Abstract
Cadmium (Cd) is an important environmental pollutant that causes varying degrees of damage to multiple systems of the body. However, the specific mechanism of Cd-induced liver mitophagy remains unclear. In the present study, 5-week-old BALB/c mice and a mouse liver parenchyma cell line (AML12) were studied using a combination of in vivo and in vitro studies. We found that Cd damaged liver cells, destroy the structure and function of mitochondria, and increased the production of superoxide anions. This study further examined the effect of Cd on mitochondrial dynamics and mitophagy and showed that Cd increased mitochondrial division and induced mitophagy. The PINK1-Parkin pathway is a classical mitophagy pathway. Cd-induced mitophagy was inhibited after significantly knocking down Pink1. Mdivi-1 can effectively inhibit mitochondrial division. In this study, Mdivi-1 inhibited the expression of DRP1 and significantly inhibited the occurrence of mitophagy induced by Cd. We further examined the effect of Cd on mitophagy flux. Cd did not increase lysosomal colocalization with mitochondria. In summary, Cd increase the level of oxidative stress, destroy the structure and function of mitochondria, destroy the homeostasis of mitochondrial division and fusion, induce mitophagy through the PINK1-Parkin pathway. Mitophagy plays a protective role in early cadmium-induced liver damage.
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