THE CRUCIAL ROLE OF HYPOXIA IN HALOTHANE-INDUCED LIPID-PEROXIDATION
THE CRUCIAL ROLE OF HYPOXIA IN HALOTHANE-INDUCED LIPID-PEROXIDATION
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DOI：
10.1016/0006-291x(84)91629-2
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发表时间：
1984-01-01
影响因子：
3.1
通讯作者：
NOLL, T
中科院分区：
文献类型：
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作者：
DEGROOT, H;NOLL, T
氟烷诱导的脂质过氧化作用的NADPH还原的肝微粒体苯巴比妥预处理的雄性大鼠进行了研究，在定义的稳态氧分压（Po 2）。在厌氧条件下，以及在Po 2高于10毫米汞柱没有氟烷诱导的丙二醛的形成被检测到。然而，当氧分压低于10 mm Hg时，最大氧分压接近1 mm Hg时，发现氟烷诱导的丙二醛形成显著，这一证据支持氟烷可诱导脂质过氧化的假设。P 〇 2（i）必须足够低以允许·CF 3CHCl-自由基的还原形成，但（ii）必须足够高以促进脂质过氧化物的形成。
Halothane-induced lipid peroxidation in NADPH-reduced liver microsomes from phenobarbital-pretreated male rats was studied under defined steady state oxygen partial pressures (Po2). Under anaerobic conditions, as well as at a Po2above 10 mm Hg no halothane-induced formation of malondialdehyde was detected. At a Po2below 10 mm Hg, however, with a maximum near 1 mm Hg oxygen, significant halothane-induced malondialdehyde formation was found. This evidence supports the hypothesis that halothane can induce lipid peroxidation. The Po2(i) must be low enough to permit the reductive formation of•CF3CHCl-radicals but (ii), it must be high enough to promote formation of lipid peroxides.