Oxidant Stress-Induced Alterations in Mitochondrial Physiology in the Presence and Absence of BCL-2

Extract

Apoptosis is an actively regulated process of cell death necessary for proper control of tissue growth. In humans, ∼100,000 cells die every second by apoptosis and are replaced by new cells of the same number. Apoptosis was originally described by Kerr, Wyllie, and Currie in 1972 as an event characterized by plasma membrane blebbing, cell shrinkage, chromatin condensation, and degradation of DNA (1). Apoptotic death is a tightly controlled process, and the cellular pathways that regulate apoptosis have been well conserved in multicellular organisms from simple to complex animals.

One of the most reproducible inducers of apoptosis is mild oxidative stress. Oxidative modification of proteins and lipids has also been observed in cells undergoing apoptosis in response to nonoxidative stimuli, suggesting that intracellular oxidation may be a general feature of the effector phase of apoptosis. Several incompletely reduced forms of oxygen are highly reactive and quite cytotoxic.