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

被引:39
作者
Pourhassanali, Nazila [1 ,2 ,3 ]
Roshan-Milani, Shiva [2 ,3 ]
Kheradmand, Fatemeh [3 ]
Motazakker, Morteza [3 ]
Bagheri, Morteza [3 ]
Saboory, Ehsan [2 ]
机构
[1] Urmia Univ Med Sci, Student Res Comm, Orumiyeh 5756115111, Iran
[2] Urmia Univ Med Sci, Dept Physiol, Neurophysiol Res Ctr, Fac Med, Orumiyeh 5756115111, Iran
[3] Urmia Univ Med Sci, Cellular & Mol Res Ctr, Orumiyeh 5756115111, Iran
关键词
Apoptosis; Caspase-3; Ethanol; Zinc; Sertoli cell; OXIDATIVE STRESS; REPRODUCTIVE-SYSTEM; HUMAN HEALTH; GERM-CELLS; MALE-RAT; IN-VIVO; ALCOHOL; DEATH; INFERTILITY; TESTIS;
D O I
10.1016/j.reprotox.2016.03.041
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
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 mu M) 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. (C) 2016 Elsevier Inc. All rights reserved.
引用
收藏
页码:97 / 103
页数:7
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