双酚A体外诱导雄性小鼠生殖细胞凋亡及其分子机制

BPA-induced apoptosis in germ cells of male mouse and apoptotic molecular mechanism in vitro

目的采用双酚A(BPA,一种典型的环境雌激素)体外诱导雄性小鼠生殖细胞凋亡,并探讨其分子机制。方法对体外培养的雄性小鼠生殖细胞以不同剂量的BPA(10-7、10-6和10-5mol/L)进行诱导,检测细胞的凋亡状况;并应用RT-PCR和免疫蛋白印记技术检测凋亡相关基因(Bax/Bcl-2、Fas/FasL)的表达变化。结果低剂量的BPA(10-7mol/L)即能够引起支持细胞和精子细胞凋亡,但精原细胞对于BPA的作用却不敏感;随着BPA处理浓度的升高,支持细胞和精子细胞中Fas/FasL、Bax表达上调,Bcl-2表达下调,而精原细胞中基因表达变化不明显。结论BPA诱导的睾丸生殖细胞凋亡,不仅是依靠调节Fas/FasL系统起作用,Bax/Bcl-2基因也能够参与这一过程的调节。

Objective To investigate the apoptotlc effect and mechanism of bisphenol A（BPA） in germ cells of male mouse in vitro. Methods With different concentrations of BPA（10^-5 , 10^-6 , 10^-7 mol/L） joined into culture medium, we observed the instance of cell apoptosis and detected expressional changes of apoptotic genes（Bax/Bcl-2, Fas/FasL） by RT-PCR and Western-blot. Results： Typical apoptotic phenomenon was detected in sertoli cells and spermatids, furthermore the expression of Fas/FasL, were are upregulated and Bcl-2 was down-regulated, however, there is no apparent apoptotic phenomenon in spermatogonias with the concentrations of BPA raised. Conclusion The apoptotie regulation that occurs in germ cells induced by BPA in vitro,depends on not only Fas/FasL system, but also Bax/Bcl-2.