Abstract
It is known that superoxide anions (O2−), one of reactive oxygen species (ROS), which damage cells, cause by electron leakage from the mitochondrial electron transport system as a major endogenous source. To further explore the relation between overproduction of O2− and cellular damage, we established a transgenic cell line with a point mutation in the cytochrome b large subunit (SDHC) of complex II, which overproduces intercellular (O2−).As expected, this increased O2− induces many apoptosis during cultivation of the cells. Interestingly, many survivors of apoptosis were transformed at higher frequencies compared to non-transgenic cell line. Oxidative stress results in damage to mitochondria as well as other cellular components, and thereby may lead to apoptosis. In addition to it, oxidative stress causes mutations in DNA and leads to cancer. These data support that oxidative stress from mitochondria plays an important role in apoptosis, which leads to precocious aging and carcinogenesis. [J Radiat Res 44:422 (2003)]
