ascorbic-acid and Cadmium-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

Topics: Animals; Antioxidants; Ascorbic Acid; Cadmium; Cadmium Poisoning; Catalase; Lipid Peroxidation; Male; Oleic Acid; Oxidative Stress; Rats; Superoxide Dismutase

Cadmium (Cd), a widely distributed toxic trace metal, has been shown to accumulate in liver after long- and short-term exposure. Cd (2 mg/kg/day CdCl2) was intraperitoneally given to rats for eight days. Vitamin C (250 mg/kg/day) + vitamin E (250 mg/kg/day) + sodium selenate (0.25 mg/kg/day) were given to rats by oral means. The animals were treated by anti-oxidants one hour prior to treatment with Cd every day. The degenerative changes were observed in the groups given only Cd and anti-oxidants + Cd. Metallothionein (MT) immunoreactivity increased in cytoplasm of hepatocytes of the rats given Cd when compared with controls. In a number of cells with Cd and anti-oxidants treatment, immunoreactivity increase was more than in the group given Cd only and nuclear MT expression was also detected. Cell proliferation was assessed with proliferating cell nuclear antigen (PCNA) immunohistochemistry. PCNA expressions increased in all groups more than in the controls. Anti-oxidants treatment increased cell proliferation. In the animals administered with Cd, an increase in serum aspartate (AST) and alanine (ALT) aminotransferases, liver glutathione (GSH) and lipid peroxidation (LPO) levels were observed. On the other hand, in the rats treated with anti-oxidants and Cd, serum AST and ALT, liver glutathione and LPO levels decreased. As a result, these results suggest that combined anti-oxidants treatment might be useful in protection of liver against Cd toxicity.

Topics: Animals; Antioxidants; Ascorbic Acid; Cadmium; Cadmium Poisoning; Chemical and Drug Induced Liver Injury; Hepatocytes; Lipid Peroxidation; Liver Diseases; Male; Metallothionein; Proliferating Cell Nuclear Antigen; Rats; Rats, Sprague-Dawley; Selenic Acid; Selenium Compounds; Vitamin E

In this study, the effects of combined antioxidants treatment against cadmium toxicity were investigated microscopically, immunohistochemically, and biochemically in small intestine of Sprague Dawley rats. The rats were subdivided into four groups as intact control, cadmium was administrated, and both control and cadmium groups treated with ascorbic acid, alpha-tocopherol, and selenium. Metallothionein expression was localized in the base of intestinal glands in control rats and similar expression was observed with antioxidants treatment. In cadmium-administrated rats, metallothionein expression was detected in surface epithelium, longitudinal muscle layer, meissner, and myenteric plexuses, but not in the base of intestinal gland. On the other hand, in the rats treated with antioxidants and cadmium, immunreactivity increased in the surface epithelium and in the base of intestinal glands according to cadmium-administrated rats but not changed in the plexuses and longitudinal muscle layer. Biochemically, lipid peroxidation levels increased and glutathione levels decreased significantly in intestine of the cadmium group compared to the control. Treatment with antioxidants in cadmium-administrated rats led to a decrease in lipid peroxidation levels and a significant increase in glutathione levels. As a result, the combination of ascorbic acid, alpha-tocopherol, and selenium shows a protective effect against cadmium toxicity in small intestine.

Topics: alpha-Tocopherol; Animals; Antioxidants; Ascorbic Acid; Cadmium; Cadmium Poisoning; Drug Synergism; Glutathione; Intestine, Small; Lipid Peroxidation; Male; Metallothionein; Random Allocation; Rats; Rats, Sprague-Dawley; Selenium

