Lucas D, Lamboeuf Y, De Saint Blanquat G, Menez J F
Laboratoire de Biochimie, Faculté de Médecine, Brest, France.
Alcohol Alcohol. 1990;25(4):395-400.
Chronic ethanol consumption results in acetaldehyde adduct formation with proteins such as haemoglobin and liver proteins in vivo. Our purpose was to study the binding of acetaldehyde to liver microsomal proteins, a site of ethanol oxidation via cytochrome P-450 (especially P-450 II E1), after chronic administration of ethanol or acetaldehyde for 21 days to rats. The liver microsomal oxidation of 1-butanol by the ethanol-inducible P-450 also was examined. Acetaldehyde bound to liver microsomal proteins was higher in ethanol-fed rats compared with acetaldehyde-treated rats (0.735 vs 0.413 nmol/mg of protein respectively). The biotransformation of n-butanol to butyraldehyde by liver microsomes was increased (by 136%) in ethanol-fed rats vs controls, whereas in acetaldehyde-treated rats this increase was much lower (only 27%). However, in this last group, a significant negative relationship between the quantity of acetaldehyde bound to microsomal proteins and the monooxygenase-catalyzed transformation of butanol by liver microsomes was demonstrated (r = -0.79, P less than 0.01). These results suggest that proteins of liver microsomes are a target for acetaldehyde binding during ethanol oxidation and such adduct formation could impair the oxidative properties of the alcohol-inducible cytochrome P-450.
长期摄入乙醇会导致体内乙醛与蛋白质（如血红蛋白和肝脏蛋白）形成加合物。我们的目的是研究在给大鼠连续21天给予乙醇或乙醛后，乙醛与肝脏微粒体蛋白的结合情况，肝脏微粒体是乙醇通过细胞色素P - 450（特别是P - 450 II E1）进行氧化的场所。同时也检测了乙醇诱导的P - 450对1 - 丁醇的肝脏微粒体氧化作用。与乙醛处理组大鼠相比，乙醇喂养组大鼠肝脏微粒体蛋白结合的乙醛含量更高（分别为0.735和0.413 nmol/mg蛋白）。与对照组相比，乙醇喂养组大鼠肝脏微粒体将正丁醇生物转化为丁醛的能力增强（提高了136%），而在乙醛处理组大鼠中，这种增加幅度要小得多（仅27%）。然而，在最后一组中，微粒体蛋白结合的乙醛量与肝脏微粒体单加氧酶催化的丁醇转化之间存在显著的负相关关系（r = -0.79，P < 0.01）。这些结果表明，肝脏微粒体蛋白是乙醇氧化过程中乙醛结合的靶点，这种加合物的形成可能会损害乙醇诱导的细胞色素P - 450的氧化特性。
