ascorbic-acid and Mercury-Poisoning

Heavy metals are among the most widespread potential chemical contaminants in the environment and may be transferred to man through diet. Cadmium, mercury and lead are those which are most dangerous to human health. The nutritional status of exposed subjects is of particular interest in the study of the biochemical and morphological changes linked to heavy metal intoxication. Some vitamins play an efficacious protective role through direct or indirect mechanisms which interfere with the intestinal absorption of heavy metals by increasing urinary excretion or creating a synergic effect on the chelating element. It is important to underline the importance of an adequate vitamin intake in the prevention and treatment of cadmium, mercury and lead intoxications.

Topics: Adult; Animals; Ascorbic Acid; Cadmium Poisoning; Child; Food Contamination; Humans; Intestinal Absorption; Lead Poisoning; Mercury Poisoning; Vitamin B Complex; Vitamin E

To study the effects of BSO, GSH, Vit-C and DMPS on the nephrotoxicity of mercury.. The rats in groups 1, 2 and 3 were sc injected with 0.75, 1.5 and 2.5 mg/kg HgCl2, respectively. Fourth group rats were ip injected with 0.5 mmol/kg BSO and 4h later sc administrated with 0.75 mg/kg HgCl2. The rats in groups 5, 6 and 7 were ip injected with 3 mmol/kg GSH, 4 mmol/kg Vit-C, 200 micromol/kg DMPS, respectively, and 2 h later sc administrated with 2.5 mg/kg HgCl2. Eighth group rats were sc injected with saline as a control. Mercury concentrations in the liver, renal cortex and urine, urinary NAG, ALP, LDH activities, protein and BUN contents were determined.. Urinary NAG, ALP activities, protein and BUN contents in the rats of BSO pretreatment group were significantly higher than that of 0.75 mg/kg HgCl2 alone group and control group. As compared with 2.5 mg/kg HgCl2 alone group, urinary NAG, ALP, LDH activities, urinary protein and BUN contents decreased significantly.. BSO pretreatment could enhance the renal toxicity of mercury and GSH, Vit-C and DMPS pretreatment had antagonistic effects on nephrotoxicity of mercury.

Topics: Animals; Antioxidants; Ascorbic Acid; Buthionine Sulfoximine; Dose-Response Relationship, Drug; Drug Interactions; Enzyme Inhibitors; Female; Glutathione; Kidney Cortex; Kidney Diseases; Liver; Male; Mercuric Chloride; Mercury Poisoning; Rats; Rats, Wistar; Unithiol

To study the renal toxicity caused by mercury administrated once and to observe the effects of buthionine sulfoximine (BSO), gluthionein (GSH), vitamin C (VC), and sodium 2,3-dimercato-1-propanesulfonate (DMPS) pretreatment on the nephrotoxicity of mercury.. Sixty-four Wistar rats were divided randomly into eight groups, i. e., control group, low, middle and high dose mercury groups and BSO, GSH, VC, DMPS pretreatment groups. The low, middle, and high dose mercury group rats were subcutaneously (sc) injected with 0.75, 1.5, and 2.5 mg/kg HgCl2, respectively. The BSO pretreatment group rats were intraperitoneally (ip) injected with 0.5 mmol/kg BSO and four hours later sc administrated with 0.75mg/kg HgCl2. The GSH, VC and DMPS pretreatment group rats were ip injected with 3 mmol/kg GSH, 4mmol/kg VC, 200 micromol/kg DMPS, respectively, and two hours later sc administrated with 2.5 mg/kg HgCl2. The control group rats were sc injected with saline at corresponding time. The volume of injection was 5 ml/kg body weight. The 12 h urine samples were collected after 12 hours. After 48 hours, the blood samples were collected and then centrifuged to get the serum. The liver and renal cortex were also removed. Mercury contents in the liver, renal cortex, and urine samples were measured. Urinary NAG, ALP, LDH activities, urinary protein and BUN contents were also determined.. Mercury concentrations in the liver, renal cortex, and urine samples increased with mercury dose increasing. Mercury contents in the renal cortex presented evident dose-effect relationship. Mercury concentrations in the liver of high-dose mercury group were higher significantly than that of low, middle-dose mercury group, and control group. The concentrations of urinary mercury in the middle and high dose mercury groups were higher significantly than that of control group. Compared with 0.75mg/kg HgCl2 alone group, BSO pretreatment increased mercury concentrations in the liver, but decreased the concentrations in the renal cortex and urine. Mercury concentrations in the liver of GSH, VC and DMPS pretreatment groups were lower than that of 2.5 mg/kg HgCl2 alone group. Urinary NAG, ALP, LDH activities, urinary protein and BUN contents increased with mercury dose increasing, and the values in the animals of 2.5 mg/kg HgCl2 mercury group were higher significantly than that of control, 0.75 and 1.5 mg/kg HgCl2 groups. Urinary NAG, ALP activities, urinary protein and BUN contents in the rats of BSO pretreatment were higher than that of 0.75 mg/kg HgCl2 alone group and control group. Compared with 2.5 mg/kg HgCl2 alone group, urinary NAG, ALP, LDH activities, urinary protein and BUN contents decreased significantly.. Mercury concentrations in the liver, renal cortex, and urine of the rats increased with mercury dose increasing. BSO pretreatment could enhance the renal toxicity induced by mercury, however, GSH, VC, and DMPS pretreatment had antagonistic effects on nephrotoxicity of the mercury.

