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低温兔脑水肿过程中硫代巴比妥酸反应性物质含量及针对过氧化损伤的酶性保护作用

Thiobarbituric acid-reactive material content and enzymatic protection against peroxidative damage during the course of cryogenic rabbit brain edema.

作者信息

Avéret N, Coussemacq M, Cohadon F

机构信息

Laboratoire de Neurochirurgie Expérimentale et Neurobiologie C.N.R.S. 040603, Université de Bordeaux II, France.

出版信息

Neurochem Res. 1990 Aug;15(8):791-5. doi: 10.1007/BF00968556.

Abstract

The relationship between free radicals reactions and the cell detoxifying system was investigated during the development of brain edema following a cryogenic lesion in the rabbit cerebral cortex. The amount of TBA-reactive material present six hours after freezing was less than in the controls, then increased at 48 and 96 hours. The activity of superoxide dismutase (SOD) decreased 6 hours post-injury; at the same time, we observed a stimulation of catalase activity. The glutathione peroxidase activity (GSH-Px) rose 96 hours post-lesion. The decrease of TBA-reactive products could result from an elimination rate that exceeds generation.

摘要

在兔大脑皮层低温损伤后脑水肿形成过程中,研究了自由基反应与细胞解毒系统之间的关系。冷冻后6小时,TBA反应性物质的量低于对照组,然后在48小时和96小时增加。超氧化物歧化酶(SOD)活性在损伤后6小时下降;同时,我们观察到过氧化氢酶活性受到刺激。谷胱甘肽过氧化物酶活性(GSH-Px)在损伤后96小时升高。TBA反应性产物的减少可能是由于消除速率超过生成速率所致。

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