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 () and protects organisms from oxidative damage during normal aging. We demonstrate that not only the cytosolic level but also the mitochondrial 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 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.