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.

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.

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.