The effects of cadmium on performance, antioxidant defense system, liver and kidney functions, and cadmium accumulation in selected tissues of broiler chickens were studied. Whether the possible adverse effects of cadmium would reverse with the antioxidant ascorbic acid was also investigated. Hence, 4 treatment groups (3 replicates of 10 chicks each) were designed in the study: control, ascorbic acid, cadmium, and cadmium plus ascorbic acid. Cadmium was given via the drinking water at a concentration of 25 mg/L for 6 wk. Ascorbic acid was added to the basal diet at 200 mg/kg either alone or with cadmium. Cadmium decreased the body weight (BW), body weight gain (BWG), and feed efficiency (FE) significantly at the end of the experiment, whereas its effect on feed consumption (FC) was not significant. Cadmium increased the plasma malondialdehyde (MDA) level as an indicator of lipid peroxidation and lowered the activity of blood superoxide dismutase (SOD). Liver function enzymes, aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH), and gamma glutamyl transferase (GGT) activities were not changed by cadmium. Cadmium ingestion did not alter serum creatinine levels. Although the serum cadmium level was not elevated, cadmium mainly accumulated in the kidneys, liver, pancreas, and muscle. Ascorbic acid supplementation resulted in a reduction of MDA level previously increased by cadmium and a restoration in SOD activity. However, ascorbic acid did not ameliorate the growth inhibitory effect of cadmium nor did it prevent accumulation of cadmium in analyzed tissues. These data indicate that oxidative stress, induced by cadmium, plays a role in decreasing the performance of broilers and that dietary supplementation by ascorbic acid might be useful in reversing the lipid peroxidation induced by cadmium and partly alleviating the adverse effect of cadmium on performance of broilers.

Topics: Animals; Antioxidants; Ascorbic Acid; Body Weight; Cadmium; Cadmium Poisoning; Chickens; Diet; Eating; Female; Lipid Peroxidation; Male; Malondialdehyde; Oxidative Stress; Superoxide Dismutase; Tissue Distribution; Weight Gain

The purpose of the present study was to evaluate the effect of a dietary vitamin C supplement on cadmium absorption and distribution in an animal model. An aqueous solution of cadmium chloride (labelled with cadmium-109) was given by gavage to male Wistar rats for 28 days at a daily dose corresponding to 10 mg Cd/kg diet (1.0-1.2 mg Cd/kg b.w.). The animals assigned to groups 1 and 2 (45 animals per group) received a standard laboratory diet LSM, and tap water or tap water supplemented with ascorbic acid (1.5 mg/l), respectively. The radioactivity of the samples was measured using a liquid scintillation counter (tissue samples) and a gas-flow automatic counter (ashed carcasses). The fractional uptake of cadmium-109 in the carcass and organs was evaluated within 32 days after treatment by dividing the cadmium-109 activity in the whole sample by the total activity of cadmium-109 administered for 28 days. Results were compared using AUC (areas under the concentration time curve) values. The vitamin C supplement decreased the carcass cadmium burden and the cadmium content in the liver, kidneys, testicles and muscles; the highest decreases were found in the testicles, the lowest ones in the muscles. In addition, the rats supplemented with vitamin C revealed an improved body weight gain during the experimental period.

Topics: Animals; Ascorbic Acid; Body Weight; Cadmium; Cadmium Chloride; Cadmium Poisoning; Evaluation Studies as Topic; Intestinal Absorption; Male; Organ Size; Rats; Tissue Distribution

The effects of acute exposure to cadmium (Cd) on the blood antioxidant defense system, lipid peroxide concentration and hematological parameters, as well as the possible protective role of vitamin E were studied. Male Wistar albino rats (3 months old) were treated with cadmium (0.4 mg Cd/kg b.m., i.p., 24 h before the experiment) or with vitamin E + Cd (20 IU Vit E/kg b.m., i.m., 48 h + 0.4 mg Cd/kg b.m., i.p., 24 h before the experiment). The hematological parameters were assessed: red blood cell counts, hematocrit value and hemoglobin concentration were significantly decreased in the blood of Cd-treated rats. Intoxication with cadmium was also followed by significantly increased lipid peroxide concentrations. We also observed increased activity of antioxidant defense enzymes: copper zinc containing superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase and glutathione-S-transferase as well as concentrations of non-enzymatic components of antioxidant defense system: reduced glutathione, vitamin C and vitamin E. Pretreatment with vitamin E exhibited a protective role on the toxic effects of cadmium on the hematological values, lipid peroxide concentration as well as on enzymatic and non-enzymatic components of antioxidant defense system.

