ascorbic-acid and Lead-Poisoning

Health hazards caused by heavy metals have become a great concern to the population. Lead and arsenic are one of the most important current global environmental toxicants. Their toxic manifestations are being considered caused primarily due to the imbalance between pro-oxidant and antioxidant homeostasis and also due to a high affinity of these metals for thiol groups on functional proteins. They also interfere with a number of other body functions and are known to affect central nervous system (CNS), hematopoietic system, liver and kidneys and produce serious disorders. They produce both acute and chronic poisoning, of which chronic poisoning is more dangerous as its very difficult to revert back to normal condition after chronic exposure to these insidious metals present in our life. Despite many years of research, we are still far from an effective treatment of chronic plumbism and arsenicosis. Current approved treatment lies in the administration of chelating agents that forms an insoluble complex with the metal and removes it. They have been used clinically as antidotes for treating acute and chronic poisoning. The most widely used chelating agents are calcium disodium ethylenediamine tetra acetic acid (CaNa2EDTA), D-penicillamine and British anti-lewisite (BAL). Meso 2,3 dimercaptosuccinic acid (DMSA), an analogue of BAL, has been tried successfully in animals as well as in humans. But it is unable to remove the metal from intracellular sites. Effective chelation therapy for intoxication by heavy metals depends on whether the chelating agents are able to reach the intracellular site where the heavy metal is firmly bound. One of the important approaches has been the use of combination therapy. This includes use of structurally different chelators or a combination of an adjuvant/ antioxidant/ herbal extracts and a chelator to provide better clinical/ biochemical recovery. A number of other strategies have been suggested to minimize the numerous problems. This article presents the recent development made in this area with possible directions for future research.

Topics: Acetylcysteine; Adjuvants, Pharmaceutic; Animals; Antioxidants; Arsenic; Arsenic Poisoning; Ascorbic Acid; Calcium; Chelating Agents; Free Radicals; Humans; Lead; Lead Poisoning; Melatonin; Metals; Micronutrients; Molecular Structure; Succimer; Taurine; Thioctic Acid; Unithiol; Vitamin E

Iron is an essential nutrient for the growth, development, and long-term survival of most organisms. High tissue iron concentrations have been associated with the development and progression of several pathological conditions, including certain cancers, liver and heart disease, diabetes, hormonal abnormalities, and immune system dysfunctions. In this review we discuss the relevance of iron toxicity on free radical-mediated tissue damage, and how iron interactions with nutrient antioxidants and other metals can affect the extent of oxidative damage to different biomolecules. It can be concluded that the ingestion of antioxidant rich foods may prevent or delay primary and secondary effects associated with iron overload-related diseases.

Topics: Animals; Antioxidants; Ascorbic Acid; Flavonoids; Humans; Iron; Iron Chelating Agents; Iron Overload; Lead Poisoning; Oxidation-Reduction; Reactive Oxygen Species; Vitamin E; Zinc

Lead-induced oxidative stress contributes to the pathogenesis of lead poisoning for disrupting the delicate prooxidant/antioxidant balance that exists within mammalian cells. Production of reactive oxygen species (ROS) is increased after lead treatment in in vitro studies. In vivo studies suggest that lead exposure causes generation of ROS and alteration of antioxidant defense systems in animals and occupationally exposed workers. The mechanisms for lead-induced oxidative stress include the effect of lead on membrane, DNA, and antioxidant defense systems of cells. From low to high doses of lead exposure, there are different responses of lead-induced oxidative stress in various target sites including lung, blood vessels, testes, sperm, liver, and brain in epidemiological as well as animal studies. Therefore, reducing the possibility of lead interacting with critical biomolecules and inducing oxidative damage, or bolstering the cell's antioxidant defenses might be associated with the beneficial role of antioxidant nutrients through exogenous supplementation of antioxidant molecules. Although many researchers have investigated the benefit of antioxidants in preventing lead toxicity, the mechanisms of antioxidant nutrients being effective via rebalancing the impaired prooxidant/antioxidant ratio are not completely clear. Antioxidant nutrients including, vitamin E, vitamin C, vitamin B(6), beta-carotene, zinc, and selenium, are addressed in this review to discuss their beneficial role in lead-induced oxidative stress.

Topics: Animals; Antioxidants; Ascorbic Acid; beta Carotene; Female; Humans; Lead; Lead Poisoning; Male; Occupational Exposure; Oxidative Stress; Pregnancy; Rats; Reactive Oxygen Species; Reproduction; Selenium; Vitamin B 6; Vitamin E; Zinc

Although several animal studies suggest a protective relationship between blood lead concentrations and ascorbic acid, there are inconclusive results regarding the beneficial effect of ascorbic acid on lead concentrations in human studies. Data from the Third National Health and Nutrition Examination Survey examined the association between ascorbic acid and blood lead concentrations in 19,578 participants ages 6-90 years without a history of lead poisoning. Elevated blood lead concentrations were found in 0.4% of adults and 0.5% of youths. Serum ascorbic acid concentrations were inversely associated with the prevalence of elevated blood lead concentrations. However, there was no significant relationship between dietary ascorbic acid intake and blood lead concentrations. This study suggests that there may be a protective relationship between ascorbic acid and lead. Questions remain regarding the unique roles of dietary vitamin C versus supplemental vitamin C in explaining this relationship.

Topics: Animals; Ascorbic Acid; Dietary Supplements; Humans; Lead; Lead 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; Ascorbic Acid; Calcium; Cattle; Citrates; Diet; Environmental Exposure; Fats; Humans; Lactose; Lead; Lead Poisoning; Milk; Milk Proteins; Phosphorus; Rats; Vitamin D

The aim of this study was to explore therapeutic efficiency of succimer used with calcium and ascorbic acid in the treatment of mildly lead-poisoned mice and preschool children. Mice were exposed to lead by drinking water, and then treated with saline solution, 50mg/kg body weight (b.w.) succimer, 100mg/kg b.w. succimer, or 50mg/kg b.w. succimer plus calcium and ascorbic acid by gavage. Seventy-two children aged 48-72 months were randomly assigned into combined treatment or nutritional intervention group. Lead levels in blood and bone were analyzed by atomic absorption spectrophotometry. Activities of aminolevulinic acid dehydratase (ALAD) in blood were determined by colorimetric method. Results of animal experiment showed that succimer used alone could reduce lead levels in blood and bone and reverse activities of ALAD in blood, however, a better therapeutic efficiency in mobilizing bone lead could be achieved by succimer used with calcium and ascorbic acid. Findings from the clinical study showed that reduction of blood lead levels (BLLs) between the end and initiation of therapy in the combined treatment group was significantly greater than that in the nutritional intervention group. Percentage of children with BLLs less than 10μg/dL at the end of therapy and the eighth week after therapy in the combined treatment group was significantly higher than that in the nutritional intervention group. In conclusion, combined use of succimer with calcium and ascorbic acid seemed to be a choice in the treatment of mildly lead poisoned children.

