patients with paraquat poisoning. VC and TAS were measured in 56 healthy subjects. Then, various concentrations (1-100 mg/dl) of VC in pooled plasma from 10 volunteers were constructed in vitro and TAS was measured. The VC and TAS were measured in vivo at 0.5, 1, 2, 3, 5, 7, 9, and 11 h after injection of VC (50 mg/kg) in seven volunteers and pharmacokinetic data were calculated. Finally, various amounts of VC (100, 500, 1000, 3000 mg/day, and 3000 mg/8 h) were given to 10 paraquat-poisoned patients for 5 consecutive days, and blood was taken for TAS 1 h after each injection. The means (SD) of VC and TAS in healthy subjects were 2.22 (0.16) mmol/l and 0.48 (0.10) mg/dl, respectively. Positive correlation between VC and TAS was observed in both in vitro and in healthy volunteers. The pharmacokinetic results in vivo were as follows: means (SD) of distribution volume, area under curve, plasma clearance, half life, C(max), and T(max) were 32.0 (4.4) l, 36.4 (11.3) mg h/dl, 2.13 (1.36) l/h, 10.2 (7.8) h, 17.1 (7.1) mg/dl, and 0.64 (0.24) h, respectively. Estimated loading and maintenance doses of VC were 2278 mg and 146 mg/h, respectively. The means of TAS were increased over 5 consecutive days as 2.26, 2.76, 2.81, 3.18, and 3.58 mmol/l in paraquat patients. All patients were recovered within mean (SD) 21.2 (5.4) admission days. Our data suggested that VC was a significant antioxidant as TAS in human plasma and that increased TAS by high doses of VC could be useful as a free radical scavenger for paraquat poisoned patients.

Topics: Adult; Antioxidants; Ascorbic Acid; Blood Cell Count; Blood Pressure; Body Temperature; Female; Free Radical Scavengers; Heart Rate; Humans; Kidney Function Tests; Liver Function Tests; Male; Middle Aged; Paraquat; Poisoning

In 2008, self-poisoning with the herbicide propanil had a case-fatality of around 11% in Sri Lanka. A simple quantitative methaemoglobinemia bedside test was developed so that treatment could be titrated according to the methaemoglobin level.. To determine whether the new method influenced patient management and changed the case fatality of propanil self-poisoning.. The bedside test (using an inexpensive validated colour chart) was introduced in three hospitals (Anuradhapura, Polonnaruwa and Galle) in Sri Lanka from 2008. Junior ward staff were given a brief training on how to use the chart for quantitative estimation of methaemoglobin in patients with propanil poisoning and utilize the results in the context of the national treatment guidelines for propanil poisoning. It was taught that the bedside test should be done repeatedly from admission until it showed consistently low values of methaemoglobin. Treatment with the antidote methylene blue was suggested for patients whose methaemoglobin was greater than 20%. Limited clinical data on poisoning have been prospectively collected from these hospitals from 2003. The case-fatality and management before and after the change were compared with data up to December 2014.. The case-fatality decreased from (38/401) 9.5% to (8/262) 3.1% [difference: -6.4%, 95% CI: -10 to -3]. Methylene blue use increased from under 10% of patients before to 55% of patients after the intervention. More patients received repeat doses and infusions, and few received ascorbic acid and exchange transfusion.. The simple bedside test for methaemoglobinemia was readily adopted into routine practice and led to large changes in management. A substantial reduction in mortality from propanil poisoning occurred after this intervention.

