Interaction between mitophagy, cadmium and zinc

Mitophagy is the selective degradation of mitochondria by autophagy. This process is considered to be one of the stages of mitochondrial quality control, as a result of which damaged depolarized mitochondria are eliminated, thus limiting the formation of reactive oxygen species and the release of apoptogenic factors. Selective degradation of mitochondria by autophagy is one of the main ways to protect cells from cadmium toxicity, which results in dysfunction of the mitochondrial electron transport chain, leading to electron leakage, production of reactive oxygen species and cells death. However, excessive autophagy can be dangerous for cells. Currently, the participation of cadmium ions in normal physiological processes has not been detected. Zn2+, unlike Cd2+, regulate the activity of a large number of functionally important proteins, including transcription factors, enzymes, and adapters. It has been shown that Zn2+ not only participate in autophagy, but are also crucial for basal or induced autophagy. It is likely that zinc drugs can be used to reduce the cadmium toxicity and in the regulation of mithophagy. •Zn2+ may have an anti-apoptotic effect.•Cd2+ cause oxidative stress in multiple ways.•Cd2+-induced oxidative stress causes activation of mitophagy.•Cd2+-induced mitophagy mediated by PINK1/Parkin.•Zinc preparations can be used to regulate Cd2+-induced autophagy.•Zinc preparations can be used to reduce the toxicity of cadmium.