Topics: Aging; Animals; Ascorbic Acid; Bone and Bones; Calcium Carbonate; Chelating Agents; Child; Child, Preschool; Colorimetry; Environmental Exposure; Female; Free Radical Scavengers; Humans; Lead; Lead Poisoning; Male; Mice; Porphobilinogen Synthase; Succimer

The study subjects were 75 adult men (20 to 30 years of age), who smoked one pack of cigarettes per day (minimum) and had no clinical signs of ascorbic acid deficiency or lead toxicity. None had a history of industrial exposure to lead, and the blood-lead levels were anticipated to be below 1.45 micromol/L, the minimum blood level associated with toxicity symptoms.. The men were randomly assigned to three study groups of 25, and each group was provided a four-week supply of one level of daily ascorbic acid supplements (placebo, 200 mg or 1000 mg of ascorbic acid). We measured baseline and weekly serum and urine ascorbic-acid levels as well as blood and urine lead levels. The weekly group means and variations of the measured data were statistically compared by means of ANOVA and Pearson's correlation.. The serum ascorbic-acid levels of the groups receiving ascorbic acid increased significantly after one week (p< or =.001). There was no effect of placebo or 200 mg ascorbic-acid supplementation on the blood or urine lead levels. However, there was a 81% decrease in blood-lead levels in the 1000 mg ascorbic acid group after one week of supplementation (p< or =.001).. Daily supplementation with 1000 mg of ascorbic acid results in a significant decrease of blood-lead levels associated with the general population. Ascorbic acid supplementation may provide an economical and convenient method of reducing blood-lead levels, possibly by reducing the intestinal absorption of lead.

Topics: Adult; Ascorbic Acid; Dietary Supplements; Humans; Lead; Lead Poisoning; Male; Smoking

Exposure to toxic elements is greatly unavoidable in our daily activities due to several routes of coming in contact with these elements. Thus lead (Pb), is one of the major causes of health hazard in human. In this study, evaluation of Zingiber officinale as mitigating measure against Pb induced biochemical and cytogenic toxicity in albino rats was investigated. Experimental rats were grouped into five with five animals per group, group I serves as control and groups 2-5 were induced intraperitoneal with lead acetate dissolved in distilled water at 3 mg/kg body weight whereas group 3-5 were orally administered with 200 mg/kg vitamin C, 200 mg/kg, and 100 mg/kg of Z. officinale, respectively for 7 d. The obtained results show that aspartate aminotransferase (AST), alkaline phosphatase (ALP), lipid peroxidation, urea, creatinine, bilirubin, and gamma-glutamyl transferase (GGT) were significantly increased (p < 0.05) and catalase (CAT) were reduced progressively in Pb alone induced rats. Hematological parameters showed a progressive reduction (p < 0.05) in lead acetate alone rats. There were significant changes in micronuclei (MN), chromosomal aberrations (CA) frequency, and oxidative damages in the bone marrow cells from lead acetate alone induced rats, although, mitotic index scores in these cells were reduced gradually (p < 0.05). The altered parameters were significantly reversed toward the levels observed in normal control rats administered with vitamin C and aqueous extract of Z. officinale. Hence, these results suggest that Z. officinale roots might contain therapeutic potential that can ameliorate the hazard effect of lead acetate poison.

Topics: Animals; Ascorbic Acid; Disease Models, Animal; Dose-Response Relationship, Drug; Lead Poisoning; Lipid Metabolism; Male; Micronuclei, Chromosome-Defective; Organometallic Compounds; Plant Extracts; Rats, Wistar; Zingiber officinale

To assess anaemia and oxidative stress in rats that were injected lead and to evaluate the possible effects of ascorbic acid supplementation on these parameters.. This randomised control trial study was conducted at the Army Medical College, Rawalpindi, Pakistan, from October 2007 to September 2008, and comprised Sprague Dawley rats. The rats were randomly divided into three groups. The rats in Group 1 were given weekly injections of sodium acetate, and rats of Group 2 and 3 were given weekly injections of lead acetate. Ascorbic acid was supplemented in the drinking water of rats of Group 3. At the end of six weeks, terminal sampling was done and blood obtained was used to assess the serum malondialdehyde levels and red cell parameters.. Of the 105 rats, each group had 35(33.33%). The overall mean age was 105±15 days and the mean weight was 225±25gm. The mean malondialdehyde level was 3.2±0.39 µmol /L in Group 1, 7.8±0.48 in Group 2 and 3.8±0.34 in Group 3 (p<0.001). The mean haemoglobin level was 13.16±0.57 g/dL, 10.64±0.86 and 12.22±0.81, respectively (p<0.001). The red blood cells count was 7.63±0.33 106/µL in Group 1, 6.29±0.54 in Group 2 and 6.83±0.45 in Group 3 (p<0.001).. Administration of ascorbic acid in drinking water significantly reduced the oxidative stress and anaemia caused by lead intoxication.

Topics: Anemia; Animals; Ascorbic Acid; Dietary Supplements; Lead Poisoning; Oxidative Stress; Pakistan; Random Allocation; Rats; Rats, Sprague-Dawley; Vitamins

Lead exposure is known to cause apoptotic neurodegeneration and neurobehavioral abnormalities in developing and adult brain by impairing cognition and memory. Coriandrum sativum is an herb belonging to Umbelliferae and is reported to have a protective effect against lead toxicity. In the present investigation, an attempt has been made to evaluate the protective activity of the hydroalcoholic extract of C. sativum seed against lead-induced oxidative stress. Male Wistar strain rats (100-120 g) were divided into four groups: control group: 1,000 mg/L of sodium acetate; exposed group: 1,000 mg/L lead acetate for 4 weeks; C. sativum treated 1 (CST1) group: 250 mg/kg body weight/day for seven consecutive days after 4 weeks of lead exposure; C. sativum treated 2 (CST2) group: 500 mg/kg body weight/day for seven consecutive days after 4 weeks of lead exposure. After the exposure and treatment periods, rats were sacrificed by cervical dislocation, and the whole brain was immediately isolated and separated into four regions: cerebellum, hippocampus, frontal cortex, and brain stem along with the control group. After sacrifice, blood was immediately collected into heparinized vials and stored at 4 °C. In all the tissues, reactive oxygen species (ROS), lipid peroxidation products (LPP), and total protein carbonyl content (TPCC) were estimated following standard protocols. An indicator enzyme for lead toxicity namely delta-amino levulinic acid dehydratase (δ-ALAD) activity was determined in the blood. A significant (p<0.05) increase in ROS, LPP, and TPCC levels was observed in exposed rat brain regions, while δ-ALAD showed a decrease indicating lead-induced oxidative stress. Treatment with the hydroalcoholic seed extract of C. sativum resulted in a tissue-specific amelioration of oxidative stress produced by lead.

