A potential mechanism associated with lead-induced spermatogonia and Leydig cell toxicity and mitigative effect of selenium in chicken.

Lead (Pb) is a toxic heavy metal pollutants and can damage male reproductive function. Selenium (Se) possesses an ability of antagonizing Pb toxicity. However, biological events in the process of Pb toxicity and mitigative effect of Se are not well understood. The aim of present research was to investigate potential mechanism of Se against Pb toxicity from the perspective of oxidative stress, heat shock response and autophagy in the spermatogonia and Leydig cell of chicken. The cells from one-day-old male Hyline chickens were treated with Se (0.5 μmol/L) and/or Pb (20 μmol/L) for 24 h, respectively. Cell viability, cell ultrastucture, Pb and Se concentrations, testosterone level, oxidative stress indicators and relative expression of heat shock proteins (HSPs) and autophagy-related genes were measured. The results showed that spermatogonia was more tolerant to Pb than Leydig cell; cell injury was confirmed via histological assessment, cell viability and testosterone level; oxidative stress was further indicated by the decrease of catalase, glutathione peroxidase, glutathione-s-transferase and superoxide dismutase activities and the increase of malondialdehyde and reactive oxygen species contents. Pb increased expression of HSPs (27, 40, 60, 70 and 90). Meanwhile Pb induced autophagy through up-regulation of autophagy-related proteins 5, Beclin 1, Dynein, light chain 3 (LC3)-I and LC3-II and down-regulation of mammalian target of rapamycin in two type cells of chicken. However, Se intervention mitigated the aforementioned alterations caused by Pb. In conclusion, Pb led to oxidative stress, which triggered heat shock response and autophagy; Se administration mitigated reproductive toxicity of Pb through strengthening antioxidant defense in the spermatogonia and Leydig cell of chicken.