抄録
In Caenorhabditis elegans (C. elegans), the effect of hormesis that extends the life-span by exposure to oxygen radicals for a short time is confirmed. We have clarified that the daf-16 gene, which is homologous to FOXO transcription factor, participates in the hormesis using AGE mutants in C. elegans. In general, it is thought that hormesis is caused by activation of antioxidant systems dependent on pre-exposure to low dosis of radicals. To clarify the mechanism of inducement in hormesis, the change in concentration of intracellular superoxide when exposed to low dosis of radicals was measured by the MPEC method. Furthermore, to demonstrate the activation of antioxidant systems when hormesis was induced immediately, the mRNA expression of antioxidant genes was measured using RT-PCR. As a result, the concentration of intracellular superoxide anion was decreased significantly by exposure to low dosis of oxygen radical that causes the life-span extension in the age-1 mutant. Moreover, mRNA expression of the antioxidant genes such as SOD and catalase in age-1 mutant was increased significantly than daf-16 mutant. This indirectly shows that antioxidant systems were activated by the exposure to low dosis of oxygen radicals. Therefore, two possibilities that antioxidant systems in C. elegans was necessary to induce the life-span extension due to hormesis, and the DAF-16 transcription factor had acted in the upstream for this activation, were suggested.
