Huang Shaoping, Cui Yiqiang, Guo Xuejiang, Wang Lei, Li Suying, Lu Ying, Bi Ye, Huang Xiaoyan, Lin Min, Xia Yankai, Wang Shoulin, Wang Xinru, Zhou Zuomin, Sha Jiahao
State Key Laboratory of Reproductive Medicine, Nanjing Medical University, Jiangsu, China; Department of Human Anatomy and Neuroscience, Medical School, Southeast University, Nanjing, Jiangsu, China.
State Key Laboratory of Reproductive Medicine, Nanjing Medical University, Jiangsu, China.
Reprod Toxicol. 2015 Jan;51:114-24. doi: 10.1016/j.reprotox.2015.01.009. Epub 2015 Feb 2.
Our objective was to explore molecular markers and mechanism of BDE47 on spermatogenesis in mammals. Adult male SD rats were gavaged daily with corn oil containing 0, 0.001, 0.03, 1 or 20mg BDE47/kg bw for eight weeks. Testes morphology was analyzed using electron microscopy, TUNEL, immunohistochemistry and morphometry. Differential proteome profile and western blotting were applied to determine molecular markers and protein expression. GC1-spg cells (mouse spermatogonial cells) were used to verify mechanism of BDE47. Data showed BDE47 reduced tubular epithelial thickness, impaired mitochondrial function and induced apoptosis in early leptotene spermatocytes. Proteomic study identified 70 differential spots corresponding to 64 proteins. 20 proteins related to apoptosis, 15 located in mitochondria. Exposure of GC1-spg cells showed BDE47 induced apoptosis, impaired mitochondria and decreased Bcl-2 in cells. Data indicate that BDE47 disrupts spermatogenesis, impairs mitochondrial function and induces apoptosis of early leptotene spermatocytes in rats probably via mitochondrial pathway.
我们的目标是探索2,2',4,4'-四溴联苯醚（BDE47）对哺乳动物精子发生的分子标志物和作用机制。成年雄性SD大鼠连续八周每天灌胃含0、0.001、0.03、1或20mg BDE47/kg体重的玉米油。使用电子显微镜、TUNEL法、免疫组织化学和形态测量法分析睾丸形态。应用差异蛋白质组图谱和蛋白质印迹法确定分子标志物和蛋白质表达。使用GC1-spg细胞（小鼠精原细胞）验证BDE47的作用机制。数据显示，BDE47降低了曲细精管上皮厚度，损害了线粒体功能，并诱导早细线期精母细胞凋亡。蛋白质组学研究鉴定出70个差异点，对应64种蛋白质。其中20种蛋白质与凋亡相关，15种定位于线粒体。GC1-spg细胞暴露实验表明，BDE47诱导细胞凋亡，损害线粒体，并降低细胞中Bcl-2的表达。数据表明，BDE47可能通过线粒体途径破坏大鼠精子发生，损害线粒体功能，并诱导早细线期精母细胞凋亡。
