Zinc attenuates ethanol-induced Sertoli cell toxicity and apoptosis through caspase-3 mediated pathways

•Cell viability decreased in TM4 Sertoli cells exposed to ethanol.•Caspase-3 mRNA expresstion increased in TM4 Sertoli cells exposed to ethanol.•Pretreatment with Zinc recovered ethanol-induced anti-proliferative effects.•Pretreatment with Zinc recovered ethanol-induced over-expression of caspase-3.•Zinc reduced ethanol-induced Sertoli cell apoptosis via caspase-3 mediated pathways.

Ethanol enhances apoptosis in testicular germ cells. Zinc reduces ethanol-induced apoptosis of somatic cells through inhibition of caspase-mediated pathways. Little is known about the effects of ethanol on Sertoli cells and the effects of Zinc on ethanol-induced testicular injury. The hypothesis tested was that ethanol enhances apoptosis of Sertoli cells through up-regulation of caspase-3 and Zinc inhibits ethanol-induced effects. Cultured Sertoli cells (TM4) were exposed to ethanol (160 mM), Zinc (8 μM) and Zinc prior to ethanol for duration of 24 or 48 h and their effects on TM4 cell viability was then investigated by MTT assay. Caspase-3 mRNA expression was also investigated using real-time RT-PCR. Cell viability decreased and caspase-3 mRNA expresstion increased in cells exposed to ethanol, while exposure to Zinc showed opposite effects. Pretreatment with Zinc recovered ethanol-induced anti-proliferative effects and over-expression of caspase-3. Zinc reduced ethanol-induced Sertoli cell toxicity and apoptosis via caspase-3 mediated pathways.