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• W133053059 abstract "DNA damage is hypothesized to be a driver of aging. In support of this, DNA damage and genetic mutations, resulting from replication of that damage, both increase in the nuclear genome as organisms age. Furthermore, long-lived species are relatively resistant to genotoxic stress. Conversely, organisms with DNA repair-deficient or genome instability disorders have decreased lifespans and age rapidly, which supports this theory. One main source of endogenous DNA damage is reactive oxygen species (ROS) generated by mitochondria. While it is true that ROS can damage other macromolecules in the cell, DNA is the only one that is repaired rather than replaced, illustrating the dire consequences of DNA damage. If repair is not 100% complete over a lifetime, it stands to reason that this unrepaired damage could be a major contributor to aging.Ercc1-/Δ mice are deficient in multiple DNA repair pathways and therefore suffer more DNA damage than normal mice. As a consequence, they age prematurely, modeling a human progeroid syndrome. This makes them a useful in vivo system for studying the contribution of DNA damage to aging. For this reason, we challenged the mice with a chemotherapeutic crosslinking agent to determine if DNA damage promotes aging, with an environmental contaminant and a diet of polyunsaturated fatty acids to see if these promote DNA damage and aging. We found that a particular class of lesions, DNA interstrand crosslinks, accelerate aging associated changes through a cytostatic, rather than cytotoxic mechanism. We also exposed the mice to a specialized antioxidant to test the hypothesis that mitochondrial-derived reactive oxygen species are the cause of endogenous DNA damage that promotes aging. Collectively, these studies identified genes, environmental influences and therapeutics that impact lifespan and healthspan. In total, the studies strongly support the hypothesis that DNA damage can promote degenerative changes associated with aging. These studies have public health significance as they reveal multiple novel strategies to decrease the DNA damage burden, therefore presenting potential opportunities to improve quality of life in old age." @default.
• W133053059 created "2016-06-24" @default.
• W133053059 creator A5066431589 @default.
• W133053059 date "2012-08-13" @default.
• W133053059 modified "2023-09-24" @default.
• W133053059 title "The Contribution of DNA Interstrand Crosslinks to Aging" @default.
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