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.

The present study evaluated the ameliorative effect of vitamin C on alteration in thyroid hormones induced by low-dose subchronic coadministration of chlorpyrifos (CPF) and lead (Pb). Forty Wistar rats were divided into 4 groups of 10 animals each. Groups I and II were administered soya oil (2 mL/kg) and vitamin C (100 mg/kg), respectively. Group III was coadministered CPF (4.25 mg/kg ~1/20th LD(50)) and Pb (250 mg/kg ~1/20th LD(50)), respectively. Group IV was pretreated with vitamin C (100 mg/kg) and then coadministered with CPF (4.25 mg/kg) and Pb (250 mg/kg), 30 min later. The regimens were administered by gavage for a period of 9 weeks. The marginal decrease in serum triiodothyronine and thyroxine and the significant increase in the concentrations of thyroid stimulating hormone and malonaldehyde in the group coadministered with CPF and Pb were ameliorated by vitamin C partly due to its antioxidant properties.

The aim of the present study was to determine changes occurring in the erythrocyte concentrations of arsenic (As), cadmium (Cd) and lead (Pb) in highly trained males, moderately trained males and sedentary men living in the same area of Extremadura (Spain). Thirty sedentary subjects (24.34 ± 3.02 years) with no sports practice and a less active lifestyle formed the control group (CG). Twenty-four moderately trained subjects (23.53 ± 1.85 years), who practised sports at a moderate level between 4 and 7 h/week, without any performance objective and without following any type of systematic training, formed the group of subjects with a moderate degree of training (MTG). And 22 professional cyclists (23.29 ± 2.73 years) at the beginning of their sports season, who trained for more than 20 h/week formed the high-level training group (HTG). Erythrocyte samples fromall subjects in a fasting stage were collected, washed and frozen at -80 °C until analysis. Erythrocyte analysis of the trace elements As, Cd and Pb was performed by inductively coupled plasma mass spectrometry (ICP-MS). As concentration was lower in CG (p < 0.01) and MTG (p < 0.01) than HTG. Cd (p < 0.001) and Pb (p < 0.05) concentrations were higher in CG than HTG. All results were expressed in μg/g Hb. Physical training produces a decrease in erythrocyte concentrations of Cd and Pb, as an adaptation in order to avoid their accumulation in the cells and preserve correct cellular functioning. The higher As concentration should be investigated in high-level sportsmen because of a possible negative effect on the cells.

Arsenic, cadmium, lead, and mercury exposures are ubiquitous. These toxic elements have no physiological benefits, engendering interest in minimizing body burden. The physiological process of sweating has long been regarded as"cleansing"and of low risk. Reports of toxicant levels in sweat were sought in Medline, Embase, Toxline, Biosis, and AMED as well as reference lists and grey literature, from inception to March 22, 2011. Of 122 records identified, 24 were included in evidence synthesis. Populations, and sweat collection methods and concentrations varied widely. In individuals with higher exposure or body burden, sweat generally exceeded plasma or urine concentrations, and dermal could match or surpass urinary daily excretion. Arsenic dermal excretion was severalfold higher in arsenic-exposed individuals than in unexposed controls. Cadmium was more concentrated in sweat than in blood plasma. Sweat lead was associated with high-molecular-weight molecules, and in an interventional study, levels were higher with endurance compared with intensive exercise. Mercury levels normalized with repeated saunas in a case report. Sweating deserves consideration for toxic element detoxification. Research including appropriately sized trials is needed to establish safe, effective therapeutic protocols.