Topics: Adult; Antidotes; Ascorbic Acid; Dose-Response Relationship, Drug; Female; Herbicides; Hospitalization; Humans; Male; Methemoglobin; Methemoglobinemia; Methylene Blue; Middle Aged; Poisoning; Propanil; Retrospective Studies; Sri Lanka; Young Adult

The study was designed to investigate the protective effect of esculin against pro-oxidant aflatoxin B1 (AFB1)-induced nephrotoxicity in mice. In this study toxicity was developed by oral administration of AFB1 at a dose of 66.60 μg/kg bw/day for 90 days in male Swiss albino mice. Esculin (150 mg/kg bw/0.2 ml/day) and standard compound ascorbic acid (300 mg/kg bw/0.2 ml/day) was given after 30 min of AFB1 administration for 90 days. Protective efficacy was assessed by measuring the levels of lipid peroxidation (LPO) and non-enzymatic antioxidants such as reduced glutathione (GSH) and also by measuring activities of enzymatic antioxidants such as glutathione peroxidase (GPX), glutathione-S-transferase (GST), glutathione reductase (GR), superoxide dismutase (SOD) and catalase (CAT) in kidney. Results were analysed at the 30(th), 60(th) and 90(th) day of the daily treatments, which showed a decrease in the level of LPO and an increase in the levels of enzymatic and non-enzymatic antioxidants. The protective effect of esculin was further proved by histopathological findings as it exhibited regenerative activities in mice renal tubules against AFB1-induced nephrotoxicity. The results obtained clearly demonstrate that the protective efficacy of esculin against pro-oxidant AFB1-induced nephrotoxicity in mice might be due to its antioxidants and free radical scavenging properties.

Topics: Administration, Oral; Aflatoxin B1; Animals; Antioxidants; Ascorbic Acid; Esculin; Histocytochemistry; Kidney; Lipid Peroxidation; Male; Mice; Poisoning

Megadose of vitamin C (MVC) has been proposed for an emergent treatment of acute paraquat (PQ) poisoning. However, the safety issue of this treatment protocol has not been evaluated. Here, we present the first evidence that vitamin C can promote aggravated production of hydroxyl radical (OH(•)) via interacting with preexisting PQ(+•)/H2O2 system in a nonmetal-catalyzed manner. This enhanced oxidative stress would therefore expect to cause more deleterious effect during acute PQ intoxication. To lend support to this possibility, we set out to attest the effects of MVC on a simulated, PQ-intoxicated, Madin-Darby canine kidney (MDCK) cell model. First, PQ alone could trigger oxidative-nitrosative stress (ONS) through robust generation of reactive oxygen species and nitric oxide (NO) that could induce apoptotic killing via promoting effective release of mitochondrial cytochrome c, an apoptogenic factor. The percentage of apoptosis for MDCK cells treated with 1.0 mM PQ for 24 h was 16.3 ± 13.0%. However, when MDCK cells were treated with a combination of PQ (1.0 mM) and MVC (20 mM) for 24 h, the severity of apoptotic killing was further exacerbated as reflected by a nearly 7-fold increase in the release of mitochondrial cytochrome c and the percentage of apoptotic cell population rose sharply to 90.7 ± 5.1%. These data indicate that MVC apparently exacerbates further killing rather than cytoprotection on this simulated, PQ-intoxicated MDCK cell model and suggest that the treatment of PQ poisoning using MVC protocol should be cautious.

Topics: Animals; Ascorbic Acid; Cells, Cultured; Dogs; Drug Synergism; Hydrogen Peroxide; Hydroxyl Radical; Madin Darby Canine Kidney Cells; Microscopy, Confocal; Nitric Oxide; Oxidative Stress; Paraquat; Poisoning; Reactive Oxygen Species

Topics: Acetylcysteine; Acute Kidney Injury; Adult; Ascorbic Acid; Charcoal; Chemical and Drug Induced Liver Injury; Combined Modality Therapy; Diuretics; Fatal Outcome; Furosemide; Gastric Lavage; Hemoperfusion; Humans; Immunosuppressive Agents; Male; Paraquat; Poisoning; Pulmonary Fibrosis; Respiration, Artificial; Respiratory Insufficiency; Rhabdomyolysis; Suicide, Attempted; Vitamin E