Topics: Animals; Antioxidants; Ascorbic Acid; Brain; Coriandrum; Lead; Lead Poisoning; Lipid Peroxidation; Male; Oxidative Stress; Plant Extracts; Protein Carbonylation; Rats; Rats, Wistar; Reactive Oxygen Species; Seeds; Superoxide Dismutase

Lead poisoning is a global environmental disease that induces lifelong adverse health effects. The effect of a milk formula consisting of antioxidant of bamboo leaves (AOB), vitamin C (Vc), calcium lactate (CaLac), ferrous sulfate (FeSO₄) and zinc sulfate (ZnSO₄) on the reduction of lead and lead-induced oxidative damage in lead-exposed mice was studied. The lead-reducing effect of milk formula was investigated via a 7-week toxicokinetics study and a tissue distribution level examination. The ameliorating effect of milk formula on lead-induced oxidative damage was investigated. Results demonstrated current milk formula could effectively reduce blood lead levels (BLLs) and lead distribution levels of liver, kidneys, thighbones and brain in mice based on metal ion-mediated antagonism and chelation mechanisms. This milk formula could not only protect lead-susceptible tissues against lead poisoning, but also maintain normal absorption and distribution of essential elements in vivo. Meanwhile, current milk formula could prevent the reduction of δ-aminolevulinic acid dehydratase (δ-ALAD) activity and enhancement of free erythrocyte protoporphyrins (FEP) levels in blood erythrocytes of mice. Also, this formula could indirectly protect blood cell membranes against lead-induced lipid peroxidation. We conclude that current optimized milk formula effectively reduces lead poisoning and lead-induced in vivo oxidative damage in lead-exposed mice.

Topics: Animals; Antioxidants; Ascorbic Acid; Calcium Compounds; Ferrous Compounds; Food, Formulated; Lactates; Lead; Lead Poisoning; Male; Mice; Mice, Inbred ICR; Micronutrients; Milk; Oxidative Stress; Porphobilinogen Synthase; Reproducibility of Results; Sasa; Spectrophotometry, Atomic; Tissue Distribution; Zinc Sulfate

Oxidative stress may be affected by lead exposure as well as antioxidants, yet little is known about the interaction between dietary antioxidants and blood lead levels (BLL) on oxidative stress level. We investigated the interaction between dietary antioxidants and BLL on oxidative stress level. As part of the Biomarker Monitoring for Environmental Health conducted in Seoul and Incheon, Korea, between April and December 2005, we analysed data from 683 adults (female = 47·4 %, mean age 51·4 (sd 8·4) years) who had complete measures on BLL, dietary intakes and oxidative stress marker (urinary 8-hydroxy-2'-deoxyguanosine (8-OHdG)). Dietary intakes were assessed by a validated semi-quantitative FFQ, BLL was measured using atomic absorption spectrophotometry, and 8-OHdG by ELISA. Multivariate linear regression analyses were used to evaluate the influence of BLL on the association between dietary antioxidants and 8-OHdG. Geometric means of BLL and 8-OHdG concentrations were 4·1 (sd 1·5) μg/dl and 5·4 (sd 1·9) μg/g creatinine, respectively. Increases of vitamins C and E were significantly associated with the decrease of log10 8-OHdG in the adults from the lowest quartile of the BLL group (≤ 3·18 μg/dl, geometric mean = 2·36 μg/dl) than those of the highest quartile BLL group (>5·36 μg/dl, geometric mean = 6·78 μg/dl). Regarding antioxidant-related foods, vegetables excluding kimchi showed a higher inverse relationship with 8-OHdG in the lowest quartile BLL group than the highest group. These findings suggest a rationale for lowering the BLL and increasing the intake of dietary antioxidants in the urban population in Korea.

Topics: 8-Hydroxy-2'-Deoxyguanosine; Adult; Antioxidants; Ascorbic Acid; Biomarkers; Cross-Sectional Studies; Deoxyguanosine; Diet; Environmental Monitoring; Female; Humans; Lead; Lead Poisoning; Male; Middle Aged; Oxidative Stress; Republic of Korea; Severity of Illness Index; Urban Health; Vegetables; Vitamin E

Occupational and environmental exposures to lead remain a public health problem as lead alters physiological processes by inducing oxidative stress and mimicking divalent cations. This study was designed to investigate the effects of Vitamin C (VC) and Vitamin E (VE) on the reproductive function of lead exposed male rats. Experimental animals were exposed to oral doses of lead, VC and VE at 60 mg/kg body weight, 40 mg/kg body weight, and 150 mg/kg body weight respectively, while control animals received 0.9% saline solution. Oral administration spanned for six weeks after which changes in testicular redox status, lead deposition, testicular zinc content, serum androgen content, semen quality and testis histology were examined.. There were significant (p < 0.05) increases in oxidative stress indices and testicular lead content. A significant (p < 0.05) depletion of zinc in the testis of lead exposed animals was also observed. Fluctuations were observed in androgen levels of lead treated animals with a significant increase (p < 0.05) in Serum follicle stimulating hormone (FSH) and testosterone (TT) content, while there was no significant change in luteinizing hormone (LH) content. Testicular tissue showed an alteration in its normal histology with degeneration of the seminiferous epithelium accompanied by a significant reduction (p < 0.05) in the number of luminal spermatozoa. A downgrade in the semen appearance and semen quality -sperm motility, morphology, and count was also observed after lead exposure. VC and VE treatment showed a significant (p < 0.05) reversal of the physiological alteration induced by lead.. Lead exposure resulted in a decline in the reproductive function of male rats by inducing oxidative stress, inhibiting enzymes and depleting testicular zinc contents. However, results clearly showed that VC and VE attenuated the deleterious impact of lead on the reproductive system.

