Author: Perez, V.I.; Bokov, A.; Van Remmen, H.; Mele, J.; Ran, Q.; Ikeno, Y.; Richardson, A.
Description: Currently, the oxidative stress (or free radical) theory of aging is the most popular explanation of how aging occurs at the molecular level. While data from studies in invertebrates (e.g., C. elegans and Drosophila) and rodents show a correlation between increased lifespan and resistance to oxidative stress (and in some cases reduced oxidative damage to macromolecules), direct evidence showing that alterations in oxidative damage/stress play a role in aging are limited to a few studies with transgenic Drosophila that overexpress antioxidant enzymes. Over the past eight years, our laboratory has conducted an exhaustive study on the effect of under- or overexpressing a large number and wide variety of genes coding for antioxidant enzymes. In this review, we present the survival data from these studies together. Because only one (the deletion of the Sod1 gene) of the 18 genetic manipulations we studied had an effect on lifespan, our data calls into serious question the hypothesis that alterations in oxidative damage/stress play a role in the longevity of mice.
Subject headings: Aging/genetics/physiology; Animals; Catalase/genetics/metabolism; Humans; Mice; Mice, Knockout; Mice, Transgenic; Oxidative Stress/physiology; Superoxide Dismutase/genetics/metabolism; Survival Analysis
Publication year: 2009
Journal or book title: Biochimica et Biophysica Acta
Volume: 1790
Issue: 10
Pages: 1005-1014
Find the full text:Â https://www.strategian.com/fulltext/Perez2009.pdf
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Type: Journal Article
Serial number: 1929