Lead induces apoptosis in mouse TM3 Leydig cells through the Fas/FasL death receptor pathway

- Lead (Pb) is an important occupational and environmental pollutant.
- It is toxic to reproductive organs.
- Pb mediated cytotoxic responses and apoptosis in TM3 cells.
- Pb-induced TM3 cell apoptosis involved in the Fas/FasL death receptor pathway.

The study was aimed to investigate the effect of Pb toxicity on mouse Leydig cells and its molecular mechanism. The TM3 cells were cultured in vitro and exposed to Pb at different concentrations for 24 h. The effects of Pb on cell proliferation and apoptosis were analyzed with MTT and Annexin V-FITC/PI via flow cytometry, respectively. Expression levels of Fas, Fas-L and caspase-8 in TM3 cells were determined by western blot. As well as the inhibitory effect of the caspase-8 inhibitor Z-IETD-FMK on cell apoptosis. We found that Pb treatment significantly decreased the cellar viability (P < 0.05), increased the apoptosis (P < 0.01) and the Fas, FasL, and caspase-8 expression levels in Pb-treated cells as compared to the control cells (P < 0.05 or P < 0.01). Furthermore, the caspase-8 inhibitor effectively block the Pb-induced cell apoptosis. Taken together, our data suggest that Pb-induced TM3 cell toxic effect may involve in the Fas/FasL death receptor signaling pathway.