Radicals may not be that important in CR-effect

[Guest guest]

I think many of you guys have probably already read this, but I think this work is very important, as it is essential that we all "put the 90s behind us" and relegate "free radicals" to their appropriate place in a "larger matrix" of more substantial biological processes.

For too long, individuals that have overemhasized a "chemistry" perspective have ruled the debate. But, the 21st century is the golden age of molecular biology, and so it is fitting that the research community is beginning to see that the various chemicals once thought to hold primacy in the mechanisms of aging are actually the product of a larger, more integrative biological framework.

(Yes, and de Grey is a quack.)

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http://www.the-scientist.com/news/20050715/02

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"Mitochondrial DNA mutations appear to lead to aging by induced apoptosis and not by increased production of free radicals that lead to cellular damage as previously thought, scientists report in this week's Science. Tomas Prolla at the University of Wisconsin-Madison and colleagues found a rise in mtDNA mutations led to premature aging but not to increased levels of reactive oxygen species.

The researchers measured several markers of oxidative stress, including hydrogen peroxide, protein carbonyls, F2-isoprostanes, and oxidative damage to DNA and RNA, in liver and skeletal muscle. None of these markers showed any sign of increased oxidative stress."

Prolla noted that the main mechanism of action of caloric restriction, the only nutritional intervention that retards aging, "was thought to be a suppression of free radical production." Prior research had found that caloric restriction also delayed mtDNA mutation accumulation and reduced mitochondria-linked apoptotic pathways. "So our findings and those of others suggest inhibition of apoptosis may instead be one of the key mechanisms by which caloric restriction retards aging," he said."

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T. pct35768@...

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