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Published on: March 20, 2012
Zinc attenuates ethanol-induced Sertoli cell toxicity and apoptosis through caspase-3 mediated pathways
Nazila Pourhassanali1, Shiva Roshan-Milani2, Fatemeh Kheradmand3
1Student Research Committee, Urmia University of Medical Sciences, Urmia, Iran; Department of Physiology, Neurophysiology Research Center, Faculty of Medicine, Urmia University of Medical Sciences, Urmia, Iran; Cellular and Molecular Research Center, Urmia University of Medical Sciences, Urmia, Iran.
Abstract:
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 (160mM), Zinc (8μM) and Zinc prior to ethanol for duration of 24 or 48h 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.
