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
> rodents, but not in humans. (Only 4% of human centenarians
die of
> cancer.) In humans atherosclerosis is the main limiting factor,
> 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,
> and thioredoxin reductase genes on longevity in Drosophila
> The overexpression of antioxidative enzymes such as Cu-Zn superoxide
> dismutase (SOD), Mn SOD and catalase has previously been reported
> extend life span in transgenic flies (Drosophila melanogaster).
> purpose of the present study was to determine whether life-extending
> effects persist if the recipient control strains of flies are
> long-lived. Accordingly, the life spans of large numbers of
> control and overexpressor lines were determined in two long-lived
> backgrounds, involving a combined total of more than 90 000
> 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
> data from earlier studies, the results show that increasing
> activities of these major antioxidative enzymes above wild
type levels
> does not decrease the rate of aging in long-lived strains of
> although there may be some effect in relatively short-lived

     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

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