X-Message-Number: 21808 From: "Ben Best" <> Subject: free radical theory of aging falsified -- NON SEQUITURS Date: Mon, 26 May 2003 21:50:48 -0700 Sorry for the delayed response, I only read this a few minutes ago. The conclusion stated in Doug's subject line does not follow from the evidence he presented. > Message #21797 > Date: Sat, 24 May 2003 12:21:12 -0700 (PDT) > From: Doug Skrecky <> > Subject: free radical theory of aging falsified > > [...in flies at least. Motor neuron degeneration is known to limit maximum > fly longevity. By comparison cancer is the main limiting factor in > rodents, but not in humans. (Only 4% of human centenarians die of > cancer.) In humans atherosclerosis is the main limiting factor, with > declines in immunity playing a secondary role. These two factors may be > connected... There may exist no general theory of aging at all. Instead > the nature of "aging" may vary for different species.)] > > J Biol Chem 2003 May 12; [epub ahead of print] The fact that cancer is the main cause of death in rodents does not mean that cancer causes aging in rodents any more than cats cause aging in rodents. The fact that atherosclerosis is the main cause of death in humans does not mean that atherosclerosis causes aging in humans. Moreover, free radicals are known to accelerate atherosclerosis along with quite a few other degenerative diseases. > Effects of overexpression of Cu-Zn and Mn superoxide dismutases, catalase > and thioredoxin reductase genes on longevity in Drosophila melanogaster. > > The overexpression of antioxidative enzymes such as Cu-Zn superoxide > dismutase (SOD), Mn SOD and catalase has previously been reported to > extend life span in transgenic flies (Drosophila melanogaster). The > purpose of the present study was to determine whether life-extending > effects persist if the recipient control strains of flies are relatively > long-lived. Accordingly, the life spans of large numbers of replicate > control and overexpressor lines were determined in two long-lived genetic > backgrounds, involving a combined total of more than 90 000 flies. > Significant increases in the activities of both Cu-Zn SOD and catalase had > no beneficial effect on survivorship in relatively long-lived y w mutant > flies, and were associated with slightly decreased life spans in wild > type flies of the Oregon-R strain. The introduction of additional > transgenes encoding Mn SOD or thioredoxin reductase in the same genetic > background also failed to cause life span extension. In conjunction with > data from earlier studies, the results show that increasing the > activities of these major antioxidative enzymes above wild type levels > does not decrease the rate of aging in long-lived strains of Drosophila, > although there may be some effect in relatively short-lived strains. Long-liveds strains (especially of fruit flies) are often long-lived because they already have high levels of antioxidant enzymes. There is an upper limit to the ability of anti-oxidant enzymes to quench free radicals and reduce aging. The diminishing returns of additional anti-oxidant enzymes against aging does not disprove that anti-oxidant enzymes slow aging and does not disprove that free-radicals contribute to aging. -- Ben Best Rate This Message: http://www.cryonet.org/cgi-bin/rate.cgi?msg=21808