ABSTRACT
Alcoholic liver injuries such as fatty liver, hepatitis, and fibrosis are frequently observed in patients with a long history of excessive alcohol intake. It is suggested that liver injury due to ethanol may involve the interaction of polyunsaturated fatty acid (PUFA), eicosanoids, and other lipid peroxides.1-4 Abnormal lipid metabolism is also frequently
observed in severe alcoholics. One of the most significant and consistent effects of ethanol on lipid metabolism is the change in the fatty acid composition of phospholipids in liver and other tissues. A common finding in ethanol-treated animals is a decrease in arachidonic acid (20:4 n-6) and increased levels of oleic acid (18:1 n-9) and linoleic acid (18:2 n-6).5 It has been suggested that the decrease in arachidonic acid induced by ethanol is caused by the reduction in ∆6 and ∆5 desaturase activity.6 On the other hand, increased metabolism of arachidonic acid into epoxides, such as 14, 15-epoxyeicosatrienoic acid (EET), 11, 12-EET, and 8, 9-EET, was also proposed by French et al.7 as an important factor in ethanol-induced liver injury. However, they suggested that lipid peroxidation by cytochrome P450 (CYP) 2E1 could not totally account for the reduction in arachidonic acid and that the severity of liver pathology correlated negatively with the decrease in arachidonic acid in ethanol-fed rats. In addition, they suggested that reduction of arachidonic acid may be an important mechanism of ethanol-induced liver injury.
