Matsuzaki S, Gordon E, Lieber C S
J Pharmacol Exp Ther. 1981 Apr;217(1):133-7.
Rates of ethanol oxidation in isolated rat hepatocytes increased with increasing ethanol concentrations even at near-saturation of the alcohol dehydrogenase (ADH) pathway. After inhibition of ADH by pyrazole, approximately 30% of ethanol-oxidizing activity remained and this activity of the non-ADH pathway was also dependent upon ethanol concentration. The apparent Km of th non-ADH pathway for ethanol was 13 mM, which is comparable to the value for the microsomal ethanol oxidizing system. Inhibition of catalase by azide affected the activity of the non-ADH pathway by less than 10%. After chronic ethanol feeding, the rates of ethanol oxidation in isolated hepatocytes and liver slices increased significantly compared to those in pair-fed controls. This adaptive increase of ethanol oxidation was more striking at a high ethanol level (30 mM) than at a low one (10 mM). Significant differences between the two groups remained even after inhibition of ADH and catalase. The results suggest that the microsomal ethanol oxidizing system may account for the major part of the non-ADH pathway.
在分离的大鼠肝细胞中，即使在酒精脱氢酶（ADH）途径接近饱和时，乙醇氧化速率也随乙醇浓度的增加而增加。用吡唑抑制ADH后，仍保留约30%的乙醇氧化活性，且非ADH途径的这种活性也依赖于乙醇浓度。非ADH途径对乙醇的表观Km为13 mM，这与微粒体乙醇氧化系统的值相当。叠氮化物对过氧化氢酶的抑制对非ADH途径活性的影响小于10%。长期给予乙醇后，与配对喂养的对照组相比，分离的肝细胞和肝切片中的乙醇氧化速率显著增加。这种乙醇氧化的适应性增加在高乙醇水平（30 mM）时比在低乙醇水平（10 mM）时更明显。即使在抑制ADH和过氧化氢酶后，两组之间仍存在显著差异。结果表明，微粒体乙醇氧化系统可能占非ADH途径的主要部分。
