Protein carbonyl accumulation in aging dauer formation-defective (daf) mutants of Caenorhabditis elegans

Abstract

It is known that a dauer-constitutive gene, daf-2, controls both larval development and adult life span in Caenorhabditis elegans. The increased life span caused by the daf-2 mutation can be enhanced by a daf-12 mutation and suppressed by a daf-16 mutation. In order to determine the correlation between longevity and oxidative stress in these mutants, protein carbonyl (a good indicator of oxidative damage during aging) was measured. Mean life spans of these mutants were in the order of daf-16 < daf-2;daf-16 ≃ wild type < daf-2 < daf-2;daf-12. Accumulations of protein carbonyl in these wild- type and daf mutants were in a mirror image of the order of their life spans. These results strongly support the notion that oxidative damage is one of the major causal factors for lifespan determination in C. elegans.