Topics: Administration, Oral; Animals; Antioxidants; Ascorbic Acid; Drug Therapy, Combination; Environmental Pollutants; Lead; Lead Poisoning; Lipid Peroxidation; Male; Oxidative Stress; Rats; Rats, Sprague-Dawley; Sperm Count; Sperm Motility; Spermatozoa; Testis; Vitamin E; Zinc

This study is intended to evaluate the efficacy of vitamin C (VC) in ameliorating the detrimental effects of long-term lead intoxication on the liver, kidneys, brain and testes as assessed by histopathology. A total of forty male Wistar rats (six-weeks-old) was divided into 4 groups: control group; lead-acetate (PbAc)-treated group (20 mgPbAc/kgbwt); PbAc+VC-treated group (20 mgPbAc/kgbwt plus 20 mg VC/kgbwt); and VC-treated group (20 mgVC/kgbwt). The Experimental period was lasted for 60 successive days in which PbAc was administered once daily while VC was supplemented every other day using intra-gastric intubation. At the end of the experimental period, all rats were sacrificed and pathological examinations were performed. Control and VC-supplemented rats showed normal liver, kidney, brain, and testes histology. In contrast, the liver of PbAc-intoxicated rats exhibited degenerated hepatocytes and portal inflammatory cell infiltrations. The kidneys showed degenerated glomeruli and formation of karyomegalic cells containing intranuclear inclusions in the proximal tubular epithelium. Cerebellar edema, cerebral satellitosis and encephalomalacia observed in the brain. Testicular tissues showed arrest of spermatogenesis and interstitial edema. Co-administration of VC with PbAc diminished the severity of pathological changes and reduced the number of affected organs compared to PbAc-intoxicated rats. These results show that low level of VC ameliorated and mitigated the adverse pathological impacts of chronic lead toxicity.

Topics: Animals; Antioxidants; Ascorbic Acid; Brain; Kidney; Lead Poisoning; Liver; Male; Organometallic Compounds; Rats; Rats, Wistar; Testis

Lead exposure is a global environmental problem that induces lifelong adverse health effects. Our aim was to investigate the effect of dietary supplements and natural antioxidants on blood lead levels (BLL) in lead-exposed mice, and observe their impact on the absorption of calcium, iron and zinc in vivo.. All of selected dietary supplements (calcium lactate, zinc sulfate, ferrous sulfate, ascorbic acid and calcium-rich milk) and natural antioxidants (extract of Chinese wolfberry, extract of Hangzhou white chrysanthemum and antioxidant extract of bamboo leaves) have promising capacity of reducing BLL in lead-exposed mice with an reduction range from 56.2% to 65.1%. The metal ion-mediated chelating and competitively inhibitory mechanisms may elucidate their reduction effect. Besides, blood calcium, iron and zinc levels were not significantly changed in all of the experimental groups, indicating that the intake of all additives does not disturb the absorption of essential mineral elements in mice.. All the studied additives not only effectively reduce BLL, but also maintain normal calcium, iron and zinc absorption in mice. The formulation of calcium, iron and zinc supplements and/or polyphenol and vitamin-rich antioxidants may constitute an important secondary prevention effort to reduce BLL and lead exposure.

Topics: Animals; Antioxidants; Ascorbic Acid; Calcium, Dietary; Dietary Supplements; Drugs, Chinese Herbal; Iron, Dietary; Lead; Lead Poisoning; Male; Mice; Mice, Inbred ICR; Micronutrients; Phytotherapy; Plants, Medicinal; Zinc

The present study was designed to determine whether the treatment with an ethanolic extract of pomegranate (EEP) (Punica granatum) can be useful for the treatment of the deleterious effect of lead acetate (LA) administration on sperm production in rats. The effects of EEP were compared with those of ascorbic acid (AA) that is a strong antioxidant and has been shown to reverse lead-induced damage on the reproductive system. The rats were divided into five different groups: those received distilled water (control group), LA, LA with EEP, LA with AA, and EEP alone, respectively. LA administration inhibited spermatogenesis by reducing the length of the stages related to spermiation (VII and VIII) and onset of mitosis (IX-XI). LA-treated rats also showed a reduction in epididymal sperm number and daily sperm production (DSP). Administration of EEP or AA resulted in longer VIII and IX-XI stages when compared with LA-treated rats. Moreover, EEP and AA administration reduced the deleterious effect of LA on DSP and epididymal sperm number. EEP showed an antioxidant activity similar to that of AA. EEP prevented LA-induced spermatogenic disruption in rats and its antioxidant activity could explain its capacity to reverse the damage produced by LA on spermatogenesis.

Topics: Animals; Antioxidants; Ascorbic Acid; Cell Count; Epididymis; Fruit; Lead Poisoning; Lythraceae; Male; Mitosis; Organometallic Compounds; Phytotherapy; Plant Extracts; Random Allocation; Rats; Rats, Sprague-Dawley; Seminiferous Tubules; Spermatogenesis; Spermatozoa

We carried out animal experiments based on the orthogonal design L(8)(2(7)) setting seven factors with two different levels of each and 10 groups of rats. The nutrients tested were tyrosine, glycine, methionine, taurine, ascorbic acid, thiamine and zinc.. The objective of this study was to explore the optimal combinations of nutrients for prevention or amelioration of lead-induced learning and memory impairment.. Rats were supplemented with nutrients by gavage once a day in two experiments: one was simultaneous nutrient supplementation with lead acetate administration (800 mg l(-1)) for 8 weeks (prophylactic supplementation) and the other was nutrient supplementation for 4 weeks after the cessation of 4 weeks of lead administration (remedial supplementation). Morris water maze was initiated at ninth week. Rats were terminated for assays of levels of Pb in blood, activities of superoxide dismutase (SOD) and nitric oxide synthase (NOS) in hippocampus, levels of nitric oxide (NO) in hippocampus and expressions of Ca2+/calmodulin-dependent protein kinase II (CaMKII) and cyclic adenosine monophosphate (cAMP) response element-binding protein messenger RNA in hippocampus.. Results showed that in prophylactic supplementation, methionine, taurine, zinc, ascorbic acid and glycine were the effective preventive factors for decreasing prolonged escape latency, increasing SOD and NOS activities and NO levels in the hippocampus, respectively. On the other hand, in remedial supplementation, taurine was the effective factor for reversing Pb-induced decrease in activities of SOD, NOS and levels of NO.. In conclusion, the optimum combinations of nutrients appear to be methionine, taurine, zinc, ascorbic acid and glycine for the prevention of learning and memory impairment, while taurine and thiamine appear to be the effective factors for reversing Pb neurotoxicity.

