Mice, at weaning, were placed on a diet supplemented with beef tallow (BT), linoleic acid (18: 2n-6)-rich safflower oil (SO), α-linolenic acid (18: 3n-3)-rich perilla oil (PO) or docosahexaenoic acid (22: 6n-3, DHA)- rich fish oil (FO) to modify membrane fatty acid vulnerability to peroxidation, then carbon tetrachloride (CCl4) was administered chronically. CCl4-induced liver injury, estimated using serum alanine aminotransferase activity and liver hydroxyproline content, was not different among the 4 dietary groups; however, the FO diet lowered the liver triacylglycerol (TG) level when compared with the BT and SO diets. The FO diet group exhibited a significantly higher level of thiobarbituric acid-reactive substances (TBARS) in the liver when compared with the three other dietary groups. Chronic CCl4 treatment decreased the proportion of eicosanoid precursors (arachidonate and cicosapentatenoate) rather than that of DHA, with the highest peroxidizability among major fatty adds in liver, and did not enhance TBARS formation in any of the dietary groups. The protein carbonyl content in the liver was similar among the 4 dietary groups but was decreased following CCl4 treatment. Liver α-tocopherol contents were affected both by diet and CCl4 treatment, and a positive correlation was ObServed between α- tocopherol and TG contents. These results indicate that increasing the autoxidizability of dietary fatty acids or the chronic CCl4 treatment did not synergistically enhance liver injury or the accumulation of oxidation products in mice.
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