EFFECT OF SUPEROXIDE-DISMUTASE AND SUCCINATE ON DEVELOPMENT OF HYPERBARIC-OXYGEN TOXICITY

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  • 1 January 1977
    • journal article
    • research article
    • Vol. 48  (7) , 645-648
Abstract
Prolonged exposure to hyperbaric O2 (HBO) caused seizures and eventual death. The precise molecular basis for O2 toxicity is not known but may be due to increased biological production of superoxide anion (O2-). Superoxide dismutase (SOD), an enzyme that catalyzes the dismutation of O2- to less toxic forms, was evaluated for its ability to protect against HBO-induced seizures and death and the results were compared to those concurrently obtained with succinate (SUCC), an agent previously reported to protect against HBO-induced seizures. Preconvulsion time and survival time in normal and vitamin E-deficient rats exposed to 100% O2 at 5 ATA [atmospheres absolute pressure] were not significantly prolonged by pretreatment with 2-20 mg/kg SOD i.p. or 0.1-1.0 mg/kg SOD intrathecally. SUCC 12 mmol/kg i.p. significantly prolonged preconvulsion time in normal and vitamin E-deficient rats and survival time in normal rats. The ability of SUCC to stimulate ATP production may account for its protective role. Reasons for the failure of SOD to protect against O2 toxicity are discussed.

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