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Protection from hyperbaric oxidant stress by administration of buthionine sulfoximine.

作者信息

Komadina K H, Duncan C A, Bryan C L, Jenkinson S G

机构信息

Lung Metabolic Unit, University of Texas Health Science Center, San Antonio.

出版信息

J Appl Physiol (1985). 1991 Jul;71(1):352-8. doi: 10.1152/jappl.1991.71.1.352.

DOI:10.1152/jappl.1991.71.1.352
PMID:1680846
Abstract

To explore the role of glutathione in protecting rats from hyperbaric hyperoxia, we administered buthionine sulfoximine (BSO) to block gamma-glutamyl cysteine synthase activity and decrease tissue glutathione synthesis. We then exposed these animals and their vehicle-treated matched controls to 100% oxygen at 4 ATA or room air at 1 ATA. After BSO treatment, glutathione concentrations in air-exposed controls decreased 62% in lung, 76% in liver, 28% in brain, and 62% in plasma. Paradoxically, BSO-treated rats were protected from hyperbaric hyperoxia. The BSO-treated animals seized significantly later and had a markedly prolonged time of survival compared with the vehicle-treated controls. We conclude that BSO treatment protects rats from hyperbaric hyperoxia, despite its effects of lowering plasma and tissue glutathione concentrations. This protection may be related to a direct effect of the compound in decreasing free radical-mediated tissue injury, increasing tissue antioxidant defenses, or increasing seizure threshold.

摘要

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