Topics: Animals; Antioxidants; Ascorbic Acid; Buthionine Sulfoximine; Dose-Response Relationship, Drug; Female; Glutathione; Kidney Cortex; Kidney Diseases; Male; Mercuric Chloride; Mercury Poisoning; Random Allocation; Rats; Rats, Wistar; Unithiol

The present study evaluates the effects of Na(2)SeO(3) and HgCl(2) on kidney and liver of adult rats. In vivo, HgCl(2) (17 micromol/kg, sc) reduced ascorbic acid levels in liver ( approximately 15%), whereas in kidney it reduced ALA-D activity ( approximately 60%) and ascorbic acid levels ( approximately 35%) and increased TBARS content ( approximately 50%). Na(2)SeO(3) (17 micromol/kg, sc) exposure increased the content of nonprotein thiol groups in liver (35-60%) and kidney ( approximately 50-160%), partially prevented mercury-induced ALA-D inhibition in kidney, and completely prevented a mercury-induced increase of TBARS content and decrease of ascorbic acid levels in kidney. In vitro, HgCl(2) and Na(2)SeO(3) inhibited renal and hepatic ALA-D, while HgCl(2) increased TBARS in renal and hepatic tissue preparations. Na(2)SeO(3) increased the rate of glutathione oxidation in vitro. Results indicated that Na(2)SeO(3) protected against HgCl(2) effects in vivo (prevention of mercury interaction with thiol groups and of mercury-induced oxidative damage). In vitro, Na(2)SeO(3) did not prevent mercury effects, but potentiated ALA-D inhibition by mercury, probably due to its ability to oxidize thiol groups.

Topics: Analysis of Variance; Animals; Ascorbic Acid; Drug Interactions; Enzyme Activation; Glutathione; Kidney; Liver; Male; Mercuric Chloride; Mercury Poisoning; Oxidative Stress; Porphobilinogen Synthase; Rats; Rats, Wistar; Sodium Selenite; Thiobarbituric Acid Reactive Substances

Some medical practitioners prescribe GSH and vitamin C alone or in combination with DMPS or DMSA for patients with mercury exposure that is primarily due to the mercury vapor emitted by dental amalgams.. This study tested the hypothesis that GSH, vitamin C, or lipoic acid alone or in combination with DMPS or DMSA would decrease brain mercury.. Young rats were exposed to elemental mercury by individual nose cone, at the rate of 4.0 mg mercury per m3 air for 2 h per day for 7 consecutive days. After a 7-day equilibrium period, DMPS, DMSA, GSH, vitamin C, lipoic acid alone, or in combination was administered for 7 days and the brain and kidneys of the animals removed and analyzed for mercury by cold vapor atomic absorption.. None of these regimens reduced the mercury content of the brain. Although DMPS or DMSA was effective in reducing kidney mercury concentrations, GSH, vitamin C, lipoic acid alone, or in combination were not.. One must conclude that the palliative effect, if any, of GSH, vitamin C, or lipoic acid for treatment of mercury toxicity due to mercury vapor exposure does not involve mercury mobilization from the brain and kidney.

Topics: Administration, Inhalation; Animals; Antioxidants; Ascorbic Acid; Brain; Chelating Agents; Drug Therapy, Combination; Glutathione; Kidney; Male; Mercury Poisoning; Rats; Rats, Sprague-Dawley; Succimer; Thioctic Acid; Unithiol; Volatilization

The effect of zinc on mercuric chloride-induced lipid peroxidation in the rat kidney was investigated. The rats received zinc acetate (2.0 mmol/kg, po) for 2 days before being given mercuric chloride (15 mumol/kg, sc) and were killed 6, 12, and 24 hr after the last injection. Lipid peroxidation occurred in the rat kidney 12 hr after mercury administration, and this mercury-induced lipid peroxidation was significantly reduced by zinc pretreatment. A decrease in vitamin C and E contents in the kidney was observed 12 hr after the administration of mercury, and this decrease was prevented by zinc pretreatment. In the kidney of rats pretreated with zinc, the activities of the protective enzymes, glutathione peroxidase and glucose-6-phosphate dehydrogenase, were increased after mercury injection. Non-protein sulfhydryl content (mostly glutathione) also rose markedly. The results indicate that zinc not only induces metallothionein, but also increases protective enzyme activities and glutathione content, which would tend to inhibit lipid peroxidation and suppress mercury toxicity.

