Ribiere C, Sinaceur J, Sabourault D, Nordmann R
Alcohol. 1985 Jan-Feb;2(1):31-3. doi: 10.1016/0741-8329(85)90010-2.
The administration of an acute ethanol load (2.3 g/kg, IP) to rats is followed by a decrease of the hepatic activity of cytosolic catalase, a decrease which precedes a reduction in the cytosolic Cu, Zn-superoxide dismutase (SOD) activity. Desferrioxamine, an iron chelator and scavenger of superoxide radicals, administered prior to ethanol, prevents the changes in the cytosolic catalase activity, changes which are unaffected by the administration of allopurinol, an inhibitor of xanthine oxidase. These data favour the hypothesis that acute ethanol results in an overproduction of oxygen free radicals which affects primarily the cytosolic catalase activity and increases hereby susceptibility of Cu, Zn-SOD to these radicals. They suggest also that xanthine oxidase does not play a major role in oxygen radical production in the liver cytosol during acute alcohol intoxication.
给大鼠腹腔注射急性乙醇负荷量（2.3克/千克）后，胞质过氧化氢酶的肝脏活性会降低，这种降低先于胞质铜锌超氧化物歧化酶（SOD）活性的降低。去铁胺是一种铁螯合剂和超氧自由基清除剂，在乙醇给药前给予，可防止胞质过氧化氢酶活性的变化，而这些变化不受黄嘌呤氧化酶抑制剂别嘌呤醇给药的影响。这些数据支持以下假设：急性乙醇会导致氧自由基过度产生，主要影响胞质过氧化氢酶活性，从而增加铜锌超氧化物歧化酶对这些自由基的敏感性。它们还表明，黄嘌呤氧化酶在急性酒精中毒期间肝脏胞质溶胶中的氧自由基产生中不起主要作用。
