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衰老会影响大脑皮层对缺氧/复氧的酶促抗氧化反应,但不会消除这种反应。

Aging affects but does not eliminate the enzymatic antioxidative response to hypoxia/reoxygenation in cerebral cortex.

作者信息

Martínez-Romero R, Cañuelo A, Martínez-Lara E, Hernández R, Del Moral M L, Pedrosa J A, Peinado M A, Siles E

机构信息

Department of Experimental Biology, University of Jaén, Paraje Las Lagunillas s/n, 23071-Jaén, Spain.

出版信息

Exp Gerontol. 2006 Jan;41(1):25-31. doi: 10.1016/j.exger.2005.09.009. Epub 2005 Nov 2.

DOI:10.1016/j.exger.2005.09.009
PMID:16260109
Abstract

The effect of aging on basal and hypoxia/reoxygenation levels of both oxidative stress (protein carbonyl and TBARS) and antioxidative-enzyme activity (Cu/Zn-SOD; Mn-SOD; Catalase, CAT; Se-independent and Se-dependent glutathione peroxidase, GPX; glutathione transferase, GST and glutathione reductase, GR) has been studied in the cerebral cortex of adult and old rats. Oxidative stress markers increased with aging and show an age-dependent post-hypoxic response. Moreover, aging caused either no change (GST, GR and CAT) or an increase (Se-GPX, Cu/Zn-SOD, Mn-SOD) in the basal activity of the enzymes analysed. Only Se-independent GPX activity decreases. However, we detected an age-dependent response of SODs to the hypoxic injury. The early and sustained Cu/Zn-SOD activity rise in adult animals became late and weak in aged animals. Meanwhile, aging slowed the Mn-SOD post-hypoxic response although this activity was consistently higher in aged rats. Aging eliminated the post-hypoxic CAT response, but, perhaps offset by increased GPX activity, did not affect the GST response and slightly reduced post-hypoxic GR activity. In conclusion, aging rise basal ROS production, does not diminish or even increase the antioxidative-enzyme activity, and may slow but does not usually eliminate the enzymatic antioxidant response to the increased post-hypoxic ROS generation.

摘要

在成年和老年大鼠的大脑皮层中,研究了衰老对氧化应激(蛋白质羰基和硫代巴比妥酸反应物)以及抗氧化酶活性(铜/锌超氧化物歧化酶;锰超氧化物歧化酶;过氧化氢酶,CAT;硒非依赖性和硒依赖性谷胱甘肽过氧化物酶,GPX;谷胱甘肽转移酶,GST和谷胱甘肽还原酶,GR)基础水平和缺氧/复氧水平的影响。氧化应激标志物随衰老增加,并呈现出年龄依赖性的缺氧后反应。此外,衰老导致所分析酶的基础活性要么没有变化(GST、GR和CAT),要么增加(硒依赖性GPX、铜/锌超氧化物歧化酶、锰超氧化物歧化酶)。只有硒非依赖性GPX活性降低。然而,我们检测到超氧化物歧化酶对缺氧损伤的年龄依赖性反应。成年动物中早期且持续的铜/锌超氧化物歧化酶活性升高在老年动物中变得延迟且微弱。同时,衰老减缓了锰超氧化物歧化酶的缺氧后反应,尽管老年大鼠中该活性始终较高。衰老消除了缺氧后过氧化氢酶反应,但可能被增加的GPX活性所抵消,不影响GST反应,并略微降低缺氧后GR活性。总之,衰老增加基础活性氧生成,不降低甚至增加抗氧化酶活性,可能减缓但通常不会消除对缺氧后增加的活性氧生成的酶促抗氧化反应。

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