Toxicants can influence the mitochondrial apoptotic pathway in various ways. Many chemicals and drugs induce oxidative stress, leading to mitochondrial dysfunction. This results in the opening of the mitochondrial permeability transition pore, loss of mitochondrial membrane potential, and the release of cytochrome c into the cytosol. Once in the cytosol, cytochrome c binds to Apaf-1, forming the apoptosome, which subsequently activates caspase-9. This activation cascade ultimately leads to the activation of effector caspases, such as caspase-3, culminating in apoptosis.
