Hoppe S A, Terrell D J, Gottlieb S F
Aviat Space Environ Med. 1984 Oct;55(10):927-30.
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.
长时间暴露于高压氧环境会导致中枢神经系统（CNS）氧中毒，表现为癫痫大发作。超氧阴离子被认为是中枢神经系统氧中毒时组织损伤的一个原因，并且有人提出黄嘌呤氧化酶活性是超氧阴离子的主要来源之一。给几组小鼠分别给予等量的别嘌呤醇、次黄嘌呤或生理盐水，然后使其暴露于5个绝对大气压的氧气环境中。有人提出，作为黄嘌呤氧化酶抑制剂的别嘌呤醇会降低超氧阴离子的形成速率，从而延迟氧诱导癫痫发作的起始时间。还有人提出，次黄嘌呤会增加超氧阴离子的形成速率，缩短惊厥前潜伏期。数据表明，别嘌呤醇和次黄嘌呤均未改变对氧中毒中枢神经系统表现的易感性。这些结果不支持黄嘌呤氧化酶是小鼠脑中超氧阴离子主要来源的理论。