Topics: Animals; Antioxidants; Ascorbic Acid; Food; Glycine; Hippocampus; Lead Poisoning; Lead Poisoning, Nervous System; Learning Disabilities; Male; Maze Learning; Memory Disorders; Methionine; Models, Animal; Organometallic Compounds; Rats; Rats, Sprague-Dawley; Taurine; Thiamine; Tyrosine; Zinc

The aim of this study was to explore the therapeutic efficacies of combined use of meso-2,3-dimercaptosuccinic acid (DMSA) with calcium and ascorbic acid in the treatment of mild to moderately lead-intoxicated mice. Female albino mice were exposed to lead by drinking water contaminated with 0.1% (moderate lead exposure) or 0.05% (mild lead exposure) lead acetate. After the cessation of lead exposure, mice were supplemented by gavage with saline solution, 50 mg/kg body weight (b.w) DMSA, 100 mg/kg b.w DMSA, calcium and ascorbic acid, or 50 mg/kg b.w DMSA and calcium as well as ascorbic acid, respectively. Atomic absorption spectrophotometric method was used to analyze lead levels in blood, bone, liver, kidney and brain. Activities of blood delta-aminolevulinic acid dehydratase (ALAD) were determined by colorimetric method. DMSA supplemented alone could reduce lead levels in both soft tissues and bone and reverse lead-inhibited activities of blood ALAD in mild to moderately lead-intoxicated mice. On the other hand, combined use of DMSA with calcium and ascorbic acid achieved better therapeutic efficacies in mobilizing lead in blood, liver and kidney, and reversing lead-inhibited activities of blood ALAD in moderately lead intoxicated mice than DMSA supplemented alone. Moreover, the better therapeutic efficacies were also found in mildly lead intoxicated mice in mobilizing lead in blood and bone achieved by combined use of DMSA with calcium and ascorbic acid. Combined use of DMSA with calcium and ascorbic acid seems to be the better choice in the treatment of mild to moderate lead-intoxication.

Topics: Animals; Ascorbic Acid; Calcium; Drug Therapy, Combination; Female; Lead; Lead Poisoning; Mice; Porphobilinogen Synthase; Severity of Illness Index; Succimer; Vitamins

To observe the effect of vitamin C and E on blood lead (Pb) levels and SOD, GSH-Px, NOS activity and NO, MDA content in hippocampus of rats with lead poisoning.. Rat lead poisoning model was established by oral administration of 0.615 mmol/L lead acetate in drinking water for 4 weeks; and animals were fed with vitamin C 100 mg/kg. bw and/or vitamin E 100 mg/kg. bw for 1 week. Then blood Pb levels and SOD, GSH-Px, NOS activity and MDA, NO contents in hippocampus of rats were determined by corresponding kits.. Compared with control group, blood Pb level was decreased significantly (P<0.05) after given vitamin C, vitamin E or combination of vitamin C and E. The concentrations of SOD, GSH-Px, NO and NOS were significantly higher in vitamin C and/or E groups than those in control group (P<0.05). The concentration of MDA in vitamin treatment groups was significantly lower than that in lead control group (P<0.05); furthermore concentration of MDA in combination of vitamin C and E group was significantly higher than that in vitamin C alone group (P<0.05).. Administration of vitamin C and E can decrease blood lead level, alleviate damage of lipid peroxidation in hippocampus by lead toxicity and reverse NO, NOS levels in rats with lead poisoning.

Topics: Animals; Antioxidants; Ascorbic Acid; Glutathione Peroxidase; Hippocampus; Lead; Lead Poisoning; Lipid Peroxidation; Male; Malondialdehyde; Nitric Oxide; Nitric Oxide Synthase; Random Allocation; Rats; Rats, Sprague-Dawley; Superoxide Dismutase; Vitamin E

Lead is a neurotoxin that affects the developing central nervous system and may potentially induce apoptotic cell death. We investigated the effect of ascorbic acid against lead-induced neurotoxicity in the developing rat hippocampus. Female Sprague-Dawley rats were divided into three groups: control group, lead-treated group and lead plus ascorbic acid-treated group. Lead (0.2% lead acetate) was administered to female rats during pregnancy and lactation, in their drinking water. During this period, rats in the lead plus ascorbic acid-treated group received 100 mg/kg/day ascorbic acid, orally. At the end of the treatment, neuronal damage, apoptosis and blood lead levels were determined and the levels of Bax and Bcl-2 were immunodetected in the hippocampus of 21-day-old male pups. Histopathological evaluation demonstrated that ascorbic acid significantly attenuates apoptosis in the developing hippocampus and also spares hippocampal CA1, CA3 and dentate gyrus (DG) neurons. Simultaneous administration of ascorbic acid and lead lowered the level of Bax protein and increased Bcl-2 in pup hippocampus and reduced lead level in blood of dams compared with lead-treated only. Based on these results, it seems that ascorbic acid may potentially be beneficial in treating lead-induced brain injury in the developing rat brain.

Topics: Animals; Animals, Newborn; Apoptosis; Ascorbic Acid; bcl-2-Associated X Protein; Disease Models, Animal; Drug Interactions; Female; Gene Expression Regulation, Developmental; Hippocampus; In Situ Nick-End Labeling; Lead; Lead Poisoning; Male; Nerve Degeneration; Neuroprotective Agents; Pregnancy; Proto-Oncogene Proteins c-bcl-2; Rats

The aim of the present study was to investigate the impact of the combined administration of Vitamin C and silymarin on lead toxicity. Male albino rats were subdivided into three groups: the first was a control group, the second received lead acetate in diet as 500 mg/kg diet daily, the third received the same lead acetate dose and supplemented with Vitamin C (1 mg/100g body weight) and silymarin (1 mg/100g body weight) by gastric tube three times per week. Blood samples were taken after 2, 4 and 6 weeks of treatment. Significant lead-induced elevations in serum ALT, AST, GGT and ALP activities were observed after different periods of treatment. However, serum LDLc was decreased. The intensities of RNA and apoptotic fragments of DNA were measured as optical density by Gel-pro program. Lead acetate decreased the intensity of DNA at 6 weeks and induced apoptotic DNA fragments reversibly with time. After 2 weeks of lead administration dilation and congestion of terminal hepatic veins and portal vein branches were observed. Lead also induced hepatocyte proliferation without any localized distribution among zones 1-3. Portal inflammatory infiltrate with disruption of the limiting plates (interface hepatitis), steatosis, apoptosis and mild fibrosis were detected especially by sixth week of lead administration. Combined treatment of lead-exposed animals with Vitamin C and silymarin showed marked improvement of the biochemical, molecular and histopathological findings. These experimental results strongly indicate the protective effect of Vitamin C and silymarin against toxic effects of lead on liver tissue.

Topics: Administration, Oral; Alkaline Phosphatase; Animals; Apoptosis; Ascorbic Acid; Cell Proliferation; Cholesterol, LDL; Dietary Supplements; Disease Models, Animal; Drug Therapy, Combination; Hepatocytes; Lead Poisoning; Liver; Male; Organometallic Compounds; Protective Agents; Rats; Silymarin; Transaminases

Blood lead concentration of an infant is largely affected by maternal blood lead recycling. This study aimed to identify sociodemographic, lifestyle, and nutritional determinants for blood lead levels (BLLs) of women of reproductive age in the United States.. Subjects (n = 4,394) were women (20-49 years old) included in the most recent complete National Health and Nutritional Survey (NHANES III). Certain sociodemographic, lifestyle and nutritional determinants for BLL were identified.. The BLL of reproductive age women was 1.78 microg/dL geometric mean, The BLL was inversely associated with poverty income ratio and education level, hematocrit, intake of thiamine, and serum levels of folate, and positively associated with ethnicity (Black, Hispanic), living in urban areas or the Northeast region, age, alcohol consumption, cigarette smoking, serum protoporphyrin, and intake of pyridoxine, iron, and folate. Subjects in the lowest decile for serum ascorbic acid had significantly higher BLLs than those in the 2nd through 8th deciles.. Infants born to women who smoke, drink and maintain poor nutritional status for selected nutrients are at a greater risk of lead toxicity than those born to other women. Nutritional manipulation of thiamine, ascorbic acid and folate may impact BLL in women.

