Koch O R, De Leo M E, Borrello S, Palombini G, Galeotti T
Institute of General Pathology, Catholic University, Rome, Italy.
Biochem Biophys Res Commun. 1994 Jun 30;201(3):1356-65. doi: 10.1006/bbrc.1994.1853.
On the basis of the well-known effect of ethanol poisoning on the prooxidant/antioxidant balance of human and rodent liver we tested the response of the mitochondrial manganese-containing superoxide dismutase (MnSOD) in the liver of rats following an acute ethanol load or chronically intoxicated with an alcohol-supplemented solid diet for three weeks. In both conditions the enzyme activity and messenger RNA were monitored. In the acutely treated animals MnSOD was induced (post-)translationally already at 3 hours after ethanol injection, reached the maximum level (about 50% increment) at 9 hours and decreased thereafter. Chronic ethanol feeding caused an up-regulation of the enzyme at the mRNA level, with a good correlation between the transcript and the enzyme activity during the first two weeks of treatment. After 20 days the mRNA level dropped to normal, whereas the activity still remained high. Chronic alcohol intake also led to a significant decrease in the content of vitamin E in the liver mitochondrial and microsomal fractions, suggesting the occurrence of an enhanced lipid peroxidation, consequent to the ethanol-induced oxidative stress. The response of MnSOD appears to be a protective mechanism that the genetic machinery builds up to partially overcome such a condition.
基于乙醇中毒对人和啮齿动物肝脏的促氧化剂/抗氧化剂平衡的众所周知的影响，我们测试了急性乙醇负荷或用含酒精的固体饮食慢性中毒三周后大鼠肝脏中线粒体含锰超氧化物歧化酶（MnSOD）的反应。在这两种情况下，都监测了酶活性和信使核糖核酸。在急性处理的动物中，乙醇注射后3小时MnSOD就被（翻译后）诱导，9小时达到最高水平（增加约50%），此后下降。慢性乙醇喂养导致该酶在信使核糖核酸水平上调，在治疗的前两周转录本与酶活性之间有良好的相关性。20天后信使核糖核酸水平降至正常，而酶活性仍然很高。慢性酒精摄入还导致肝脏线粒体和微粒体部分中维生素E含量显著降低，表明由于乙醇诱导的氧化应激，脂质过氧化增强。MnSOD的反应似乎是一种保护机制，是遗传机制为部分克服这种状况而建立的。
