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线粒体介导的细胞凋亡参与了 BPA 对雄性大鼠生殖损伤的作用。

Mitochondrion-mediated apoptosis is involved in reproductive damage caused by BPA in male rats.

机构信息

Department of Clinical Laboratory, The First College of Clinical Medical Science of China Three Gorges University and Yichang Central People's Hospital, Yichang 433003, Hubei, China.

Department of Clinical Laboratory, The First College of Clinical Medical Science of China Three Gorges University and Yichang Central People's Hospital, Yichang 433003, Hubei, China.

出版信息

Environ Toxicol Pharmacol. 2014 Nov;38(3):1025-33. doi: 10.1016/j.etap.2014.10.018. Epub 2014 Nov 1.

DOI:10.1016/j.etap.2014.10.018
PMID:25461564
Abstract

Bisphenol A (BPA) is a widely used environmental endocrine disruptor. Many studies have reported that BPA exposure shows reproductive toxicity and causes apoptosis in spermatogenic cells. However, few studies have investigated the relationship between the mitochondrial pathway and BPA-induced apoptosis. This study investigated the role of the mitochondrial pathway in apoptosis induced by BPA, which resulted in compromised male rat spermatogenesis and reproductive damage. Rats were exposed to various BPA concentrations (0, 50, 100, or 200mg of BPA/kg body weight per day), and factors in the mitochondrial signal transduction pathway and the apoptosis indices of spermatogenic cells were measured and sperm characteristics were analyzed. Our data revealed that BPA exposure increased the protein and mRNA levels of cytochrome C, apoptosis-inducing factor, caspase-3/9, and Bax; caspase-3 and caspase-9 activities; and the apoptosis indices of spermatogenic cells. In addition, abnormal structure of mitochondria and decreased protein and gene levels of Bcl-2 were observed following BPA exposure. These results suggest that apoptosis in the mitochondrial pathway mediates compromised reproductive system function caused by BPA exposure.

摘要

双酚 A(BPA)是一种广泛使用的环境内分泌干扰物。许多研究报告称,BPA 暴露表现出生殖毒性,并导致生精细胞凋亡。然而,很少有研究调查线粒体途径与 BPA 诱导的细胞凋亡之间的关系。本研究探讨了线粒体途径在 BPA 诱导的凋亡中的作用,导致雄性大鼠生精功能受损和生殖损伤。大鼠暴露于不同浓度的 BPA(0、50、100 或 200mg/kg 体重/天),测量线粒体信号转导途径中的因子和生精细胞的凋亡指数,并分析精子特征。我们的数据显示,BPA 暴露增加了细胞色素 C、凋亡诱导因子、caspase-3/9 和 Bax 的蛋白和 mRNA 水平;caspase-3 和 caspase-9 的活性;以及生精细胞的凋亡指数。此外,BPA 暴露后观察到线粒体结构异常,Bcl-2 的蛋白和基因水平降低。这些结果表明,线粒体途径中的细胞凋亡介导了 BPA 暴露导致的生殖系统功能受损。

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