论文部分内容阅读
实验使用的昆明种雄性小鼠随机分为脂质体包封超氧化物歧化酶(L-SOD)组、空白脂质体(对照)组和游离超氧化物酶(F-SOD)组。结果发现,L-SOD 组小鼠比其他两组出现氧中毒的时间明显推迟,死亡率降低,血循中超氧负离子浓度较低,脑细胞超微结构变化较轻。L-SOD 组与其他两组比,小鼠肝细胞AKP、G-6-P_(ase)和CCO 活性减弱较轻,而过氧化氢酶活性减弱程度最严重。这些资料表明,L-SOD 对高压氧下小鼠的急性氧中毒有显著预防作用;同时也提示高压氧下,氧在机体内产生过多的氧自由基是造成急性氧中毒的直接原因。
Kunming male mice used in the experiment were randomly divided into L-SOD group, blank liposome (control) group and free superoxide dismutase (F-SOD) group. The results showed that the mice in L-SOD group were significantly delayed in oxygen poisoning than the other two groups, the mortality was decreased, the concentration of superoxide anion in blood was low, and the ultrastructure of brain cells was less changed. Compared with the other two groups, the activities of AKP, G-6-Psease and CCO in the L-SOD group were weaker than those in the other two groups, while the activity of catalase was the weakest. These data indicate that L-SOD has a significant preventive effect on acute oxygen toxicity in mice under hyperbaric oxygenation. It also suggests that excessive oxygen free radicals are the direct cause of acute oxygen poisoning in the body under hyperbaric oxygenation.