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.

Ascorbic acid (AA), one of the best-known reactive oxygen species (ROS) scavengers, exhibits numerous functions such as antioxidant, anti-cancer, and anti-inflammatory effects. Increasing evidence demonstrates that oxidative stress plays an important role in testicular toxicity. In the present study, we investigated the protective effect of AA against cadmium (Cd)-induced blood-testis barrier (BTB) disruption. Sprague-Dawley (SD) rats were divided into four groups: the Cd-treated group received a single dose (s.c.) of 2 mg/kg BW cadmium chloride; the AA antagonism group received an injection of AA at a dose of 400 mg/kg BW (200 mg 24 h prior to Cd treatment and 200 mg 24 h following Cd treatment); and the control groups received an equal volume of saline or an equal dose of AA. As expected, ROS expression was upregulated in the Cd-treated rats, accompanied by an increase in malondialdehyde (MDA). Interestingly, AA suppressed Cd-induced oxidative stress by decreasing the levels of ROS and MDA and increasing the activity of superoxide dismutase (SOD) and catalase (CAT). In addition, AA also reduced BTB disruption by inhibiting TGF-β3 activation and p38 MAPK phosphorylation. Significant decreases in occludin and claudin-11 expression were observed in the Cd-treated rats, whereas AA administration attenuated this effect. Moreover, testicular histopathology and transmission electron microscopy further demonstrated the protective effects of AA against Cd-induced BTB damage. In conclusion, the results of the present study suggest that AA protects BTB destruction via the inhibition of oxidative stress and the TGF-β3/p38 MAPK signalling pathway in the testis of Cd-exposed rats.