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

Paraquat (PQ) poisoning is an extremely difficult condition to manage clinically because of the lack of effective treatments. The purpose of this study was to assess the effect of high doses of vitamin C in combination with anti-inflammatory and immunosuppressant therapy in patients with PQ poisoning. The medical records of 134 patients who presented to the emergency department within 24 hours after PQ poisoning were reviewed retrospectively. The 57 patients presented between January 2004 and September 2005 were group 1; they received pulse therapy, which included cyclophosphamide and methylprednisolone, followed by the administration of dexamethasone over 2 weeks. The 77 patients that presented between October 2005 and January 2008 were group 2; they received the above-mentioned therapy and high-dose vitamin C for 2 weeks. There was no difference in the distribution of baseline variables between the 2 groups. However, group 2 showed a significant reduction in acute kidney injury related to PQ. Furthermore, a multivariate logistic regression analysis showed that the addition of vitamin C to the treatment was significantly associated with an increased survival of the patients. Larger trials will be needed to verify the effect of high-dose vitamin C on survival in patients with PQ poisoning.

Topics: Anti-Inflammatory Agents; Antioxidants; Ascorbic Acid; Cohort Studies; Dose-Response Relationship, Drug; Drug Therapy, Combination; Female; Hospitals, University; Humans; Immunosuppressive Agents; Logistic Models; Male; Medical Records; Middle Aged; Paraquat; Poisoning; Retrospective Studies; Suicide, Attempted; Treatment Outcome

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

Chlorpyrifos (CPF) is one of the most widely used organophosphorous insecticides in agriculture with its attendant adverse health outcomes. This study aimed at evaluating the effect of subchronic oral CPF administration on hematological and serum biochemical indices, and the possible ameliorating effect of vitamin C on the indices in mice. Thirty mice divided into 3 groups of 10 mice each were used for this study. Mice in group I (control) were dosed with vegetable oil, while those in group II were given CPF (21.3 mg/kg~ 1/5(th) LD(50)) only. Mice in group III were pretreated with vitamin C (100 mg/kg) prior to dosing with CPF 30 min later (Vitamin C + CPF-treated group). This regime was given to each group of mice three times a week for a period of ten weeks. During the study period, mice were examined for signs of toxicity, and weight of each mouse was measured every week. At the end of the study period, blood samples were collected from the mice and analyzed for packed cell volume (PCV), total red blood cell (RBC), white blood cell (WBC) and total protein (TP). Serum obtained from the blood was analyzed for Na( +, K+ and Cl-), urea, creatinine, alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP). The results showed that mice in the vitamin C + CPF-treated group exhibited milder signs of toxicity and significant increase in weight gain (p<0.01) compared to the CPF-treated group. No significant increase in weight in the CPF-treated group was observed compared to the control. There was a significant increase in PCV, RBC, Hb, TP and creatinine, but a significant decrease was obtained in WBC, ALT and AST in the CPF-treated group compared to the control. All the parameters with the exception of WBC, ALT and AST (which increased significantly), were significantly decreased in the vitamin C + CPF-treated group compared to CPF-treated group. ALP was significantly elevated in the CPF-treated group compared to both the control and vitamin C + CPF-treated group. No significant changes in urea and the measured electrolytes in all three groups, except a significant decrease in the concentration of Na(+) was observed in the CPF-treated group compared to the control. The study demonstrated that pretreatment of CPF-administered mice with vitamin C significantly altered some important hematological and serum biochemical parameters, revealing the protective action of the vitamin against some organ damage induced by CPF.

Topics: Animals; Antioxidants; Ascorbic Acid; Blood Proteins; Body Weight; Chemistry, Clinical; Chlorpyrifos; Drug Antagonism; Erythrocyte Indices; Female; Hematologic Tests; Insecticides; Leukocytes; Male; Mice; Poisoning

