Attenuation of cerebral oxygen toxicity by sound conditioning

Hypothesis: Sound conditioning might reduce cerebral oxygen toxicity. Background: Cerebral oxygen toxicity is related to high levels of reactive oxygen species. Noise-induced hearing loss has been shown to result from ischemia-reperfusion, in which reactive oxygen species play a major role. Repeated exposure to loud noise at levels below that which produces permanent threshold shift prevented noise-induced hearing loss and was associated with significant elevation of the antioxidant enzymes measured in the inner ear. We tested the hypothesis that sound conditioning might reduce cerebral oxygen toxicity. Methods: Forty-five guinea pigs were prepared for electroencephalography and auditory brainstem recording. The auditory brainstem recording detection threshold was determined to confirm baseline normal hearing. The animals were divided into three equal groups and subjected to the following procedures: Group 1, electroencephalography electrode implantation and auditory brainstem recording only; Group 2, exposure to oxygen at 608 kPa (the latency to the first electrical discharge in the electroencephalogram preceding the appearance of seizures was measured); and Group 3, sound conditioning followed by oxygen exposure. The animals were killed, and the brains were excised and homogenized. Brain levels of superoxide dismutase, catalase, glutathione peroxidase, glutathione transferase, glutathione reductase, glucose-6-phosphate dehydrogenase, and thiobarbituric acid reactive substances were compared among the groups. Results: Latency to the first electrical discharge was compared between Groups 2 and 3, and was found to be significantly longer in Group 3 (27.9 ± 11 versus 20.4 ± 7.6 min, p < 0.03). No significant changes were found in brain levels of superoxide dismutase, catalase, glutathione peroxidase, glutathione transferase, glutathione reductase, glucose-6-phosphate dehydrogenase, or thiobarbituric acid reactive substances. Conclusion: Our data show that sound conditioning prolongs the latency to oxygen-induced convulsions. This effect was not accompanied by significant changes in whole-brain antioxidant enzyme activity or the magnitude of lipid peroxidation.