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铜锌超氧化物歧化酶缺乏会加速黑腹果蝇中与衰老相关标志物的进程。

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

作者信息

Rogina B, Helfand S L

机构信息

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

出版信息

Biogerontology. 2000;1(2):163-9. doi: 10.1023/a:1010039813107.

Abstract

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.

摘要

在衰老的氧化应激假说中,假定随着时间的推移氧化损伤的随机积累会导致衰老。氧化损伤积累的速度决定了衰老的速率,但尚不清楚随机损伤的积累如何能导致衰老的刻板模式。有人提出氧化损伤会诱导基因表达的变化,将随机的损伤输入转化为有模式的输出。为支持这一观点,我们表明,在成年黑腹果蝇中,抗氧化酶铜锌超氧化物歧化酶(Sod)缺乏,氧化应激增加,寿命缩短,无翅基因表达的正常年龄相关时间模式加速。无翅基因表达时间模式的加速与寿命缩短成正比,这表明Sod缺陷动物寿命缩短不是由于异常的病理过程,而是由于衰老速率的增加。

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