Abstract

Tissue damage due to hyperbaric oxygen treatment or radiation treatment may be mediated by free radicals and lipid peroxidation by-products. We have found that the retinas of animals deficient in antioxidant nutrients are very susceptible to tissue damage induced by hyperbaric oxygen treatment. Hyperbaric oxygen treatment was found to adversely affect the electroretinograms of rats fed either a diet deficient in both vitamin E and selenium (the basal or B diet) or a diet deficient in vitamin E alone (B + Se diet). Vitamin E and selenium are micronutrients thought to play essential roles in preventing in vivo lipid peroxidation. After 4 weeks of hyperbaric oxygen treatment (3.0 ATA of 100% oxygen, 1.5 hr per day, 5 days/ week), rats fed the B diet deficient in vitamin E and selenium showed decreased (p < 0.05) a-wave amplitudes (85 ± 10 μV, N = 11) compared with a-wave amplitudes (150 ± 10 μV, N = 21) for rats fed an identical diet but not treated with hyperbaric oxygen. Rats fed a basal diet supplemented with both vitamin E and selenium (the B + E + Se diet) or with vitamin E alone (the B + E diet) showed constant a-and b-wave amplitudes that did not decrease after 15 weeks of hyperbaric oxygen treatment. After 15 weeks of hyperbaric oxygen treatment, rats fed the B + Se diet deficient in vitamin E alone showed decreased (p < 0.01) a-wave (61 ± 9 μV, N = 4) and b-wave (253 ± 23 μV, N = 4) amplitudes compared with a-wave (115 ± 7 μV) and b-wave amplitudes (450 ± 35 μV) for rats fed the same diet but not treated with hyperbaric oxygen. Dietary antioxidants appeared to provide protection from hyperbaric oxygen damage to the retina. Quantitative histopathology studies are now under way to determine which cell types in the retina of antioxidant-deficient rats have been damaged by hyperbaric oxygen treatment.

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