The 22 supersetnd Hohenheim Consensus Workshop took place in at the University of Stuttgart-Hohenheim. The subject of this conference was vitamin C and its role in the treatment of endothelial dysfunction. Scientists, who had published and reviewed scientific and regulatory papers on that topic were invited, among them basic researchers, toxicologists, clinicians and nutritionists. The participants were presented with eleven questions, which were discussed and answered at the workshop, with the aim of summarising the current state of knowledge. The explicatory text accompanying the short answers was produced and agreed on after the conference and was backed up by corresponding references. The therapeutic relevance of administration of the physiological antioxidant vitamin C in high parenteral doses in Endothelial Dependent Pathophysiological Conditions (EDPC) was discussed. Endothelial dysfunction is defined as including disturbed endothelial dependant relaxation of resistance vessels, breakdown of the microvascular endothelial barrier and/or loss of anti-adhesive function. It occurs in severe burn injury, intoxications, acute hyperglycemia, sepsis, trauma, and ischemic-reperfusion tissue injury and is induced by oxidative stress. Reduced plasma ascorbate levels are a hallmark of oxidative stress and occur in severe burns, sepsis, severe trauma, intoxication, chemotherapy/radiotherapy and organ transplantation. Vitamin C directly enhances the activity of nitric oxide synthase, the acyl CoA oxidase system and inhibits the actions of proinflammatory lipids. There is experimental evidence that parenteral high-dose vitamin C restores endothelial function in sepsis. In vitro, supraphysiological concentrations (> 1mM) of ascorbate restore nitric oxide bioavailability and endothelial function. Only parenterally, can enough vitamin C be administered to combat oxidative stress. There is no evidence that parenteral vitamin C exerts prooxidant effects in humans. Theoretical concerns in relation to competitive interactions between vitamin C and glucose cellular uptake are probably only relevant for oxidised vitamin C (dehydroascorbate).

Topics: Acute Disease; Acyl-CoA Oxidase; Ascorbic Acid; Burns; Endothelium, Vascular; Glucose; Heart Failure; Humans; Hyperglycemia; Infusions, Parenteral; Myocardial Ischemia; Nitric Oxide Synthase Type III; Oxidative Stress; Poisoning; Reperfusion Injury; Sepsis

Topics: 8-Hydroxy-2'-Deoxyguanosine; Acetylcysteine; Adolescent; Ascorbic Acid; beta 2-Microglobulin; Biomarkers; Charcoal; Chromium; Creatinine; Deoxyguanosine; DNA Damage; Female; Humans; Kidney Tubules, Proximal; Oxidation-Reduction; Poisoning; Potassium Dichromate; Retinol-Binding Proteins; Suicide, Attempted

Methidathion (MD) is one of the most widely used organophosphate insecticides (OPIs) for public health programmes and agricultural purposes. However it causes side effects such as liver disorders. We examined the ameliorating effects of a combination of vitamins E and C against MD induced liver toxicity in rats. MD was given orally with a single dose of 8 mg/kg body weight at 0 h. Vitamin E and vitamin C were injected 30 min after the treatment of MD at doses of 150 mg/kg body weight i.m. and 200 mg/kg body weight i.p., respectively. Liver tissue samples were taken 24 h after the MD administration. In MD treated group, some histopathological changes like infiltration with mononuclear cells at parenchymal tissue, sinusoidal dilatation, focal necrotic areas, granular degeneration and picnotic nuclei in the hepatocytes were observed. The severity of these lesions was reduced by administration of vitamins. It is concluded that MD caused liver damage and single-dose treatment with a combination therapy of vitamins E and C after the administration of MD can reduce the toxic effects of MD on liver tissue of rats.

Topics: Administration, Oral; Animals; Antioxidants; Ascorbic Acid; Dose-Response Relationship, Drug; Drug Interactions; Female; Insecticides; Liver; Organothiophosphorus Compounds; Poisoning; Rats; Rats, Wistar; Vitamin E