Topics: Animals; Antioxidants; Ascorbic Acid; Cadmium; Cadmium Poisoning; Catalase; Erythrocyte Count; Erythrocytes; Glutathione; Glutathione Peroxidase; Glutathione Reductase; Glutathione Transferase; Hematocrit; Hemoglobins; Lipid Peroxides; Male; Rats; Rats, Wistar; Superoxide Dismutase; Vitamin E

Ascorbic acid and selenium are important antioxidants for the reactive forms of oxygen. The purpose of these experiments was to determine the influence of various concentrations of cadmium on ascorbic acid and selenium concentrations in certain tissues of rats. The results showed that cadmium, added to rats' feed, influenced the concentration of ascorbic acid in blood serum and tested rats' tissues. Cadmium influenced the concentration of selenium in certain tissues as well. Furthermore, it has been demonstrated that ascorbic acid and selenium concentrations are dependent on the type of tissue tested as well as on the size of cadmium concentrations and length of the experiments.

Topics: Animals; Ascorbic Acid; Cadmium; Cadmium Poisoning; Dose-Response Relationship, Drug; Male; Rats; Rats, Wistar; Selenium; Time Factors; Tissue Distribution

The critical organ of chronic cadmium (Cd) exposure are kidneys. Long-term exposure leads to Cd accumulation in kidneys and causes renal tubular dysfunctions. Cd-induced renal changes are irreversible, so the primary prevention by different nutrients can play an important role. In this study, male guinea pigs which, like humans, do not synthetize ascorbic acid (AA) received low (2 mg/animal/day) or high (100 mg/animal/day) dosage of AA and cadmium (1 mg Cd/animal/day) in drinking water for 12 weeks. Characteristic finding in renal morphology of Cd-intoxicated guinea pigs was dilatation of interstitial veins with apparent paravenous lymphatic infiltrates. Histomorphological changes were more evident in Cd-intoxicated guinea pigs with low AA intake. High AA intake apparently reduced in Cd-intoxicated guinea pigs the extent of renal damage. Cadmium significantly increased serum creatinine and urea levels in the group of guinea pigs with low AA intake but not in guinea pigs receiving high concentration of AA. The results showed that AA can be effective in the protection of Cd-induced nephrotoxicity.

Topics: Animals; Ascorbic Acid; Cadmium Poisoning; Dose-Response Relationship, Drug; Guinea Pigs; Kidney; Kidney Diseases; Male

Cadmium in the dose of 1 mg/animal/day was administered to guinea-pigs in the form of CdCl2 dissolved in drinking water during short-term (5 weeks) and subchronic (12 weeks) experiments. Both the control and cadmium-treated groups were divided into two subgroups, according to low (2 mg/animal/day) and high (100 mg/animal/day) vitamin C intake. Subchronic cadmium treatment caused copper deficiency indicated by a dramatic decrease of copper concentration in the liver and serum and by its moderate decrease in the testes and brain. Cadmium significantly increased zinc concentrations in the kidneys during the whole experiment and decreased the level of zinc in the serum after subchronic cadmium treatment. In the control groups, the levels of zinc and copper in the serum were lowered after 5 weeks of high vitamin C doses. High doses of vitamin C in cadmium-treated guinea-pigs decreased the levels of copper in the testes, brain and serum. These observations suggest that cadmium intake in relatively high doses might potentiate the development of copper deficiency, and high doses of vitamin C aggravate, to a certain extent, copper depletion in some important organs and serum of guinea-pigs.

Topics: Administration, Oral; Animals; Ascorbic Acid; Cadmium Poisoning; Copper; Guinea Pigs; Male; Tissue Distribution; Zinc

