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脂质体介导的脑超氧化物歧化酶和过氧化氢酶增强可抑制中枢神经系统的氧毒性。

Liposome-mediated augmentation of brain SOD and catalase inhibits CNS O2 toxicity.

作者信息

Yusa T, Crapo J D, Freeman B A

出版信息

J Appl Physiol Respir Environ Exerc Physiol. 1984 Dec;57(6):1674-81. doi: 10.1152/jappl.1984.57.6.1674.

Abstract

Enzymes specific for O-2 and H2O2 metabolism [superoxide dismutase (SOD) and catalase] can be delivered to the rat brain following entrapment in liposomes and intravenous injection and will protect against hyperbaric O2-induced convulsions in rats. Liposome-mediated superoxide dismutase and catalase augmentation of brain enzyme activity was 2.7-fold and 1.9-fold, respectively, 15 min after intravenous injection of superoxide dismutase plus catalase-entrapped liposomes. Rats treated with liposomes containing superoxide dismutase plus catalase 2 h before 6 ATA 100% O2 exposure had the time to convulsion extended three times that of controls. This protective effect was dose-dependent and was primarily due to augmentation of catalase activity. These findings show O-2 and H2O2 are important mediators of hyperbaric O2-induced central nervous system toxicity and that liposome-mediated augmentation of brain antioxidant enzymes has a biological effect.

摘要

参与O₂和H₂O₂代谢的特异性酶[超氧化物歧化酶(SOD)和过氧化氢酶],经脂质体包裹并静脉注射后,能够被递送至大鼠脑内,并且可以预防大鼠因高压氧引起的惊厥。静脉注射包裹有超氧化物歧化酶和过氧化氢酶的脂质体15分钟后,脂质体介导的脑内超氧化物歧化酶和过氧化氢酶活性增强分别为2.7倍和1.9倍。在6个绝对大气压的100% O₂暴露前2小时,用含有超氧化物歧化酶加过氧化氢酶的脂质体处理的大鼠,惊厥发作时间延长至对照组的三倍。这种保护作用具有剂量依赖性,主要是由于过氧化氢酶活性增强。这些发现表明,O₂和H₂O₂是高压氧诱导的中枢神经系统毒性的重要介质,并且脂质体介导的脑内抗氧化酶增强具有生物学效应。

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