The mitochondria is the site of metabolic pathways like the Krebs cycle and the electron transport chain that allow our cells to produce ATP. However, it also plays a role in apoptosis, a form of programmed cell death. Note the distinction between necrosis, an uncontrolled form of cell death that usually occurs in response to extreme stress, and apoptosis, which is controlled and often confers an advantage to an organism. For example, during embryonic development, the digits on our hands are “carved” out of an initial paw-like structure through apoptosis of the unwanted tissue, ultimately producing a hand with five separate fingers.
In addition to sculpting tissues during embryonic development, apoptosis can be triggered by various other factors. These include extensive DNA damage that cannot be repaired by DNA repair mechanisms, viral infection, environmental stress (such as oxygen or nutrient deprivation), and a loss of physical proximity or a chemical signal (such as growth factors) from neighboring cells.
Apoptosis can also be triggered by reactive oxygen species (ROS), which are oxygen molecules with an unstable number of electrons that are highly reactive and can result in toxic reactions with cellular components like DNA, proteins, and lipid membranes. ROS include the negatively charged superoxide anion, the neutrally charged hydroxide molecule, and hydrogen peroxide, which can be formed in our cells. Recall that oxygen is the final electron acceptor in the electron transfer chain, necessary for the production of ATP. However, up to 4% of oxygen molecules are improperly reduced during oxidative phosphorylation, leading to the production of ROS. Although enzymatic mechanisms exist to convert ROS to less reactive species, extensive oxidative damage can induce apoptosis.