Some studies have indicated that cadmium-induced lethality and selective injurious effects to specific tissues, such as testes or liver, can be prevented by pretreatment with the antioxidant L-ascorbic acid (ascorbic acid). However, the basis of this tolerance is unclear. We examined the effects of ascorbic acid pretreatment on cadmium toxicity in male Fischer (F344/NCr) rats. Cadmium treatment alone (25 mumol CdCl2/kg, s.c.) proved lethal, causing a 93% mortality within 72 h, but in rats pretreated with ascorbic acid (2 g/kg, s.c. 24, 12 and 1 h) cadmium-induced lethality was nearly prevented. Hepatic lesions, including hepatocellular necrosis, induced by cadmium were at least partially ameliorated by ascorbic acid pretreatment. Ascorbic acid pretreatment had no effect on cadmium-induced testicular lesions nor on cadmium content in testes, liver, kidney and urine. Ascorbic acid alone modestly increased hepatic metallothionein (MT), but not renal MT and had no effect on induction of hepatic or renal MT by cadmium. In contrast to liver and kidney, testicular cadmium-binding protein (TCBP) in rats exposed to cadmium alone decreased markedly. Moreover, the level of TCBP decreased unexpectedly in ascorbic acid pretreated rats as compared with control. These results indicate that ascorbic acid pretreatment decreases the toxicity of cadmium in the rat without markedly modifying its toxicokinetics or markedly stimulating MT synthesis.

Topics: Animals; Ascorbic Acid; Base Sequence; Cadmium Poisoning; Kidney; L-Lactate Dehydrogenase; Liver; Male; Metallothionein; Molecular Sequence Data; Oligonucleotide Probes; Rats; Rats, Inbred F344; RNA, Messenger; Testis; Tissue Distribution

The study investigated the possibility of influencing immunotoxic effects of Cd through ascorbic acid. Guinea pigs with high and low intake of ascorbic acid were perorally exposed to cadmium chloride (1 mg Cd/animal/day). The daily vitamin C intake was 2 and 100 mg per animal, respectively. Phagocytic activity of polymorphonuclear leucocytes and monocytes as well as the percentage of active and total T lymphocytes in peripheral blood of animals were evaluated. Five- and 12-week experiments showed a mutual potentiation of negative effects of Cd on the immune system by suboptimal intake of ascorbic acid. Toxic effects of Cd on the immune system can be reduced by a sufficient intake of vitamin C.

Topics: Animals; Ascorbic Acid; Ascorbic Acid Deficiency; Body Weight; Cadmium; Cadmium Poisoning; Drug Interactions; Environmental Exposure; Guinea Pigs; Immunity, Cellular; Liver; Lymphocyte Activation; Male; Monocytes; Neutrophils; Organ Size; Phagocytosis; Rosette Formation; Spleen; T-Lymphocytes

Cadmium (as CdCl2) administered at a dose of 1 mg Cd/animal/day in drinking water to guinea pigs with a low intake of ascorbic acid (2 mg/animal/day) increased lipid peroxidation (LPO) in the kidney, liver and serum after 5 wk of treatment. A high intake of ascorbic acid (100 mg/animal/day) decreased LPO (determined from malondialdehyde levels) in the kidney, liver and serum of Cd-treated guinea pigs. Administration of Cd to guinea pigs with a low intake of ascorbic acid significantly increased LPO in the kidney at 5 wk, in comparison with controls given low levels of ascorbic acid but no Cd. However, at 12 wk, LPO in the kidney of Cd-treated guinea pigs was significantly lower than in the controls. These results indicate that the level of lipid peroxides in the kidney of guinea pigs with a low intake of ascorbic acid depends on the amount of accumulated cadmium.

Topics: Administration, Oral; Animals; Ascorbic Acid; Cadmium; Cadmium Chloride; Cadmium Poisoning; Chlorides; Chromatography, High Pressure Liquid; Dose-Response Relationship, Drug; Guinea Pigs; Kidney; Lipid Peroxidation; Liver; Male; Malondialdehyde

The concentration of metallothionein in mouse tissues after administration of ascorbic acid was determined by the Cd-hem method. The concentration of metallothionein in the liver was increased significantly after an intraperitoneal injection of L-ascorbic acid at the dose of 1000 mg/kg. A simultaneous injection of cycloheximide inhibited the increase of the metallothionein concentration. Mortality of mice injected with a lethal dose of cadmium was decreased significantly by the pre-injection of L-ascorbic acid. All of these results indicate that metallothionein is induced in the liver after the administration of ascorbic acid.