Topics: Animals; Ascorbic Acid; Glucosephosphate Dehydrogenase; Glutathione; Glutathione Peroxidase; Kidney; Lipid Peroxides; Male; Mercuric Chloride; Mercury; Mercury Poisoning; Rats; Rats, Inbred Strains; Sulfhydryl Compounds; Vitamin E; Zinc

An increased environmental exposure to various toxic heavy metals such as lead, cadmium, or mercury seems to be a fact of 20th-century life. But relatively little attention has been paid to the possible implications of sucy exposure for the nutritional status of humans and animals. This review summarizes the information available concerning the effect of various nutritional factors in resistance to metal toxicants and the effect of heavy metal toxicity on nutritional status. In particular, the following questions are considered: 1) Are there any examples of heavy metal toxicity that are potentiated by a nutritional deficiency? 2) Is there any evidence that nutritional deficiency can be caused by heavy metal toxicity? 3) Is there any proof that heavy metal toxicity can be decreased by an excess intake of nutrients: 4) Is there any proof that heavy metal toxicity can be increased by an excess intake of nutrients? The discussion is focused primarily on studies with animal models but, wherever possible, implications for human health are pointed out.

Topics: Animals; Ascorbic Acid; Cadmium; Cadmium Poisoning; Calcium; Copper; Dose-Response Relationship, Drug; Humans; Iron; Iron Deficiencies; Lead; Lead Poisoning; Mercury Poisoning; Metals; Molecular Weight; Nutritional Physiological Phenomena; Protein Deficiency; Selenium; Vitamin E Deficiency; Zinc

1. Rats toxicated with mercury showed drastic fall in growth rate and supplementation of L-ascorbic acid to these rats could not reverse this effect. The contents of L-ascorbic acid and of D-glucuronic acid in the urine of the toxicated animals were decreased which could be counteracted by subsequent L-ascorbic acid supplementation. 2. The concentration of L-ascorbic acid in the liver tissues of mercury toxicated rats was decreased markedly and administration of L-ascorbic acid to this group could raise the tissue reserve considerably. 3. Severe damages of the normal histological pattern of the kidney tissues of rats viz. cellular and glomerular degeneration were observed under mercury toxicity. 4. In the liver tissues of the mercury toxicated rats, the rate of L-ascorbic acid synthesis was reduced along with increased catabolism of L-ascorbic acid. Subsequent supplementation of L-ascorbic acid to these toxicated rats was, however, found to be effective in reversing these alterations almost to the basal level.

Topics: Animals; Ascorbic Acid; Depression, Chemical; Diet; Glucuronates; Kidney; Liver; Male; Mercury Poisoning; Rats; Stimulation, Chemical

Topics: Alkaline Phosphatase; Animals; Ascorbic Acid; Calcium; Chelating Agents; Glutamates; Glycine; Kidney; Male; Mercury Poisoning; Necrosis; Potassium; Pyridoxine; Rats; Regeneration; Sodium

Topics: Animals; Ascorbic Acid; Blood Urea Nitrogen; Body Fluids; Histocytochemistry; In Vitro Techniques; Kidney; Kidney Diseases; Mercury Poisoning; Organ Size; Rats; Succinate Dehydrogenase; Tetracycline

Topics: Antidotes; Ascorbic Acid; Guinea Pigs; Mercury; Mercury Poisoning; Pharmacology; Research; Vitamins

Topics: Ascorbic Acid; Injections, Intraperitoneal; Kidney Diseases; Kidney Function Tests; Mercury Poisoning; Metabolism; Niobium; Phosphates; Poisons; Rats; Research; Toxicology; Uranium; Urine

Topics: Ascorbic Acid; Blood Proteins; Chemical Industry; Cholinesterases; Coronary Disease; Environmental Health; Hematopoietic System; Hexachlorocyclohexane; Humans; Influenza, Human; Lead Poisoning; Liver Function Tests; Mercury Poisoning; Methionine; Mice; Nitrobenzenes; Pituitary Hormones; Pituitary Hormones, Posterior; Pituitary-Adrenal Function Tests; Rabbits; Rats; Research; Sulfur Isotopes; Toxicology

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

Topics: Administration, Intravenous; Ascorbic Acid; Cardiotoxicity; Diuresis; Diuretics; Mercury; Mercury Poisoning; Psychotherapy

Topics: Administration, Intravenous; Ascorbic Acid; Cardiotoxicity; Diuresis; Diuretics; Mercury; Mercury Poisoning; Psychotherapy

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