In the present study, we investigated the effects of ascorbic acid on lead-exposed developing cerebellum. Female rats were divided into the following three groups: control (distilled water), lead (0.2% lead acetate), and lead plus ascorbic acid (100 mg/kg/day, 10% solution). To evaluate the effect of lead exposure and ascorbic acid treatment accurately on the cerebellar development for the gestational period, we halted further treatment with lead and ascorbic acid in the dams after delivery of the pups. Although the ascorbic acid slightly decreased the lead level in pups, lead level was still high in the group treated with lead plus ascorbic acid group compared with the control group. The blood lead levels indicated that the ascorbic acid could facilitate both the excretion and transfer of lead from a dam to its pups via milk. At postnatal day 21, lead exposure significantly reduced the number of Purkinje cells in the cerebellar cortex of pups. Additionally, lead treatment induced degenerative changes such as reduction of glutamic acid decarboxylase (GAD67) and c-kit expressions are observed in the developing cerebellar cortex. Inthe cerebellum of the pups from the lead plus ascorbic acid group, reduction of the number of Purkinje cells, GAD67 expression, and c-kit immunopositivity were remarkably restored compared with the lead group. Our present results suggested that ascorbic acid treatment to lead-exposed dam exerted protective effects on the developing cerebellum against lead-induced neurotoxicity.

We investigated the effects of the gestational administration of lead (Pb) and ascorbic acid on cerebellar development. Pregnant female rats were randomly assigned to the control, Pb, or Pb plus ascorbic acid (PA) groups; six offspring per cage were randomly selected for analysis. Compared to the control group, fewer Purkinje cells were observed in the Pb-exposed pups at postnatal day 21. However, co-administrating Pb and ascorbic acid inhibited the Pb-induced reduction in Purkinje cells. Terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) staining, which detected DNA fragmentation in the dying cells, showed more TUNEL-positive cells in the Pb group, while co-treatment with Pb and ascorbic acid mitigated the Pb-induced cellular degeneration. Using immunohistochemistry and immunoblotting, we additionally found that Pb exposure induced a rise in the apoptotic factor Bax in the cerebellum, while Pb plus ascorbic acid treatment ameliorated this Bax induction. Since, Pb competes with the iron in the cell and the accumulation of free iron triggers oxidative stress, we performed iron staining, which revealed that ascorbic acid prevented the Pb-induced rises in iron-reactive cells and iron-reactivity. The anti-oxidant enzyme manganese-dependent superoxide dismutase showed change patterns that were similar to those of iron in the cerebellum. Finally, the pups' blood Pb levels were highest in the Pb group but were reduced in the PA group. Our findings suggest that ascorbic acid effectively ameliorates Pb-induced apoptosis and oxidative stress in the cerebellum. The present results imply that ascorbic acid treatment during pregnancy may protect against Pb-mediated developmental impairments in the cerebellum.

We evaluated the effect of lead (Pb) and ascorbic acid treatment of pregnant female rats on cerebellar development in pups. Pb was administered in drinking water (0.2% Pb acetate), and ascorbic acid (100 mg/kg) was administered through oral intubation. Fifteen female rats were randomly classified into control, Pb, and Pb plus ascorbic acid (PA) groups. The treatment of Pb and ascorbic acid treatments were terminated after birth to evaluate the effects on the gestational development of the cerebellum. At postnatal day 21 (PND21), pups were sacrificed, and blood Pb level was analyzed. Blood Pb levels of pups and dams were highest in the Pb group and reduced in the PA group. Immunohistochemistry and immunoblot assays were conducted to study the cerebellar expression levels of synaptic proteins.Along with a significant reduction in Purkinje cells, the reduction in presynaptic (synaptophysin) and postsynaptic (postsynaptic density protein 95, N-methyl-D-aspartate receptor subtype 1) marker proteins was observed in Pb-exposed pups. Ascorbic acid treatment significantly prevented Pb-inducedimpairment in the cerebellar synaptic proteins. Hypothesizing that brain-derived neurotrophic factor (BDNF) might be affected by Pb exposure given its importance in the regulation of synaptogenesis, we observed a Pb-induced decrease and ascorbic acid-mediated increase of BDNF in the cerebellum. Luxol fast blue staining and myelin basic protein analysis suggest that ascorbic acid treatment ameliorated the Pb exposure-induced reduction in the axonal fibers in the developing cerebellum. Overall, we conclude that ascorbic acid treatment during pregnancy can prevent Pb-induced impairments in the cerebellar development in rats.

