Takano T, Motohashi Y, Miyazaki Y, Okeda R
J Toxicol Environ Health. 1985;15(6):847-54. doi: 10.1080/15287398509530710.
The interaction of carbon monoxide (CO) with cytochrome P-450 associated with hexobarbital metabolism was observed in hemoglobin-free perfused rat liver by using a scanning reflectance spectrophotometer. The evidence obtained showed that CO bound to the substrate complexed cytochrome P-450 and, at a CO/O2 ratio of over 0.1 in the perfusate, inhibited the hexobarbital metabolism estimated from the hexobarbital uptake, and oxygen consumption. Although the oxygen supply to the liver cell was one of the major limiting factors during CO hypoxia, CO binding to cytochrome P-450 significantly enhanced the suppression of hexobarbital oxidation caused by hypoxic hypoxia.
利用扫描反射分光光度计，在无血红蛋白灌注的大鼠肝脏中观察了一氧化碳（CO）与参与己巴比妥代谢的细胞色素P - 450的相互作用。所获得的证据表明，CO与底物复合的细胞色素P - 450结合，并且当灌注液中CO/O2比率超过0.1时，抑制了根据己巴比妥摄取量和耗氧量估算的己巴比妥代谢。尽管在CO缺氧期间向肝细胞的氧气供应是主要限制因素之一，但CO与细胞色素P - 450的结合显著增强了低氧性缺氧引起的己巴比妥氧化抑制作用。
