脂质体介导的脑SOD和过氧化氢酶增强抑制CNS O2毒性。

T Yusa, J D Crapo, B A Freeman
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引用次数: 82

摘要

O-2和H2O2代谢的特异性酶[超氧化物歧化酶(SOD)和过氧化氢酶]可以通过脂质体包裹和静脉注射传递到大鼠大脑,并可以保护大鼠免受高压o2引起的惊厥。脂质体介导的超氧化物歧化酶和过氧化氢酶在静脉注射超氧化物歧化酶加过氧化氢酶包埋脂质体15 min后,脑酶活性分别提高2.7倍和1.9倍。在6ata 100% O2暴露前2 h用含有超氧化物歧化酶和过氧化氢酶的脂质体处理大鼠惊厥时间延长3倍。这种保护作用是剂量依赖性的,主要是由于过氧化氢酶活性的增强。这些发现表明,o2和H2O2是高压氧诱导中枢神经系统毒性的重要介质,脂质体介导的脑抗氧化酶增强具有生物学效应。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Liposome-mediated augmentation of brain SOD and catalase inhibits CNS O2 toxicity.

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.

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