Fujii K
Department of Anesthesiology and Critical Care Medicine, Hiroshima University School of Medicine, Japan.
Toxicology. 1996 Dec 2;114(2):147-53. doi: 10.1016/s0300-483x(96)03480-4.
Effects of the anesthetics isoflurane, enflurane, halothane and sevoflurane on the dechlorination of carbon tetrachloride to produce chloroform were investigated using guinea pig liver microsomes. Under anaerobic conditions, chloroform is produced from carbon tetrachloride by the microsomes in the presence of NADPH, and chloroform production from 86 microM carbon tetrachloride was enhanced to 146%, 133%, 123% and 115% by the addition of isoflurane, enflurane, halothane and sevoflurane, respectively. The half-life of oxidized cytochrome P450 which remained during the reduction by the addition of NADPH was shortened to 51%, 54%, 60% and 80% by isoflurane, enflurane, halothane and sevoflurane, respectively, without alteration of NADPH-cytochrome c reductase activity. These anesthetics hastened the onset of the 445 nm absorption band formation which was shown by microsomes with carbon tetrachloride in the presence of NADPH under anaerobic conditions. These results indicate that the anesthetics isoflurane, enflurane, sevoflurane and halothane stimulate the reduction of cytochrome P450 results in the acceleration of the carbon tetrachloride dechlorination. These results may have implications for other type II drugs that are administered during anesthesia.
使用豚鼠肝微粒体研究了麻醉剂异氟烷、恩氟烷、氟烷和七氟烷对四氯化碳脱氯生成氯仿的影响。在厌氧条件下，四氯化碳在微粒体存在NADPH的情况下生成氯仿，分别添加异氟烷、恩氟烷、氟烷和七氟烷后，86微摩尔四氯化碳生成氯仿的量分别提高到146%、133%、123%和115%。通过添加NADPH进行还原过程中残留的氧化型细胞色素P450的半衰期，分别被异氟烷、恩氟烷、氟烷和七氟烷缩短至51%、54%、60%和80%，而NADPH-细胞色素c还原酶活性未发生改变。这些麻醉剂加速了在厌氧条件下微粒体与四氯化碳在NADPH存在时出现的445纳米吸收带的形成。这些结果表明，麻醉剂异氟烷、恩氟烷、七氟烷和氟烷刺激细胞色素P450的还原，导致四氯化碳脱氯加速。这些结果可能对麻醉期间使用的其他II类药物具有启示意义。
