Mitochondrial response to environmental toxicants

The mitochondria are important subcellular targets of environmental contaminants. Short and long exposure with environmental toxicants is associated with a series of toxic effects on mitochondria, which originate from the respiratory chain dysfunction, mutations and damages in mitochondrial DNA (mtDNA), reactive oxygen species (ROS) formation, oxidative stress, dynamic changes in mitochondrial fusion and fission, and structure/membrane damages. The toxic effects of environmental toxicants on mitochondrial intact membranes and morphology, and their determination of cell fate, have already been broadly studied and reported on. Obviously, environmental toxicant-induced mitochondrial dysfunction can hinder ATP production, and may elevate ROS production and oxidative stress. The increased ROS induced by environmental toxicants can damage mtDNA more, and consequently lead to inactivation of some respiratory chain protein-encoding mtDNA, generating a vicious circle of amplifying mitochondrial damage. Many diseases have been identified as caused by mitochondrial dysfunction, and many environmental contaminants such as pesticides, metals, and polycyclic aromatic hydrocarbons (PAHs) have been identified as previously unrecognized mitochondrial toxicants. In this chapter, we discuss how the mitochondria are susceptible to environmental contaminants, with particular attention to factors that may modulate vulnerability. Finally, we review mitochondrial disturbance induced by environmental contaminants with a particular focus on those toxicants that target electron transport chain, mitochondrial DNA, mitochondrial permeability transition pores (MPTP), and mitochondria-related diseases.