Hyperbaric oxygen preconditioning protects rats against CNS oxygen toxicity

被引:11
作者
Arieli, Yehuda [1 ]
Kotler, Doron [1 ,2 ]
Eynan, Mirit [1 ]
Hochman, Ayala [2 ]
机构
[1] IDE Med Corps, Israel Naval Med Inst, Haifa, Israel
[2] Tel Aviv Univ, George S Wise Fac Life Sci, Dept Biochem, IL-69978 Tel Aviv, Israel
关键词
Central nervous system oxygen toxicity; Hyperbaric oxidative stress; Reactive oxygen species scavengers; ISCHEMIA-REPERFUSION INJURY; NITRIC-OXIDE PRODUCTION; OXIDATIVE STRESS; ANTIOXIDANT ENZYMES; UP-REGULATION; DNA-DAMAGE; TYROSINE NITRATION; BRAIN; GLUCOSE-6-PHOSPHATE-DEHYDROGENASE; EXPOSURE;
D O I
10.1016/j.resp.2014.03.006
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
We examined the hypothesis that repeated exposure to non-convulsive hyperbaric oxygen (HBO) as preconditioning provides protection against central nervous system oxygen toxicity (CNS-OT). Four groups of rats were used in the study. Rats in the control and the negative control (-Ctl) groups were kept in normobaric air. Two groups of rats were preconditioned to non-convulsive HBO at 202 kPa for 1 h once every other day for a total of three sessions. Twenty-four hours after preconditioning, one of the preconditioned groups and the control rats were exposed to convulsive HBO at 608 kPa, and latency to CNS-OT was measured. Ctl- rats and the second preconditioned group (PrC) were not subjected to convulsive HBO exposure. Tissues harvested from the hippocampus and frontal cortex were evaluated for enzymatic activity and nitrotyrosine levels. In the group exposed to convulsive oxygen at 608 kPa, latency to CNS-OT increased from 12.8 to 22.4 min following preconditioning. A significant decrease in the activity of glutathione reductase and glucose-6-phosphate dehydrogenase, and a significant increase in glutathione peroxidase activity, was observed in the hippocampus of preconditioned rats. Nitrotyrosine levels were significantly lower in the preconditioned animals, the highest level being observed in the control rats. In the cortex of the preconditioned rats, a significant increase was observed in glutathione S-transferase and glutathione peroxidase activity. Repeated exposure to non-convulsive HBO provides protection against CNS-OT. The protective mechanism involves alterations in the enzymatic activity of the antioxidant system and lower levels of peroxynitrite, mainly in the hippocampus. (C) 2014 Elsevier BM. All rights reserved.
引用
收藏
页码:29 / 35
页数:7
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