Topics: Adult; Alcohol Drinking; Ascorbic Acid; Educational Status; Female; Folic Acid; Humans; Infant, Newborn; Lead; Lead Poisoning; Life Style; Middle Aged; Nutrition Surveys; Prevalence; Risk Factors; Smoking; Socioeconomic Factors; Thiamine; United States

The protective action of vitamins C and E against lead acetate-induced reduced sperm count and sperm abnormalities in Swiss mice has been studied. Intraperitoneal injection of lead acetate (10mg/kg body weight) in the present study stimulates lipid peroxidation in the testicular tissue, indicated by a significant increase in malondialdehyde content in the experimental mice group. This is associated with an increased generation of noxious reactive oxygen species (ROS). Significantly reduced sperm count associated with increased sperm abnormality percentage in the lead-injected mice group compared to controls substantially proves the ongoing damaging effects of lead-induced ROS on developing germ cells. However, intraperitoneal administration of vitamin C (Vit C) at a concentration equivalent to the human therapeutic dose (10 mg/kg body weight) was able to minimize significantly the testicular malondialdehyde content with a concomitant increase in sperm count and significant decrease in the percentage of abnormal sperm population. Vitamin E (Vit E) (100 mg/kg body weight) treatment of a batch of lead-injected mice had a similar effect as Vit C but with a comparatively lower efficacy. On the other hand, coadministration of both vitamins (Vit C + Vit E) at the above mentioned doses to lead-treated mice led to the most significant decline in malondialdehyde content along with elevated sperm count and reduction in the percentage of abnormal sperm population. The protective action and the synergistic action of both vitamins (C and E) against lead-induced genotoxicity are discussed.

Topics: alpha-Tocopherol; Animals; Ascorbic Acid; Lead Poisoning; Lipid Peroxidation; Male; Mice; Organ Size; Organometallic Compounds; Reactive Oxygen Species; Sperm Count; Spermatogenesis; Spermatozoa; Testis

Ameliorative effects of few naturally occurring antioxidants like ascorbic acid (vitamin C), alpha-tocopherol (vitamin E) either alone or in combination with meso-2,3-dimercaptosuccinic acid (DMSA) or monoisoamyl DMSA (MiADMSA), on parameters indicative of oxidative stress in the liver, kidney, brain and blood of lead-exposed rats were studied. Male Wistar rats were exposed to 0.1% lead acetate in drinking water for 3 months and treated thereafter with DMSA or its analogue MiADMSA (50 mg/kg, intraperitoneally), either individually or in combination with vitamin E (5 mg/kg, intramuscularly) or vitamin C (25 mg/kg, orally) once daily for 5 days. The effects of these treatments in influencing the lead-induced alterations in haem synthesis pathway, hepatic, renal and brain oxidative stress and lead concentration from the soft tissues were investigated. Exposure to lead produced a significant inhibition of delta-aminolevulinic acid dehydratase (ALAD) activity from 8.44+/-0.26 in control animals to 1.76+/-0.32 in lead control, reduction in glutathione (GSH) from 3.56+/-0.14 to 2.57+/-0.25 and an increase in zinc protoporphyrin level from 62.0+/-3.9 to 170+/-10.7 in blood, suggesting altered haem synthesis pathway. Both the thiol chelators and the two vitamins were able to increase blood ALAD activity towards normal, however, GSH level responded favorably only to the two thiol chelators. The most prominent effect on blood ALAD activity was, however, observed when MiADMSA was co-administered with vitamin C (7.51+/-0.17). Lead exposure produced a significant depletion of hepatic GSH from 4.59+/-0.78 in control animals to 2.27+/-0.47 in lead controls and catalase activity from 100+/-3.4 to 22.1+/-0.25, while oxidized glutathione (GSSG; 0.34+/-0.05 to 2.05+/-0.25), thiobarbituric acid reactive substance (TBARS; 1.70+/-0.45 to 5.22+/-0.50) and glutathione peroxidase (GPx) levels (3.41+/-0.09 to 6.17+/-0.65) increased significantly, pointing to hepatic oxidative stress. Altered, reduced and oxidized GSH levels showed significant recovery after MiADMSA and DMSA administration while, vitamins E and C were effective in reducing GSSG and TBARS levels and increasing catalase activity. Administration of MiADMSA alone and the combined administration of vitamin C along with DMSA and MiADMSA were most effective in increasing hepatic GSH levels to 4.88+/-0.14, 4.09+/-0.12 and 4.30+/-0.06, respectively. Hepatic catalase also reached near normal level in animals co-administered v

Topics: Animals; Antidotes; Antioxidants; Ascorbic Acid; Chelating Agents; Cysteinyldopa; Disease Models, Animal; Drug Therapy, Combination; Lead Poisoning; Male; Oxidative Stress; Porphobilinogen Synthase; Protoporphyrins; Rats; Rats, Wistar; Succimer; Treatment Outcome; Vitamin E

Topics: Animals; Ascorbic Acid; Diet; Erythrocytes; Lead Poisoning; Lipids; Metals, Heavy; Mice; Microscopy, Electron, Scanning; Organometallic Compounds; Spectrophotometry, Atomic

Chronic exposure to lead results in sustained hypertension in humans and experimental animals. We investigated the possible role of reactive oxygen species (ROS) and their impact on DNA damage in lead-induced hypertension. Further the effect of short-term supplementation of vitamin C is also demonstrated.. Male Wistar rats were treated with either lead acetate (100 ppm) alone or lead acetate plus vitamin C (20 mg/rat/day). The control rats were fed regular rat chow. Blood pressure, antioxidants, total antioxidant status as measured by ferric-reducing antioxidant power, nitric oxide (NO) metabolites, malondialdehyde (MDA) and 8-hydroxy 2-deoxyguanosine were determined after 0, 1, 2 and 3 months.. The lead-exposed group showed a significant rise in blood pressure, lipid peroxidation (MDA) and a substantial oxidative damage to the DNA. A significant fall in NO metabolites, total antioxidant levels and ferric-reducing antioxidant power was also observed in this group. Concomitant administration of vitamin C ameliorated hypertension, normalized NO levels and abrogated lipid peroxidation. Also, it completely prevented oxidative damage to the DNA.. These findings point to enhanced ROS-mediated inactivation and sequestration of NO which can potentially contribute to hypertension, lipid peroxidation, reduced antioxidant status and oxidative DNA damage. The beneficial effects of vitamin C on these parameters support the role of increased ROS activity in the pathogenesis of these abnormalities in this model.