Propanil pesticide poisoning can produce methemoglobinemia, tissue hypoxia, and depression of central nervous system and respiratory system. It has been recorded only rarely worldwide and most current poison texts consider propanil to be of low toxicity. However, propanil self-poisoning is a significant clinical problem in parts of Sri Lanka and an occasional cause of death.. To report the clinical features and management of severe propanil poisoning.. We report a retrospective case series of patients who were treated in the intensive care unit of and/or died in Anuradhapura General Hospital between 1998 and early 2002.. Sixteen patients were identified. Common manifestations of toxicity included confusion, reduced conscious level, cyanosis, and respiratory depression. Marked hemolysis was noted in several patients. Nine deaths occurred due to respiratory depression and cardiorespiratory arrest. Management was difficult given the lack of i.v. methylene blue, inability to measure methemoglobin levels, and paucity of intensive care unit beds.. This series indicates that propanil poisoning can be a severe form of self-poisoning, particularly in resource-poor settings. We have now initiated the establishment of a prospective series of propanil poisoned patients to further describe its clinical features, responsiveness to therapy, and case fatality rate.

Topics: Adolescent; Adult; Aged; Antidotes; Ascorbic Acid; Blood Cell Count; Female; Herbicides; Humans; Intensive Care Units; Male; Methylene Blue; Middle Aged; Poisoning; Propanil; Sri Lanka; Suicide, Attempted

A case of recovery from acute respiratory insufficiency due to paraquat is described. A 57-year-old farmer developed breathlessness, high fever and interstitial infiltrates in the upper and middle lung fields few days after percutaneous paraquat poisoning with rapid evolution to pulmonary fibrosis. Anti-inflammatory drugs and antioxidants, were administered to the patient, though with a delay, with some improvement; the patient survived despite residual lung fibrosis. Paraquat lung, as confirmed by this paper, is not invariably fatal.

Topics: Acute Disease; Agricultural Workers' Diseases; Ascorbic Acid; Humans; Male; Methylprednisolone; Middle Aged; Paraquat; Poisoning; Pulmonary Fibrosis; Skin Absorption; Vitamin E

Topics: Accidents, Home; Ascorbic Acid; Central Nervous System; Child, Preschool; Dapsone; Humans; Male; Methemoglobinemia; Poisoning

The child ingested 7 tabl. of VICEDRIN (a combination of phenacetin, ephedrin, chinin, acid. ascorbicum), the total dose of phenacetin was 140 mg/kg of b.w. Lethal doses of phenacetin vary between 100-200 mg/kg, the sensitivity to phenacetin being increased in infants. Toxicological examination in this case revealed a high concentration of phenacetin in urine. The clinical signs of intoxication were vomiting (hematemesis), methemoglobinemia and somnolence. 2 hemoperfusions were performed lasting 6 hrs and 5 hrs resp. (HEMASORB 400 A 4), the second one were combined with hemodialysis because after the first perfusion a high concentration of metabolic products of phenacetin was detected in urine. After the second perfusion the status of the child rapidly improved and we could discharge the patient of the 10th day after admission. Hemoperfusion is recommended in severe intoxication with phenacetin, the combination with, hemodialysis is possible to remove its metabolic product.

Topics: Ascorbic Acid; Drug Combinations; Ephedrine; Female; Humans; Infant; Phenacetin; Poisoning

Topics: Antidotes; Ascorbic Acid; First Aid; Humans; Poisoning; Potassium Permanganate

The successful management of nitrobenzene poisoning in a 21-year-old patient is presented. We report our experience of ventilatory care with additional intravenous methylene blue and ascorbic acid therapy. Pulse oximeters available at present are not useful in patients treated with methylene blue and should be used cautiously in the presence of cyanosis of unknown aetiology.

