SOD-1 deletions in Caenorhabditis elegans alter the localization of intracellular reactive oxygen species and show molecular compensation.
Yanase S, Onodera A, Tedesco P, Johnson TE, Ishii N
J Gerontol A Biol Sci Med Sci (2009) 64: 530-9.
Category: aging, mitochondria, ROS ¤ Added: Jun 25, 2009 ¤ Rating: ◊◊
Superoxide dismutase (SOD) is an enzyme that catalytically removes the superoxide radical (*O2-) and protects organisms from oxidative damage during normal aging. We demonstrate that not only the cytosolic *O2- level but also the mitochondrial *O2- level increases in the deletion mutants of sod-1 gene encoding Cu/Zn SOD in Caenorhabditis elegans (C. elegans). Interestingly, this suggests that the activity of SOD-1, which so far has been thought to act mainly in cytoplasm, helps to control the detoxification of *O2- also in the mitochondria. We also found functional compensation by other SODs, especially the sod-5 gene, which was induced several fold in the mutants. Therefore, the possibility exists that the compensative expression of sod-5 gene in the sod-1 deficit is associated with the insulin/insulin-like growth factor-1 (Ins/IGF-1) signaling pathway, which regulates longevity and stress resistance of C. elegans because the sod-5 gene may be a target of the pathway.
Keywords: Animals / Caenorhabditis elegans / Gene Expression Regulation, Enzymologic / Longevity / Mitochondria / Reactive Oxygen Species / Superoxide Dismutase