Arieli Yehuda, Kotler Doron, Eynan Mirit, Hochman Ayala
Israel Naval Medical Institute, IDF Medical Corps, Haifa, Israel.
Israel Naval Medical Institute, IDF Medical Corps, Haifa, Israel; Department of Biochemistry, George S. Wise Faculty of Life Sciences, Tel Aviv University, Tel Aviv, Israel.
Respir Physiol Neurobiol. 2014 Jun 15;197:29-35. doi: 10.1016/j.resp.2014.03.006. Epub 2014 Mar 24.
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 1h 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.
我们检验了这样一种假设,即反复暴露于非惊厥性高压氧(HBO)作为预处理可提供针对中枢神经系统氧中毒(CNS - OT)的保护作用。本研究使用了四组大鼠。对照组和阴性对照组(Ctl -)的大鼠饲养于常压空气中。两组大鼠每隔一天在202 kPa下接受1小时的非惊厥性HBO预处理,共进行三次。预处理24小时后,其中一组预处理大鼠和对照组大鼠暴露于608 kPa的惊厥性HBO,并测量CNS - OT的潜伏期。Ctl -组大鼠和第二组预处理大鼠(PrC -)未接受惊厥性HBO暴露。对从海马体和额叶皮质采集的组织进行酶活性和硝基酪氨酸水平评估。在暴露于608 kPa惊厥性氧的组中,预处理后CNS - OT的潜伏期从12.8分钟增加到22.4分钟。在预处理大鼠的海马体中,观察到谷胱甘肽还原酶和葡萄糖 - 6 - 磷酸脱氢酶活性显著降低,而谷胱甘肽过氧化物酶活性显著增加。预处理动物的硝基酪氨酸水平显著较低,对照组大鼠中观察到的水平最高。在预处理大鼠的皮质中,谷胱甘肽S - 转移酶和谷胱甘肽过氧化物酶活性显著增加。反复暴露于非惊厥性HBO可提供针对CNS - OT的保护作用。保护机制涉及抗氧化系统酶活性的改变以及过氧亚硝酸盐水平降低,主要发生在海马体中。