Hyperbaric oxygen preconditioning protects rats against CNS oxygen toxicity.

Yehuda Arieli, Doron Kotler, Mirit Eynan, Ayala Hochman
Author Information
  1. Yehuda Arieli: Israel Naval Medical Institute, IDF Medical Corps, Haifa, Israel. Electronic address: yarieli@netvision.net.il.
  2. Doron Kotler: 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.
  3. Mirit Eynan: Israel Naval Medical Institute, IDF Medical Corps, Haifa, Israel.
  4. Ayala Hochman: Department of Biochemistry, George S. Wise Faculty of Life Sciences, Tel Aviv University, Tel Aviv, Israel.

Abstract

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.

Keywords

MeSH Term

Animals
Blotting, Western
Catalase
Central Nervous System Diseases
Frontal Lobe
Glucosephosphate Dehydrogenase
Glutathione Peroxidase
Glutathione Reductase
Glutathione Transferase
Hippocampus
Hyperbaric Oxygenation
Male
Oxygen
Rats, Sprague-Dawley
Time Factors
Tyrosine

Chemicals

3-nitrotyrosine
Tyrosine
Glucosephosphate Dehydrogenase
Catalase
Glutathione Peroxidase
Glutathione Reductase
Glutathione Transferase
Oxygen

Word Cloud

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