Hormesis inducing the lifespan extension decreases mitochondrial superoxide radical levels in Caenorhabditis elegans.

Abstract

The hormetic effect, which extends the lifespan by intermittent exposure to hyperoxia, is confirmed in Caenorhabditis elegans (C. elegans). To determine the mechanism of this hormesis, the mitochondrial superoxide radical (O₂^-) level in various age-related strains were measured using a chemiluminescent probe. Hence, the O₂^- level significantly decreased depending on the intermittent exposure to hyperoxia in a strain, which is activated by an insulin/insulin-like growth factor-1 (Ins/IGF-1) signaling pathway such as the age-1 mutant. Furthermore, the expression of some sod-genes was induced to the hormesis. These results suggest that a decrease in the mitochondrial O₂^- levels by activation of the antioxidant systems was associated with hormesis.