Decabromodiphenyl ether (BDE-209) tends to accumulate in lipid-rich tissues and targets the liver since its high lipophilicity. This study aimed to investigate the effects of BDE-209 on mouse liver and reveal the underlying toxicological mechanisms. Here we firstly confirmed that treatment of BDE-209 could lead to an imbalance of redox and promote apoptosis with a mitochondria-dependent manner in mice livers. Next, the transmission electron microscope (TEM) image revealed BDE-209 induced changes in mitochondrial morphology and increased endoplasmic reticulum (ER) - mitochondrial contact. ER stress was involved in the apoptosis process, which was displayed by the enhancive ER stress maker. Finally, the increased abundance of cellular pivotal Ca²⁺ signals transducer CaM, activating Ca²⁺ release channel Sig-1R and IP3R1, and the stronger fluorescence density of mitochondria-specifically Ca²⁺ labeled probe Rhod-2 in vitro, we summarized that there was overloaded mitochondrial Ca²⁺ in hepatocytes of BDE-209 treated mice. In conclusion, these results partly illustrated evidence to reveal a potential mechanism of BDE-209-induced hepatoxicity, where oxidative stress-induced-ER stress led to the over-release of Ca²⁺, followed by the overloaded mitochondrial Ca²⁺, and cell apoptosis initiated. Our findings provided a theoretical basis for further studying and provided a theoretical basis for further studying.

十溴二苯醚 (BDE-209) 倾向于在富含脂质的组织中积聚，并因其高亲脂性而靶向肝脏。本研究旨在调查 BDE-209 对小鼠肝脏的影响并揭示潜在的毒理学机制。在这里，我们首先证实了 BDE-209 的治疗可导致小鼠肝脏中氧化还原失衡并以线粒体依赖性方式促进细胞凋亡。接下来，透射电子显微镜 (TEM) 图像显示 BDE-209 诱导线粒体形态发生变化并增加内质网 (ER) - 线粒体接触。ER应激参与了细胞凋亡过程，这由增强的ER应激制造者显示。^{最后，细胞关键 Ca 2+}信号转导 CaM的丰度增加，激活 Ca ²⁺释放通道 Sig-1R 和 IP3R1，以及线粒体特异性 Ca ²⁺标记的探针 Rhod-2在体外更强的荧光密度，我们总结BDE-209 处理的小鼠肝细胞中存在超载的线粒体 Ca ^{2+ 。}总之，这些结果部分说明了揭示 BDE-209 诱导肝毒性的潜在机制的证据，其中氧化应激诱导的内质网应激导致 Ca ²⁺过度释放，随后是线粒体 Ca ²⁺超载，以及细胞凋亡开始。我们的研究结果为进一步研究提供了理论基础，也为进一步研究提供了理论依据。