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Biogerontology. 2000;1(2):163-9.

Cu, Zn superoxide dismutase deficiency accelerates the time course of an age-related marker in Drosophila melanogaster.

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Department of Genetics and Developmental Biology, School of Medicine, University of Connecticut Health Center, Farmington, CT 06030, USA.


In the oxidative stress hypothesis of aging the random accumulation of oxidative damage over time is postulated to cause aging. The pace at which oxidative damage accrues determines the rate of aging, but it is less clear how the accumulation of random damage could cause the stereotypic pattern of aging. It has been proposed that oxidative damage induces changes in gene expression, translating a random input of damage into a patterned output. In support of this we show that in adult Drosophila melanogaster, with a deficiency in the anti-oxidant enzyme Cu, Zn superoxide dismutase (Sod), an increase in oxidative stress, and a shortened life span, there is acceleration in the normal age-related temporal pattern of wingless gene expression. The acceleration in the temporal pattern of wingless gene expression is proportional to the shortened life span suggesting that the shortened life span of Sod deficient animals is due, not to an abnormal pathological process, but to an increase in the rate of aging.

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