Topics: Animals; Antioxidants; Ascorbic Acid; Deoxyadenosines; Dietary Supplements; Disease Models, Animal; DNA Damage; Hypertension; Lead Poisoning; Lipid Peroxidation; Male; Malondialdehyde; Nitric Oxide; Organometallic Compounds; Oxidation-Reduction; Random Allocation; Rats; Rats, Inbred WKY; Reactive Oxygen Species; Time Factors

It was suggested that ascorbic acid as a natural chelating agent can influence lead toxicokinetics and improve chelating properties of dimercaptosuccinic acid (DMSA) in adult rats. In this paper potential benefits of ascorbic acid supplementation, alone or combined with DMSA, in decreasing lead retention in suckling rats were evaluated. Such data in young mammals are not available. L-Ascorbic acid (daily dose 650 mg/kg b.wt.) and/or DMSA (daily dose 91 mg/kg b.wt.) were administered orally to suckling Wistar rats either during ongoing 8-day oral lead exposure (as acetate; daily dose 2 mg lead/kg b.wt.) or after 3-day lead exposure (total dose 12 mg lead/kg b.wt.). Lead concentrations were analysed in the carcass (skeleton), liver, kidneys and brain by atomic absorption spectrometry. By ascorbic acid supplementation lead retention was not reduced under either lead exposure condition. Lead concentration was even increased in the carcass. Treatment with DMSA under both exposure conditions significantly reduced lead in all analysed tissues. Combined treatment with ascorbic acid and DMSA during ongoing lead exposure was substantially less effective than DMSA treatment alone, and did not affect DMSA efficacy when administered after lead exposure. It was concluded that ascorbic acid administered either during or after lead exposure in suckling rats has no beneficial effect on either lead retention or DMSA chelation effectiveness.

Topics: Administration, Oral; Animals; Animals, Suckling; Antidotes; Ascorbic Acid; Chelating Agents; Drug Synergism; Drug Therapy, Combination; Female; Lead; Lead Poisoning; Male; Rats; Rats, Wistar; Succimer

The refining of silver from old silver ornaments, articles and jeweller's waste by smelting these with lead scraps for the fabrication of new jewellery is an important small scale industry in India. The present survey and clinical investigations have shown that 31 out of 50 silver refiners with a mean blood lead level of 32.84+/-1.78 microg/dl (range 20.3-64.9), decrease in blood delta-aminolevulinic acid dehydratase (ALAD) activity and thiamine (as pyruvate) level and an enhanced urinary excretion of ALA as compared to control, were suffering from lead poisoning. Most of these workers have shown anaemia, abdominal colic, blue lining of gum and muscular wasting indicative of lead toxicity. Twenty-four workers with relatively high blood lead levels were equally divided into two groups and given either vitamin B1 (75 mg, once a day) or vitamin C (250 mg. twice a day) for 1 month. The treatment with both the vitamins significantly lowered the blood lead levels and reduced blood thiamine and copper deficiency. In addition, vitamin C was also effective in reversing the inhibition of blood ALAD activity while the effect of vitamin B1 on its activity was marginal. The daily intake of vitamin B1 and vitamin C may prevent the accumulation of lead and reduce its toxic effects particularly in those regularly exposed to lead.

Topics: Adolescent; Adult; Anemia; Ascorbic Acid; Atrophy; Colic; Health Surveys; Humans; India; Lead Poisoning; Male; Metallurgy; Middle Aged; Muscle, Skeletal; Porphobilinogen Synthase; Preventive Medicine; Silver; Thiamine

Effect of vitamin C supplementation in restoring lead induced alterations in hematopoietic system and drug metabolizing enzymes were investigated in male rats. Intraperitoneal administration of 20 mg/kg lead produced a significant inhibition of heme synthesis in blood and liver and drug metabolism in liver. Toxic insult by lead also resulted into a marked decline in tissue thiols and vitamin C levels. Oral supplementation of vitamin C (100 mg/kg for 3 days) completely restored blood delta aminolevulinic acid dehydratase, uroporphyrinogen I synthetase and a few drug metabolizing enzymes. Level of vitamin C and sulfhydryl contents too recovered to a great extent. A marked reduction in blood and liver lead concentration occurred on vitamin C supplementation although renal lead contents were marginally reduced in lead exposed animals. The results, thus, indicate a significant protective action of vitamin C against toxic effects of lead on heme synthesis and drug metabolism.

Topics: Administration, Oral; Aniline Hydroxylase; Animals; Ascorbic Acid; Hematopoiesis; Heme; Hydroxymethylbilane Synthase; Kidney; Lead; Lead Poisoning; Liver; Male; Microsomes, Liver; Mixed Function Oxygenases; Porphobilinogen Synthase; Rats; Sulfhydryl Compounds

Mammalian cell cultures were used to determine the capacity of antidotes to modify (a) lead uptake, (b) lead toxicity and (c) lead release from cells. The following chelating agents were tested: Na, Ca-ethylenediaminetetraacetic acid (EDTA), diethylenetriaminepentaacetic acid (DTPA), nitriloacetic acid, ethylene glycol-bis(aminoethyl)tetraacetic acid (EGTA), D,L-mercaptosuccinic acid (MSA), meso-2,3-dimercaptopropanesuccinic acid (MSA), D,L-2,3-dimercaptopropane-1-sulfonic acid (DMPS), penicillamine (PA), N-acetylpenicillamine (NAPA), and diethylcarbodithioate (DDTC). The following vitamins were tested: thiamine (B1), riboflavine (B2), pyridoxine (B6), cobalamin (B12) and ascorbic acid (C). Inhibition of lead uptake was produced by EDTA, EGTA, DMSA, DMPS, MSA, PA, NAPA and vitamins B1, B6 and C, vitamins B2 and B12 being ineffective. The same compounds reduced lead cytotoxicity. Interestingly DDTC and DTPA increased lead uptake, but did not exacerbate lead toxicity. Significant release of lead from preloaded cells was caused by DTPA, NAPA, DMPS and PA, while the other chelators were ineffective.

