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DNA oxidative damage and life expectancy in houseflies
The objective of this study was to explore the relationship between oxidative molecular damage and the aging process by determining whether such damage is associated with the rate of aging, using the adult housefly as the experimental organism. Because the somatic tissues in the housefly consist of...
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Published in: | Proceedings of the National Academy of Sciences - PNAS 1994-12, Vol.91 (25), p.12332-12335 |
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Main Authors: | , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that cite this one |
Online Access: | Get full text |
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Summary: | The objective of this study was to explore the relationship between oxidative molecular damage and the aging process by determining whether such damage is associated with the rate of aging, using the adult housefly as the experimental organism. Because the somatic tissues in the housefly consist of long-lived postmitotic cells, it provides an excellent model system for studying cumulative age-related cellular alterations. Rate of aging in the housefly was manipulated by varying the rate of metabolism (physical activity). The concentration of 8-hydroxydeoxyguanosine (80HdG) was used as an indicator of DNA oxidation. Exposure of live flies to x-rays and hyperoxia elevated the level of 80HdG. The level of 80HdG in mitochondrial as well as total DNA increased with the age of flies. Mitochondrial DNA was 3 times more susceptible to age-related oxidative damage than nuclear DNA. A decrease in the level of physical activity of the flies was found to prolong the life-span and correspondingly reduce the level of 80HdG in both mitochondrial and total DNA. Under all conditions examined, mitochondrial DNA exhibited a higher level of oxidative damage than total DNA. The 80HdG levels were found to be inversely associated with the life expectancy of houseflies. The pattern of age-associated accrual of 80HdG was virtually identical to that of protein carbonyl content. Altogether, results of this study support the hypothesis that oxidative molecular damage is a causal factor in senescence |
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ISSN: | 0027-8424 1091-6490 |
DOI: | 10.1073/pnas.91.25.12332 |