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Glutathione and non-protein sulfhydryl in cerebral cortex and lung in mice exposed to high oxygen pressure
Abstract:
Mice were exposed to 6 atm of 100% O2, and killed at the onset of hyperactivity, convulsions, and 10(s) post convulsions. Examination of brain cortex from mice killed at these stages of O2 toxicity revealed no change in oxidized glutathione (GSSG), non-protein sulfhydryls (NPSH), total glutathione (GSH + GSSG), the GSH/GSSG ratio, glutathione reductase and glutathione peroxidase. Mice exposed to 4 atm for 1 h or 6 atm for 16 min exhibited a 36% and 33% decrease in lung NPSH respectively, but no change in cortical NPSH was observed. Although intraventricular diethylmaleate (DEM) decreased cerebral NPSH 72%, no change in the susceptibility of mice to O2 convulsions was found. Disulfiram, an effective O2 convulsive protectant had no effect on either cortical NPSH or total glutathione.
Insights
High oxygen levels did not alter brain glutathione levels in mice, even during convulsions. Lung sulfhydryl levels decreased, but this did not affect oxygen convulsion susceptibility.
Area of Science:
- Biochemistry
- Physiology
- Toxicology
Background:
- Oxygen toxicity is a significant concern in hyperbaric environments.
- Glutathione (GSH) and sulfhydryls are critical antioxidants.
- Their role in oxygen-induced seizures is not fully understood.
Purpose of the Study:
- To investigate the changes in glutathione and non-protein sulfhydryl levels in the brain cortex and lungs of mice during oxygen toxicity.
- To determine if these biochemical changes correlate with the onset of oxygen-induced convulsions.
- To assess the effect of agents that modify sulfhydryl levels on oxygen convulsion susceptibility.
Main Methods:
- Mice were exposed to hyperbaric 100% oxygen (6 atm).
- Biochemical assays were performed on brain cortex and lung tissue at various stages of oxygen toxicity.
- Diethylmaleate (DEM) was used to deplete cerebral sulfhydryls, and disulfiram was used as a protective agent.
Main Results:
- No significant changes were observed in brain cortical glutathione (oxidized, reduced, total, or ratio) or related enzymes (reductase, peroxidase) during oxygen toxicity.
- Lung non-protein sulfhydryls (NPSH) decreased significantly at 4 atm and 6 atm oxygen exposure.
- Cortical NPSH remained unchanged, and depletion of cerebral NPSH with DEM did not alter susceptibility to oxygen convulsions. Disulfiram did not affect cortical NPSH or total glutathione.
Conclusions:
- Brain glutathione homeostasis is maintained during acute oxygen toxicity in mice.
- Lung sulfhydryl depletion does not appear to be a primary factor in the development of oxygen convulsions.
- Cerebral sulfhydryl levels and their modulation do not play a critical role in the susceptibility to oxygen-induced seizures.