作者: Ellen R. Taylor , Fiona Hurrell , Richard J. Shannon , Tsu-Kung Lin , Judy Hirst
关键词:
摘要: Increased production of reactive oxygen species (ROS) by mitochondria is involved in oxidative damage to the organelle and committing cells apoptosis or senescence, but mechanisms this increase are unknown. Here we show that ROS mitochondrial complex I increases response oxidation glutathione pool. This correlates with thiols on 51- 75-kDa subunits forming mixed disulfides glutathione. Glutathionylation superoxide complex, when reduced, returns basal levels. Within intact pool disulfide also leads glutathionylation I, which increased formation. In case, most converted hydrogen peroxide, can then diffuse into cytoplasm. mechanism reversible suggests how might regulate redox signaling shows could contribute pathological changes occur during stress.