Methylmercury disrupts autophagic flux by inhibiting autophagosome-lysosome fusion in mouse germ cells

文献类型： 外文期刊

第一作者： Chen, Na

作者： Chen, Na;Tang, Xiaofeng;Xiao, Xianjin;Ye, Zhaoyang;Wang, Shanshan

作者机构：

关键词： Methylmercury; GC2-spd cells; Apoptosis; Autophagy; Mitophagy; Lysosome

期刊名称：ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY （ 影响因子：6.291； 五年影响因子：6.393 ）

ISSN： 0147-6513

年卷期： 2020 年 198 卷

页码：

收录情况： SCI

摘要： Methylmercury (MeHg) is an extremely toxic environmental pollutant that can cause serious male reproductive developmental dysplasia in humans and animals. However, the molecular mechanisms underlying MeHg-induced male reproductive injury are not fully clear. The purpose of this study was to explore whether mitophagy and lysosome dysfunction contribute to MeHg-induced apoptosis of germ cell and to determine the potential mechanism. First, we confirmed the exposure of GC2-spd cells to mercury. In GC2-spd cells (a mouse spermatocyte cell line), we found that MeHg treatment led to an obvious increase of cell apoptosis accompanied by a marked rise of LC3-II expression and an elevated number of autophagosomes. These results were associated with the induction of oxidative stress and mitophagy. Interestingly, we found that MeHg did not promote but prevented autophagosome-lysosome fusion by impairing the lysosome function. Furthermore, as a lysosome inhibitor, chloroquine pre-treatment obviously enhanced LC3-II expression and mitophagy formation in MeHg-treated cells. This further proved that the induction of mitophagy and the injury of the lysosome played an important role in the GC2-spd cell apoptosis induced by MeHg. Our findings indicate that MeHg caused apoptosis in the GC2-spd cells, which were dependent on oxidative stress-mediated mitophagy and the lysosome damaging-mediated inhibition of autophagic flux induced by MeHg.

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