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 vitamin C with DMSA or MiADMSA (82.5+/-4.5 and 84.2+/-3.5, respectively). Combined treatments with vitamins and the thiol chelators were also able to effectively reduce lead-induced decrease in renal catalase activity and increase in TBARS and GPx level. Combination therapy, however, was unable to provide an effective reversal in the altered parameters indicative of oxidative stress in different brain regions, except in catalase activity. The result also suggests a beneficial role of vitamin E when administered along with the thiol chelators (particularly with MiADMSA) in reducing body lead burden. Blood lead concentration was reduced from 13.3+/-0.11 in lead control to 0.3+/-0.01 in MiADMSA plus vitamin E-treated rats. Liver and kidney lead concentration also showed a most prominent decrease in MiADMSA plus vitamin E co-administered rats (5.29+/-0.16 to 0.63+/-0.02 and 14.1+/-0.21 to 1.51+/-0.13 in liver and kidney, respectively). These results thus suggest that vitamin C administration during chelation with DMSA/MiADMSA was significantly beneficial in reducing oxidative stress however, it had little or no additive effect on the depletion of lead compared with the effect of chelators alone. Thus, the co-administration of vitamin E during chelation treatment with DMSA or MiADMSA could be recommended for achieving optimum effects of chelation therapy.

OBJECTIVE:The neuroprotective effects of both garlic and ascorbic acid (AA) have been documented. In this study the effects of garlic and ascorbic acid on memory deficits and brain tissue oxidative damages induced by lead exposure was investigated.

METHODS:The juvenile rats were divided and treated: (1) Control, (2) Lead (lead acetate in drinking water, 8 weeks), (3) Lead - Ascorbic Acid (Lead-AA), (4)  Lead - Garlic (100 mg/kg, daily, gavage) (Lead-Gar).

RESULTS:In Morris water maze (MWM), the escape latency and traveled path in the Lead group were significantly higher while, the time spent in the target quadrant (Q1) was lower than Control. Both Lead-Gar and Lead-AA groups spent more times in Q1than to lead group. There were no significant differences in swimming speed between the groups. In passive avoidance (PA) test, the time latency for entering the dark compartment by Lead group was lower than Control. Treatment of the animals by AA and garlic significantly increased the time latency. In Lead group, the total thiol concentration in brain tissues was significantly lower while, MDA was higher than Control. Treatment by both garlic and AA increased total thiol concentrations and decreased MDA. Both garlic and AA decreased the lead content of brain tissues.

CONCLUSION:It is suggested that treatment with garlic attenuates the learning and memory impairments due to lead exposure during juvenile rat growth which is comparable to AA. The possible mechanism may be due to its protective effects against brain tissues oxidative damage as well the lowering effects of brain lead content.

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 (20mgPbAc/kgbwt); PbAc+VC-treated group (20mgPbAc/kgbwt plus 20mg VC/kgbwt); and VC-treated group (20mgVC/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.

BACKGROUND:Lead toxicity is a public health concern. Lead is one of the dispensable and non-biodegradable heavy metals and is toxic even at low concentrations.

OBJECTIVE:This study was to investigate the effect of oral administration of Vitamin C and Vitamin E on lead-induced hepatotoxicity and oxidative stress in the brain of rats.

METHODS:Thirty Sprague-Dawley albino male albino rats (115.58 +/- 4.96g) were divided equally into five groups. The rats were fed rat chow and water ad libitum. Group 1 rats served as control and were orally administered 2ml saline every day for 7 weeks. Group 2 rats received orally 2ml lead acetate solution (60mg/kg body weight) every day for 7 weeks. Group3 rats received orally 2ml lead acetate solution (60mg/kg body weight) and vitamin C (40mg/kg body weight) every other day for 7 weeks. Group 4 rats received orally 2ml lead acetate solution (60mg/kg body weight) and vitamin E (150mg/kg body weight)every day for 7weeks. Group 5 received orally lead acetate solution at 60mg/kg body weight and vitamin C (40mg/kg body weight)and vitamin E (150mg/kg body weight) every other day for 7weeks. Three rats from each group were sacrificed after the fourth week. The remaining rats were sacrificed after the seventh week. Changes in body weight, liver weight, brain weight, activities of liver function enzymes (aspartate amino transferase (AST), alanine amino transferase (ALT) and alkaline phosphatase(ALP) in the serum at week 4 and week 7 were assayed.The oxidative stress markers (reduced glutathione (GSH), nitric oxide(NO), malondialdehyde(MDA), levels, catalase(CAT) and superoxide dismutase (SOD) activities) were determined in the brain of rats. Serum lead level of rats was also determined.

