Human erythrocyte superoxide dismutase activity during deep diving

Area of Science:

• Biomedical Science
• Occupational Health
• Marine Biology

Background:

• High pressure oxygen (HPO) is increasingly used in clinical settings and offshore industries.
• Understanding HPO's toxic effects, particularly on red blood cells, is crucial for safety.

Purpose of the Study:

• To investigate the impact of high pressure exposure on erythrocyte superoxide dismutase (SOD) activity in divers.
• To determine the mechanism behind SOD activity changes and assess red blood cell resistance to oxygen toxicity.

Main Methods:

• Monitoring erythrocyte SOD activity in divers at depths greater than 150m.
• Assaying total red cell SOD protein and activity, and examining for intra-cellular Heinz bodies.
• Measuring intra-membrane lipid peroxidation products in red blood cell fractions.
• Conducting in vitro experiments on pressure-stressed human red blood cells at varying oxygen pressures.

Main Results:

• Erythrocyte SOD activity decreased by an average of 20% at depths exceeding 150m.
• The reduction in SOD activity was attributed to the loss of immuno-measurable enzyme, not Heinz body formation.
• Increased intra-membrane lipid peroxidation products were observed in denser red cell fractions.
• Human red blood cells demonstrated resistance to oxygen up to 0.021 MPa (0.21 bar), after which SOD activity loss and hemolysis occurred during decompression.

Conclusions:

• High pressure oxygen exposure significantly impacts erythrocyte SOD activity in divers.
• The primary mechanism involves the loss of functional SOD enzyme, with lipid peroxidation as a secondary effect.
• Human red blood cells have a defined tolerance limit to high pressure oxygen before experiencing detrimental effects like hemolysis.