Topics: Animals; Ascorbic Acid; Cells, Cultured; Chelating Agents; Cricetinae; Lead Poisoning; Penicillamine; Pentetic Acid; Pyridoxine; Thiamine; Vitamins

Topics: Aminolevulinic Acid; Animals; Ascorbic Acid; Lead; Lead Poisoning; Male; Porphobilinogen Synthase; Protoporphyrins; Rats; Succimer; Sulfhydryl Compounds; Thiamine

The influence of the administration of thiamine (vitamin B1), ascorbic acid (vitamin C) or their combination on the efficacy of two thiol metal chelators, viz. alpha-mercapto-beta-(2-furyl) acrylic acid (MFA) and 2,3-dimercaptosuccinic acid (DMS), in counteracting lead (Pb) toxicity was investigated in rats. Ascorbic acid or its combination with thiamine enhanced the urinary elimination of Pb, reduced the hepatic and renal burden of Pb, and reversed the Pb-induced inhibition of the activity of blood delta-aminolevulinic acid dehydratase (delta-ALA-D). All these effects were more evident in DMS- than in MFA-treated rats. The combination of MFA and DMS treatments further improved the performance of the animals in enhancing urinary Pb excretion and in reducing Pb hepatic levels.

Topics: Animals; Ascorbic Acid; Chelating Agents; Lead; Lead Poisoning; Male; Rats; Sulfhydryl Compounds; Thiamine; Tissue Distribution

Topics: Adult; Ascorbic Acid; Electronics; Humans; Lead Poisoning; Male; Middle Aged; Occupational Diseases; Time Factors; Vitamin E

Topics: Adrenal Glands; Aminolevulinic Acid; Animals; Ascorbic Acid; Body Weight; Catecholamines; Cholesterol; Lead; Lead Poisoning; Male; Organ Size; Rats; Time Factors

Thiamine, ascorbic acid and their combination were investigated for their ability to prevent or treat the experimental lead intoxication in rats. The combination of the two vitamins was most effective in reducing the lead induced inhibition in the activity of blood delta-aminolevulinic acid dehydratase, elevation in the level of blood zinc protoporphyrin and the urinary excretion of delta-aminolevulinic acid and the uptake of lead in blood, liver and kidney. The combined treatment post lead exposure was also most effective in restoring the lead induced biochemical alterations and mobilizing lead from the tissues. The order of effectiveness was, thiamine + ascorbic acid less than ascorbic acid less than thiamine. The lead induced changes in brain biogenic amines and the brain concentration of lead remained unaffected by these vitamins.

Topics: Animals; Ascorbic Acid; Drug Therapy, Combination; Lead; Lead Poisoning; Male; Porphobilinogen Synthase; Rats; Thiamine

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

Ascorbic acid has been found to interact with several elements in such a manner as to render them less available for animals. This property of the vitamin has a negative effect on the animals fed a copper-deficient diet, but a positive effect on those fed toxic levels of copper, selenium, vanadium, and cobalt. The effect of ascorbic acid in alleviating cadmium toxicity has been attributed to the effect of the vitamin on iron metabolism, since ferrous iron will also alleviate cadmium toxicity in the Japanese quail. The results of studies reported here indicate that iron will alleviate lead toxicity but ascorbic acid is ineffective. Ascorbic acid will alleviate mercury toxicity, but iron exacerbates this condition. For these two elements, the effects of iron and ascorbic acid are independent of each other.

Topics: Animals; Ascorbic Acid; Cadmium; Chickens; Cobalt; Copper; Humans; Intestinal Absorption; Lead; Lead Poisoning; Mercury; Selenium; Vanadium

Topics: Aminolevulinic Acid; Animals; Ascorbic Acid; Bone and Bones; Drug Therapy, Combination; Edetic Acid; Lead; Lead Poisoning; Male; Rats; Time Factors; Tissue Distribution

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 high levels of dietary iron and ascorbic acid on moderately long-term toxicity in rats were examined. In rats fed a diet containing 500 ppm of lead for 56 days, growth retardation, reduction of food consumption, anemia, hypertrophy of the kidney and accumulation of lead in the bone and kidney were observed, however, activities of alkaline phosphatase and GOT in the plasma did not change. Addition of 400 ppm of iron and 1% of ascorbic acid to the lead containing diet prevented the growth depression, reduction of food consumption, anemia and decreased the accumulation of lead in tissues. When these compounds were added to the lead containing diet for 18 days after feeding the lead diet alone for 38 days, almost no curative effects on lead toxicity were observed. In contrast to cadmium toxicity, dietary iron and ascorbic acid have no curative effect on established lead toxicity.

Topics: Animals; Ascorbic Acid; Bone and Bones; Diet; Iron; Lead Poisoning; Male; Metals; Rats

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. Lead toxicated rats became severely anaemic which could be recovered to a considerable extent by simultaneous supplementation of L-ascorbic acid to these rats. 2. The concentrations of L-ascorbic acid in the liver tissues and in the urine of the toxicated rats were increased significantly while that in the kidney tissues was markedly reduced and supplementation of L-ascorbic acid to the toxicated rats could not raise appreciably this reduced L-ascorbic acid level in the kidney tissues. 3. The kidney of rats maintained on lead supplemented basal diet were enlarged significantly; the normal histological pattern of the kidney tissues was severely disturbed under the experimental condition exhibited by cellular necrosis and membrane rupture. 4. In the liver tissues of lead toxicated rats, the rate of L-ascorbic acid synthesis was enhanced and this was brought to the basal level by supplementation of L-ascorbic acid. Synthesis of L-xylulose in the kidney tissues of rats was drastically reduced under lead toxicosis and administration of L-ascorbic acid to the toxicated animals could not protect this effect.

Topics: Animals; Ascorbic Acid; Glucuronates; Hemoglobins; Kidney; Lead Poisoning; Liver; Male; Organ Size; Rats

Topics: Acetates; Animals; Ascorbic Acid; Body Weight; Creatinine; Diet; Heme; Lead; Lead Poisoning; Levulinic Acids; Male; Nicotinic Acids; Phenylhydrazines; Pyridoxine; Rats; Vitamin B 12; Vitamins

Topics: Animals; Ascorbic Acid; Barbiturates; Catalase; Diet; Humans; Lead Poisoning; Levulinic Acids; Lipid Metabolism; Liver; Magnesium; Mice; Mitochondria; Porphyrias; Purines; Rats

Topics: Anemia, Sideroblastic; Animals; Ascorbic Acid; Cobalt; Erythropoiesis; Erythropoietin; Humans; Lead Poisoning; Porphyrias; Porphyrins; Rats

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: Ascorbic Acid; Humans; Lead Poisoning; Magnesium Sulfate

Topics: Ascorbic Acid; Flavonoids; Lead Poisoning; Rutin; Vitamins

Topics: Ascorbic Acid; Central Nervous System; Cholesterol; Humans; Lead Poisoning

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