Topics: Animals; Ascorbic Acid; Cadmium Poisoning; Cycloheximide; Intestine, Small; Kidney; Liver; Male; Metallothionein; Mice; Pancreas; Zinc

Topics: Adolescent; Adult; Aged; Animals; Ascorbic Acid; Cadmium Poisoning; Child; Environmental Exposure; Female; Food Analysis; Humans; Kinetics; Lead Poisoning; Middle Aged; Neoplasms; Nitrosamines; Nitroso Compounds; Pesticide Residues; Pregnancy; Rats; Risk

In former papers it was stated that the fetus can be exposed a considerable burden by traces of heavy metals and that a combined therapy with calcium phosphate and ascorbic acid has a good detoxifying effect. In fourty lead-burdened mothers who were treated in this way the excretion of 5-aminolevulinic acid in urine decreased by 65%, the lead content of placenta by 90% and the lead content of mother's milk by 15% compared with a control group without treatment. The cadmium content of the placenta was reduced to 4% of the content in untreated mothers.

Topics: Aminolevulinic Acid; Ascorbic Acid; Cadmium; Cadmium Poisoning; Calcium Phosphates; Female; Humans; Lead; Lead Poisoning; Maternal-Fetal Exchange; Milk, Human; Pregnancy; Pregnancy Complications; Zinc

In our laboratory, the protective and therapeutic effects of surplus dietary iron and ascorbic acid on cadmium toxicity in rats have been studied and in this experiment, an effect of surplus iron and ascorbic acid on lead toxicity was examined. In young rats ingesting a diet containing 500 ppm of lead, growth retardation and anemia were observed. Suplementation of 400 ppm of iron and 1% of ascorbic acid to the lead containing diet prevented the growth depression and anemia and caused reductions of concentrations of lead in the kidney and tibia. Whereas, addition of 50 ppm of cadmium to the lead containing diet aggravated the growth retardation and anemia, but reduced the concentrations of lead in the kidney and tibia. Dietary supplementation of iron to the lead containing diet prevented the growth depression and anemia and reduced the accumulation of lead in the kidney, however the supplementation of ascorbic acid alone did not show any ameliolative effects. Rats were fed the lead containing diet and then transferred to the basal diet with or without iron and ascorbic acid. Recoveries from the growth retardation and anemia were not observed in rats within a week after the transfer to the non-lead diet with or without iron and ascorbic acid. These results suggest that iron prevents the growth depression and anemia in rats ingesting lead by an inhibition of lead asborption.

Topics: Animals; Ascorbic Acid; Cadmium; Cadmium Poisoning; Diet; Iron; Lead Poisoning; Male; Rats

The protective and curative effects of dietary iron and ascorbic acid on chronic (180 days) cadmium toxicity in rats were examined. Growth retardation and anemia were observed in rats fed a diet containing 50 ppm of cadmium for 180 days; during this period the contents of iron in the liver, kidney, spleen, testis, intestine, and tibia decreased and the zinc contents of the liver and kidney increased, but the calcium content of bone did not change. Addition of 400 ppm of iron and 1% of ascorbic acid to the cadmium-containing diet overcame the growth retardation and anemia due to cadmium toxicity and reduced the tissue levels of cadmium; however, it did not restore the zinc contents in the liver, kidney, and bone to normal. Similar effects were observed when these compounds were added to cadmium containing diet for 90 days after feeding the cadmium diet alone for 90 days. The glutamic-pyruvic transminase and glutamic-oxaloacetic transminase activities in the plasma of rats fed the cadmium diet increased significantly and these increases were prevented by supplementing the diet with iron and ascorbic acid. Glucose, urea, and alkaline phosphatase in the plasma and glycogen in the liver were not changed by feeding the cadmium diet for 180 days. These results indicate the long-term effectiveness of supplementing the diet with iron and ascorbic-acid for preventing and curing dietary cadmium toxicity in rats.

Topics: Animals; Ascorbic Acid; Cadmium; Cadmium Poisoning; Chronic Disease; Iron; Male; Rats; Tissue Distribution; 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

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

Topics: Acute Disease; Animals; Ascorbic Acid; Cadmium Poisoning; Male; Manganese; Mice; Testis; Thiamine; Zinc

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