SOD-1 deletions in Caenorhabditis elegans alter the localization of intracellular reactive oxygen species and show molecular compensation.
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.
Yanase
Sumino
S
Department of Health Science, Daito Bunka University School of Sports and Health Science, Saitama, Japan.
Onodera
Akira
A
Tedesco
Patricia
P
Johnson
Thomas E
TE
Ishii
Naoaki
N
D000818:Animals; D017173:Caenorhabditis elegans; D015971:Gene Expression Regulation, Enzymologic; D008136:Longevity / Q000235:genetics*; D008928:Mitochondria / Q000201:enzymology*; D017382:Reactive Oxygen Species / Q000378:metabolism*; D013482:Superoxide Dismutase / Q000235:genetics*; D000072105:Superoxide Dismutase-1
D017382:Reactive Oxygen Species; D013482:Superoxide Dismutase; D000072105:Superoxide Dismutase-1