Hexavalent chromium [Cr(VI)] has aroused the main interest of environmental health researchers due to its high toxicity. Liver is the main target organ of Cr(VI), and the purpose of this study was to explore whether mitophagy contributes to Cr(VI)-induced hepatotoxicity and to demonstrate the potential mechanisms. Cr(VI) exposure induced mitochondrial loss, energy metabolism disorders and cell apoptosis, which were associated with the occurrence of excessive mitophagy characterized by the increased number of green fluorescent protein-microtubule-associated protein light chain 3 (GFP-LC3) puncta and lysosomal colocalization with mitochondria. In addition, the suppression of mitophagy by autophagy-related 5 (ATG5) siRNA can effectively inhibit Cr(VI)-induced mitochondrial loss and cytotoxicity. In summary, we reached the conclusion that Cr(VI)-induced overactive mitophagy contributes to mitochondrial loss and cytotoxicity in L02 hepatocytes, which will further reveal the possible mechanisms of Cr(VI)-induced hepatotoxicity, and provide a new experimental basis for the study of the health hazard effects of chromium.

中文翻译：

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Cr（VI）诱导的过度吞噬导致L02肝细胞中的线粒体丢失和细胞毒性。

六价铬[Cr（VI）]由于其高毒性而引起了环境健康研究人员的主要兴趣。肝脏是Cr（VI）的主要靶器官，本研究的目的是探讨线粒体是否有助于Cr（VI）诱导的肝毒性并证明其潜在机制。Cr（VI）暴露引起线粒体丢失，能量代谢紊乱和细胞凋亡，这与过度线粒体的发生有关，其特征在于绿色荧光蛋白-微管相关蛋白轻链3（GFP-LC3）点和溶酶体的数量增加与线粒体共定位。此外，自噬相关5（ATG5）siRNA抑制线粒体可以有效抑制Cr（VI）诱导的线粒体丢失和细胞毒性。综上所述，