The effect of allopurinol on oxygen-induced seizures in mice.
Prolonged exposure to hyperbaric oxygen causes central nervous system (CNS) oxygen toxicity manifested by grand mal seizures. The superoxide anion is believed to be a cause of tissue damage in CNS oxygen toxicity and it is proposed that xanthine oxidase activity is one of the prime sources of superoxide. Groups of mice were given equivalent doses of allopurinol, hypoxanthine, or saline, and exposed to five atmospheres absolute of oxygen. It was proposed that allopurinol, a xanthine oxidase inhibitor, would decrease the rate of superoxide formation thus delaying the onset of oxygen-induced seizures. It was further proposed that hypoxanthine would increase the rate of superoxide formation decreasing the preconvulsive latency. The data indicated that neither allopurinol nor hypoxanthine altered susceptibility to the CNS manifestations of oxygen toxicity. The results do not support the theory that xanthine oxidase is a prime source of superoxide anions in mouse brain.
D000493:Allopurinol / Q000627:therapeutic use*; D000818:Animals; D001921:Brain / Q000187:drug effects / Q000378:metabolism; D004830:Epilepsy, Tonic-Clonic / Q000209:etiology / Q000517:prevention & control*; D005260:Female; D005609:Free Radicals; D006931:Hyperbaric Oxygenation / Q000009:adverse effects*; D007042:Hypoxanthines / Q000627:therapeutic use; D008297:Male; D051379:Mice; D010100:Oxygen / Q000633:toxicity; D013481:Superoxides / Q000378:metabolism; D014969:Xanthine Oxidase / Q000037:antagonists & inhibitors*
D005609:Free Radicals; D007042:Hypoxanthines; D013481:Superoxides; D000493:Allopurinol; D014969:Xanthine Oxidase; D010100:Oxygen