Fatty acid ω- and (ω-1)-hydroxylation in experimental alcoholic liver disease: Relationship to different dietary fatty acids

Arachidonic acid concentrations in liver are decreased in response to ethanol administration. In addition, the oxygenated products of arachidonic acid metabolites could affect the severity of alcoholic liver injury. Selective utilization of arachidonic acid by the cytochrome P-450 system could, in part, account for the decrease in arachidonic acid. To evaluate this pathway further, male Wistar rats were fed different dietary fats: medium chain triglycerides, palm oil, and corn oil or fish oil with either ethanol or isocaloric amounts of dextrose. Histopathology, cytochrome P- 4502E1 (CYP2E1) and cytochrome P-4504A (CYP4A), and ω- and (ω-1)- hydroxylation products of lauric and arachidonic acids were evaluated. Ethanol induction of CYP2E1 was related to the concentration of polyunsaturated fatty acids in the diet; induction of CYP4A by ethanol was seen in all groups. The highest levels of 11-hydroxy-lauric acid and 19- hydroxyarachidonic acid (ω-1) were seen in rats fed ethanol with palm oil and corn oil. Highly significant correlations were seen between the (ω-1)- hydroxylation products and CYP2E1 activity. No correlation was seen between the ω-hydroxylation products and CYP2E1 activity. In contrast, the levels of ω-hydroxylation products correlated with CYP4A. The overall results showed a significant increase in (ω-1)-hydroxylation products in rats fed diets containing significant amounts of linoleic acid (i.e., palm oil and corn oil).