RESULTS:The lead Pb exposed rats caused a significant (p<0.01) increase in bioavailable lead in the blood (p<0.05) as compared to the control. AST, ALT and ALPactivities were significantly increased (p<0.05) in the serum of rats exposed to lead as compared to the control. NO and MDA levels were significantly increased (p<0.05) in the brain of rats exposed to lead, while GSH level, SOD and CAT activities were significantly reduced (p<0.05) in the brain of rats exposed to lead when compared with the control.

CONCLUSION:Data of the study indicate that oral administration of vitamin C and vitamin E significantly reduced the blood lead concentration, ameliorates the hepatic damage and significantly reduced the oxidative stress in the brain of rats.

The preventive effect of Coriandrum sativum, Fam. UMBELLIFERAE (Chinese parsley) on lead deposition was investigated in male ICR mice given lead (1000 ppm) as lead acetate trihydrate in drinking water for 32 days. Administration of Chinese parsley to mice by gastric intubation was performed for 25 days from day 7 after the start of lead exposure up to the end of the experiment. The mice were then sacrificed for comparison of lead distribution. The lead reached its highest concentration in the femur but localized lead deposition in the femur was significantly decreased by meso-2,3-dimercaptosuccinic acid (DMSA), a chelating agent used as a positive control to validate this experimental model. Administration of Chinese parsley also significantly decreased lead deposition in the femur and severe lead-induced injury in the kidneys. In addition, urinary excretion of delta-aminolevulinic acid (ALA) which is known to increase with lead intake was significantly decreased after administration of Chinese parsley. The MeOH extract of Chinese parsley also reduced lead-induced inhibition of delta-aminolevulinic acid dehydratase (ALAD) activity in vitro. These results suggest that Chinese parsley has suppressive activity on lead deposition, probably resulting from the chelation of lead by some substances contained in Chinese parsley.

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.

Lead belongs to the heavy metal group and is considered as an environmental contaminant. Acute or chronic contact to lead can change the physiological function of human organs. One of the most important disorders following the lead exposure is neurotoxicity. Lead neurotoxicity consists of the neurobehavioral disturbances like cognitive impairment. The aim of the current study is to evaluate the possible protective effect of vitamin C (Vit C), vitamin B12 (Vit B12), omega 3 (ω-3), or their combination on the lead-induced memory disorder. Adult wistar rats were orally administered Vit C (120 mg/kg/day) or Vit B12 (1 mg/kg/day) or ω-3 (1000 mg/kg/day) or their combination for 3 weeks in groups of 7 animals each. Then lead acetate (15 mg/kg/day) was injected intraperitoneally for one week to all pretreated animals. The control group received normal saline as a vehicle while the positive control for cognitive impairment received just lead acetate. At the end of treatments animal memories were evaluated in Object Recognition Task. The results showed, although 15 mg/kg lead acetate significantly declines the memory-evaluating parameters, pretreatment with Vit C, Vit B12, ω-3, or their combination considerably inverted the lead induced reduction in discrimination (d2) index (P<0.001) and recognition (R) index (P<0.001, P<0.05, P<0.05, and P<0.001, respectively). Our findings indicate while lead acetate impairs spatial memory in rat, administration of Vit C, Vit B12,ω-3, or their combination prior to the lead exposure inhibits the lead induced cognitive loss. There was no remarkable difference in this effect between the used supplements.

