Heavy metal pollution not only poses a serious threat to both animal growth and public health, but also to aquatic life. Mitochondria are the first target sites for a variety of
heavy metals, and recently great attention has been made on the mechanisms of toxicity of
heavy metals on mitochondria. The underlying molecular mechanisms of
heavy metals that may induce abnormal mitochondrial functions combined with different other
environmental pollutants in the body reached a certain level, result in
stunted growth and development, abnormal physiological and biochemical changes, over expression of genes, altered behavior and series of toxicological effects including inadequate metabolism. The
heavy metals alter mitochondrial membrane permeability, generate increased amount of
reactive oxygen species (ROS), by changing the structure of ROS clearance
enzyme (
antioxidant enzymes) to inhibit its activity. Due to rapid and increased generation of ROS and decreased status of
antioxidant enzymes, different
environmental pollutants accumulate in the exposed organisms and lead to induction of oxidative stress on the mitochondria. The increased generation of ROS also causes damage to mitochondrial respiratory chain, oxidative phosphorylation decoupling,
ATP synthesis disorders, and mitochondrial apoptosis. This review mainly expounds various molecular mechanisms and progress of mitochondrial functional damage to explore the molecular mechanisms of
heavy metal damage to mitochondrial functions, which provides a basis for the treatment of
heavy metal poisoning, and protects the animal and animal-derived food safety from the source.