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- W203492124 abstract "Living organisms are constantly exposed to oxidative stress from environmental agents and from endogenous metabolic processes. The resulting oxidative modifications occur in proteins, lipids, and DNA. Many different DNA base changes have been seen following oxidative stress, and these lesions are widely considered as instigators for the development of cancer, aging, and neurological degradation. There are over 100 oxidative base modifications in DNA and one of these is 8-hydroxyguanosine (8-oxoG), which is the lesion that has been most widely studied. Oxidative DNA damage is thought to contribute to carcinogenesis, and studies have shown that oxidative DNA damage accumulates in cancerous tissue. There is evidence for the accumulation of oxidative DNA damage with age, based on studies mainly measuring the increase in 8-oxoG. Human premature aging syndromes are rare disorders where the patients exhibit many of the features of normal aging at an early stage in life. These conditions are also termed “segmental progerias,” indicating that several, but not all of the symptoms, reflect the normal aging process. They are natural human mutants and serve as good model systems for molecular aging research. Two of these conditions are the progeroid disorders: Cockayne syndrome (CS) and Werner syndrome (WS), which share several clinical features that are associated with normal aging." @default.
- W203492124 created "2016-06-24" @default.
- W203492124 creator A5089917586 @default.
- W203492124 date "2001-01-01" @default.
- W203492124 modified "2023-09-27" @default.
- W203492124 title "DNA damage and its processing with aging: Human premature aging syndromes as model systems" @default.
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- W203492124 doi "https://doi.org/10.1016/s1566-3124(01)04033-0" @default.
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