Abstract
To elucidate the role of hydroxyl radical ( OH) species in the generation mechanism of the cochlear pathology induced by transient asphyxia and subsequent re-ventilation, the concentrations of 2,3-hydroxybenzoic acid (DHBA) and 2,5-DHBA, major products arising from the attack of OH upon salicylate, were measured in the perilymph of the guinea pig by the high performance liquid chromatography–electrochemical/UV method. The mean value of 2,3-DHBA concentration in the perilymph significantly increased from the pre-asphyxic level (6.4 μM) to 7.6 μM and 8.8 μM during asphyxia of 3 min duration and at 5 min after the onset of re-ventilation, respectively. The 2,5-DHBA concentration was 7.9 μM before asphyxia, and also significantly increased to 11.5 μM and 16.2 μM during and after asphyxia, respectively. These results strongly indicated that OH was generated in the perilymph of the asphyxic and re-ventilated guinea pig cochlea, and the significance of this increased OH in generating anoxia and re-perfusion injury is discussed with respect to iron and oxygen-derived free radicals.
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