Ryle P R, Chakraborty J, Thomson A D
Biochem J. 1985 Dec 15;232(3):877-82. doi: 10.1042/bj2320877.
Feeding of ethanol in a liquid diet to male Wistar rats caused decreases in the hepatic cytosolic and mitochondrial [NAD+]/[NADH] ratios. This redox-state change was attenuated after 16 days of feeding ethanol as 36% of the total energy intake. Supplementation of the ethanol-containing liquid diet with Methylene Blue largely prevented the ethanol-induced redox state changes, but did not significantly decrease the severity of the hepatic lipid accumulation that resulted from ethanol ingestion. Methylene Blue did not affect body-weight gain, ethanol intake or serum ethanol concentrations in ethanol-fed rats, nor did the compound influence the hepatic redox state or liver lipid content of appropriate pair-fed control animals. These findings suggest that the altered hepatic redox state that results from ethanol oxidation is not primarily responsible for the production of fatty liver after long-term ethanol feeding in the rat.
给雄性Wistar大鼠喂食含乙醇的液体饲料会导致肝脏细胞溶质和线粒体中[NAD+]/[NADH]比值降低。当乙醇作为总能量摄入的36%喂食16天后,这种氧化还原状态的变化会减弱。在含乙醇的液体饲料中添加亚甲蓝在很大程度上可防止乙醇诱导的氧化还原状态变化,但并不能显著降低因摄入乙醇而导致的肝脏脂质积累的严重程度。亚甲蓝不影响喂食乙醇大鼠的体重增加、乙醇摄入量或血清乙醇浓度,该化合物也不影响适当配对喂养的对照动物的肝脏氧化还原状态或肝脏脂质含量。这些发现表明,在大鼠长期喂食乙醇后,由乙醇氧化导致的肝脏氧化还原状态改变并非脂肪肝产生的主要原因。