Lead exposure has negative effects on developing nervous system and induces apoptosis in newly generated neurons. Natural antioxidants (i.e. Ascorbic acid and Garlic) might protect against lead-induced neuronal cell damage. The aim of the present study was to investigate the protective effects of Ascorbic acid and Garlic administration during pregnancy and lactation on lead-induced apoptosis in rat developing hippocampus. Timed pregnant Wistar rats were administrated with Lead (1500 ppm) via drinking water (Pb group) or lead plus Ascorbic acid (Pb + AA Group, 500 mg/kg, IP), or lead plus Garlic Extract (Pb + G Group, 1 ml garlic juice/100 g BW, via Gavage) from early gestation (GD 0) until postnatal day 50 (PN 50). At the end of experiments, the pups' brains were carefully dissected. To identify neuronal death, the brain sections were stained with TUNEL assay. Mean of blood and brain lead levels increased significantly in Pb group comparing to other studied groups (P < 0.01). There was significant reduction in blood and brain lead level in Pb + AA and Pb + G groups when compared to those of Pb group (P < 0.01). The mean number of TUNEL positive cells in the CA1, CA3, and DG was significantly lower in the groups treated by either Ascorbic acid or Garlic (P < 0.05). Administration of Ascorbic acid and Garlic during pregnancy and lactation protect against lead-induced neuronal cell apoptosis in the hippocampus of rat pups partially via the reduction of Pb concentration in the blood and in the brain.

OBJECTIVE: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.

METHODS: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.

RESULTS: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).

CONCLUSIONS:Administration of ascorbic acid in drinking water significantly reduced the oxidative stress and anaemia caused by lead intoxication.

Lead is a ubiquitous environmental and industrial pollutant that may have toxic effects on the male. Vitamins may protect against toxic effects of lead in the liver and reproductive system, which is confirmed by our initial research. The aim of this study was to further investigate the protective effects of vitamins (ascorbic acid combined with thiamine) on lead acetate (Pb)-induced reproductive toxicities in mice and study the possible mechanisms underlying these effects. Forty-five male mice were randomly divided into 3 groups, 15 mice in each and received daily intragastric administration with control, Pb (20 mg/kg), and Pb+vitamins (ascorbic acid of 420 mg/kg+thiamine of 30 mg/kg) for 6 weeks, respectively. The Pb-treated animals showed significant decreases in the epididymal sperm count and motility compared to the control group, while the Pb+vitamins group had significant increases for these variables. Moreover, an increasing apoptosis of germinal cells induced by Pb was reduced by vitamin treatment. Pb induced the activation of Caspase-3, Fas/Fas-L and Bcl-2 with elevated levels, and the adaptor protein primarily regulated signaling through Fas and required for Fas-induced apoptosis. In conclusion, ascorbic acid combined with thiamine exhibited protective effect on reproductive system by inhibiting Pb-induced excessive cell apoptosis.

Oxidative stress is a major pathogenic mechanism of lead neurotoxicity. The antioxidant ascorbic acid protects hippocampal pyramidal neurons against cell death during congenital lead exposure; however, critical functions like synaptic transmission, integration, and plasticity depend on preservation of dendritic and somal morphology. This study was designed to examine if ascorbic acid also protects neuronal morphology during developmental lead exposure. Timed pregnant rats were divided into four treatment groups: (1) control, (2) 100mg/kg ascorbic acid once a day via gavage, (3) 0.05% lead acetate in drinking water, and (4) 0.05% lead+100mg/kg oral ascorbic acid. Brains of eight male pups (P25) per treatment group were processed for Golgi staining. Changes in hippocampal CA1 pyramidal neurons' somal size were estimated by cross-sectional area and changes in dendritic arborization by Sholl's analysis. One-way ANOVA was used to compare results among treatment groups. Lead-exposed pups exhibited a significant decrease in somal size compared to controls (P<0.01) that was reversed by cotreatment with ascorbic acid. Sholl's analysis revealed a significant increase in apical dendritic branch points near cell body (p<0.05) and a decreased total dendritic length in both apical and basal dendritic trees of CA1 neurons (p<0.05). Ascorbic acid significantly but only partially reversed the somal and dendritic damage caused by developmental lead exposure. Oxidative stress thus contributes to lead neurotoxicity but other pathogenic mechanisms are also involved.

It was found that being a hygienic procedure sauna essentially improves well-being of the workers, activates the cardiovascular system and mechanism of general adaptation of the body. Sauna increased excretion with sweat fluid of toxic substances (lead, thiuram, captax, sulphenamide C) that penetrated the body during work. Sauna is recommended as an effective procedure in conditions where chemical and physical factors are the leading professional noxae.