Involvement of PINK1/Parkin-mediated mitophagy in paraquat- induced apoptosis in human lung epithelial-like A549 cells

Paraquat (PQ) is one of the most popular herbicides and has been widely used all over the world over the past several decades. However, PQ exposure can cause multiple organ failure, especially acute lung injury in humans as well as in rodent animals. Mitochondrial dysfunction plays a crucial role in PQ-induced lung cell damage. Mitophagy, defined as the selective autophagic elimination process of mitochondria, is a significant mechanism controlling mitochondrial quality. In this study, we investigated PINK1/Parkin-mediated mitophagy activated in the process of the PQ-induced cell apoptosis by using human lung epithelial-like A549 cells. We showed that PQ inhibited cell viability and induced mitochondrial damage as well as cell apoptosis in A549 cells. During this process, PQ induced PINK1/Parkin-mediated mitophagy. Knocking down the expression of Parkin gene by the transient transfection of Parkin small interfering RNA mitigated PQ-induced mitophagy and worsened A549 cell apoptosis. On the contrary, overexpression of Parkin attenuated PQ-induced cell injury by promoting mitophagy. These results indicated PINK1/Parkin-mediated mitophagy played a protective role in PQ-induced A549 cell damage and provided a potential therapeutic strategy for enhancing mitophagy against PQ poisoning