Topics: Adult; Ascorbic Acid; Humans; Male; Methemoglobinemia; Methylene Blue; Nitrobenzenes; Oximetry; Poisoning

Topics: Animals; Antioxidants; Ascorbic Acid; Butylated Hydroxytoluene; Drug Combinations; Drug Evaluation, Preclinical; Environmental Exposure; Hydrogen Sulfide; Lipid Peroxides; Male; Poisoning; Rats; Time Factors; Vitamin E

Topics: Animals; Ascorbic Acid; Ascorbic Acid Deficiency; Cytochrome P-450 Enzyme System; Guinea Pigs; Humans; Methylene Blue; Microsomes, Liver; NADH Dehydrogenase; Oxidoreductases, N-Demethylating; Poisoning; Sulfones

Using ascorbic acid as a model, this paper proposes that the concept of the RDA should be broadened to take into account the effects of ubiquitous pollutants on human health, a factor presently not incorporated in RDA derivations. It is now widely accepted that ascorbic acid nutritional status markedly affects the toxicity and/or carcinogenicity of greater than 50 pollutants, many of which are ubiquitous in the air, water, and food environments. At the present time, the data do not warrant changing the ascorbic acid RDA in light of the knowledge of pollutant interactions.

Topics: Animals; Ascorbic Acid; Carcinogens; Dose-Response Relationship, Drug; Drug Interactions; Environmental Pollutants; Food; Humans; Inactivation, Metabolic; Metals; Nitrosamines; Nutritional Physiological Phenomena; Nutritional Requirements; Pesticides; Poisoning; Smoking

A case of self-poisoning with sodium selenate sheep drench, along with blood and urine levels of selenium, is reported. Treatment included gastric lavage, diuresis, vitamin C, and dimercaprol, and the patient recovered without sequelae.

Topics: Acute Disease; Adolescent; Ascorbic Acid; Dimercaprol; Female; Humans; Poisoning; Selenium

Topics: Animals; Ascorbic Acid; Chronic Disease; Growth; Guinea Pigs; Kidney; Liver; Lung; Motor Activity; Poisoning; Spleen; Vinyl Chloride; Vinyl Compounds

Topics: Adrenal Glands; Animals; Ascorbic Acid; Body Weight; Bone and Bones; Cadmium Poisoning; Chemical and Drug Induced Liver Injury; Coturnix; Deficiency Diseases; Duodenum; Erythrocytes; Esophagus; Female; Heart; Hematocrit; Hemoglobinometry; Iron; Kidney; Liver; Male; Poisoning; Spleen; Testis; Zinc

Topics: Acetates; Animals; Antioxidants; Ascorbic Acid; Chick Embryo; Fatty Acids, Unsaturated; Fertilization; Helianthus; Methylene Blue; Nutritional Requirements; Oils; Petroleum; Poisoning; Time Factors; Vitamin E

Topics: Alcohol Oxidoreductases; Anemia; Animals; Ascorbic Acid; Body Weight; Cadmium; Cadmium Poisoning; Esterases; Hepatitis, Animal; Ketones; Kidney; Liver; Male; Pentoses; Poisoning; Rats; Sugar Acids

Topics: Alcoholic Intoxication; Aluminum; Aminopyrine; Anti-Inflammatory Agents; Ascorbic Acid; Benzyl Compounds; Child; Child, Preschool; Cosmetics; Female; Hallucinations; Humans; Hyperkinesis; Male; Methylamines; Nalidixic Acid; Perfume; Phenethylamines; Piperidines; Poisoning; Pyrazoles; Rutin; Shock; Speech Disorders

Topics: Aniline Compounds; Ascorbic Acid; Child, Preschool; Diarrhea, Infantile; Erythrocytes; Glycolysis; Humans; Infant; Male; Methemoglobinemia; Methylene Blue; Oxidation-Reduction; Poisoning

Topics: Anemia; Animals; Antioxidants; Ascorbic Acid; Birds; Body Weight; Bone and Bones; Cadmium; Cadmium Poisoning; Calcium; Copper; Deficiency Diseases; Depression, Chemical; Erythrocytes; Growth; Hematocrit; Hemoglobins; Iron; Kidney; Liver; Metals; Poisoning; Stereoisomerism; Zinc

Topics: Animal Feed; Animals; Ascorbic Acid; Chickens; Cottonseed Oil; Food Additives; Gossypol; Male; Poaceae; Poisoning; Poultry Diseases; Vanadium

Topics: Accidents, Home; Ascorbic Acid; Child, Preschool; Cytochromes; Disulfiram; Humans; Male; Poisoning

