Superoxide in Apoptosis

作者：Jiyang Cai, Dean P. Jones · 发表于：Journal of Biological Chemistry · 年份：1998 · DOI：10.1074/jbc.273.19.11401 · 被引用次数：765 · 研究领域：Cell death mechanisms and regulation、Mitochondrial Function and Pathology、ATP Synthase and ATPases Research

Activation of apoptosis is associated with generation of reactive oxygen species. The present research shows that superoxide is produced by mitochondria isolated from apoptotic cells due to a switch from the normal 4-electron reduction of O2 to a 1-electron reduction when cytochrome c is released from mitochondria. Bcl-2, a protein that protects against apoptosis and blocks cytochrome c release, prevents superoxide production when it is overexpressed. The switch in electron transfer provides a mechanism for redox signaling that is concomitant with cytochrome c-dependent activation of caspases. The block of cytochrome c release provides a mechanism for the apparent antioxidant function of Bcl-2.