Binding of acetaldehyde to rat liver microsomes: enhancement after chronic alcohol consumption.
Binding of acetaldehyde to rat liver microsomes: enhancement after chronic alcohol consumption.
复制标题
乙醛与大鼠肝微粒体的结合：长期饮酒后增强。
DOI：
10.1016/s0006-291x(81)80073-3
复制
发表时间：
1981
影响因子：
3.1
通讯作者：
Lieber,CS
中科院分区：
文献类型：
--
作者：
Nomura,F;Lieber,CS
评估了大鼠肝微粒体制剂在微粒体乙醇氧化系统（MEOS）中结合外源14c -乙醛和由14c -乙醇内源性形成的14c -乙醛的能力。发现外源性乙醛与大鼠肝微粒体结合。用位点特异性试剂（吡哆醛5′-磷酸和对羟基汞苯甲酸酯）阻断游离氨基和巯基，可减少乙醛的结合。由乙醇内源性形成的乙醛也与肝微粒体结合。这在长期饮酒后增加，与MEOS活性增强有关。MEOS产生的乙醛的结合明显大于等量的外源乙醛。因此，原位产生的乙醛可能对内质网产生局部毒性作用。
Rat hepatic microsomal preparations were assessed for their capacity to bind exogenous14C-acetaldehyde and14C-acetaldehyde formed endogenously from14C-ethanol in the microsomal ethanol-oxidizing system (MEOS). Exogenous acetaldehyde was found to bind to rat liver microsomes. Blocking of the free amino groups and thiol groups with site specific reagents (pyridoxal 5′-phosphate and p-hydroxymercuribenzoate) reduced the binding of acetaldehyde. Acetaldehyde formed endogenously from ethanol also bound to hepatic microsomes. This was increased after chronic alcohol consumption, in association with enhanced MEOS activity. The binding of acetaldehyde produced by MEOS was significantly greater than that of an equivalent amount of exogenous acetaldehyde. Thus, acetaldehyde produced in situ may exert local toxic effects on the endoplasmic reticulum.