Topics: Acetanilides; Ascorbic Acid; Cyanosis; Drug Industry; Humans; Methemoglobinemia; Methylene Blue; Occupational Diseases; Poisoning

Topics: Acute Disease; Adolescent; Ascorbic Acid; Autopsy; Brain Chemistry; Chromates; Chromium; Dimercaprol; Humans; Kidney; Liver; Male; Peritoneal Dialysis; Poisoning; Potassium

Topics: Adolescent; Adult; Ascorbic Acid; Biological Assay; Child; Drowning; Female; Humans; Hypothalamo-Hypophyseal System; Hypothalamus; Luteinizing Hormone; Male; Middle Aged; Neoplasms; Ovary; Pituitary Hormone-Releasing Hormones; Poisoning; Uremia; Vascular Diseases; Wounds and Injuries

Topics: Ammonia; Animals; Arginine; Ascorbic Acid; Autoradiography; Bicarbonates; Blood-Brain Barrier; Carbon Isotopes; Chickens; Citrulline; Hydrogen-Ion Concentration; Injections, Intraperitoneal; Male; Mice; Ornithine; Phosphates; Poisoning; Rats; Sulfates; Time Factors

Topics: Animals; Anura; Ascorbic Acid; Birds; Cats; Citrus; Fruit; Mice; Pharmacology; Poisoning; Rats; Research; Seizures; Strychnine; Toxicology

Topics: Ascorbic Acid; Diseases in Twins; Humans; Methemoglobinemia; Piperazine; Piperazines; Poisoning; Toxicology; Twins

Topics: Animals; Ascorbic Acid; Pesticides; Poisoning; Rats

Topics: Ascorbic Acid; Mice; Poisoning; Pyridoxine; Research; Toxicology

Topics: Adrenocorticotropic Hormone; Anemia; Anemia, Myelophthisic; Anti-Bacterial Agents; Ascorbic Acid; Benzene; Biopsy; Blood Transfusion; Cortisone; Female; Hematologic Diseases; Hematology; Leukemia; Liver Extracts; Mortality; Occupational Diseases; Pathology; Poisoning; Prednisolone; Prednisone; Pregnancy; Pregnancy Complications; Pregnancy Complications, Hematologic; Tetracycline; Toxicology; Vasopressins; Vitamin B 12

Topics: Animals; Antidotes; Ascorbic Acid; Humans; Mercuric Chloride; Mercury; Mercury Poisoning; Poisoning; Vitamins

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

Topics: Ascorbic Acid; Benzene; Bone Marrow; Carbohydrate Metabolism; Chronic Disease; Humans; Poisoning; Vegetables; Vitamins

Topics: Acetates; Antidotes; Ascorbic Acid; Edetic Acid; Ethylenes; Poisoning; Vanadium; Vitamins

Topics: Acrolein; Ascorbic Acid; Humans; Inositol; Lung Diseases; Poisoning; Vitamin A; Vitamin E; Vitamin K; Vitamins

Topics: Ascorbic Acid; Humans; Lead Poisoning; Poisoning; Thiamine; Vitamins

Topics: Ascorbic Acid; Humans; Poisoning; Poisons; Vitamins

Topics: Ascorbic Acid; Benzene; Corrinoids; Hematinics; Poisoning; Poisons; Vitamin B 12; Vitamins

Topics: Anesthesia, Local; Ascorbic Acid; Poisoning; Poisons

Topics: Ascorbic Acid; Poisoning; Poisons

Topics: Ascorbic Acid; Drug-Related Side Effects and Adverse Reactions; Phosphorus; Poisoning; Poisons

Topics: Ascorbic Acid; Mercury; Mercury Poisoning; Poisoning; Poisons

Topics: Ascorbic Acid; Barium; Cholinesterases; Poisoning; Poisons

Topics: Antacids; Antidiarrheals; Ascorbic Acid; Bismuth; Cholinesterases; Poisoning; Poisons