Effects of oxygen on protein carbonyl and aging in Caenorhabditis elegans mutants with long (age-1) and short (mev-1) life spans.

Protein carbonyl accumulation is an indicator of oxidative damage during aging. The relationship between oxidative stress and protein carbonylation during aging was studied by using a long (age-1) and a short (mev-1) life span mutant of Caenorhabditis elegans. Protein carbonyl concentrations were similar in young adults of both mutants and wild type; however, the subsequent age-dependent accumulation was different with the genotype. The mev-1 mutant (with 50% superoxide dismutase activity) accumulated protein carbonyl at a faster rate than did wild type, whereas the age-1 mutant exhibited no obvious increase except a significant accumulation at the end of extended life span. Exposure to 70% oxygen between the ages of 4 and 11 days caused afar greater accumulation of carbonyl in mev-1 than in wild type, but not in age-1. In addition, rates of aging were enhanced by oxygen in a concentration-dependent fashion. The age-1 mutant was more resistant to, but mev-1 was more sensitive to, such oxygen enhancements of aging than was wild type. These results provide further evidence that oxidative damage is one of the major causal factors for aging in C. elegans, and that the age-1 and mev-1 genes govern resistance to oxidative stress.