Hasumura Y, Teschke R, Lieber C S
Science. 1975 Aug 29;189(4204):727-9. doi: 10.1126/science.168641.
Prolonged consumption of ethanol significantly reduces the capacity of rat liver mitochondria to oxidize acetaldehyde. This is associated with decreased mitochondrial respiration with acetaldehyde as substrate. The reduced ability of mitochondria to metabolize acetaldehyde may explain the high levels of acetaldehyde in the blood of alcoholics, which in turn could promote the perpetuation of liver injury.
长期摄入乙醇会显著降低大鼠肝脏线粒体氧化乙醛的能力。这与以乙醛为底物时线粒体呼吸作用的降低有关。线粒体代谢乙醛能力的下降可能解释了酗酒者血液中乙醛水平较高的现象，而这反过来又可能促使肝损伤持续存在。
