EFFECTS OF DIETARY UNSATURATED FATTY-ACID AND CHRONIC CARBON-TETRACHLORIDE TREATMENT ON THE ACCUMULATION OF OXIDATION-PRODUCTS, ALPHA-TOCOPHEROL AND LIVER-INJURY IN MICE

Citation
S. Yasuda et al., EFFECTS OF DIETARY UNSATURATED FATTY-ACID AND CHRONIC CARBON-TETRACHLORIDE TREATMENT ON THE ACCUMULATION OF OXIDATION-PRODUCTS, ALPHA-TOCOPHEROL AND LIVER-INJURY IN MICE, Biological & pharmaceutical bulletin, 21(10), 1998, pp. 1050-1056
Citations number
41
Categorie Soggetti
Pharmacology & Pharmacy
ISSN journal
09186158
Volume
21
Issue
10
Year of publication
1998
Pages
1050 - 1056
Database
ISI
SICI code
0918-6158(1998)21:10<1050:EODUFA>2.0.ZU;2-I
Abstract
Mice, at weaning, were placed on a diet supplemented with beef tallow (BT), linoleic acid (18:2n-6)-rich safflower oil (SO), alpha-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 chr onically, CCl4-induced liver injury estimated using serum alanine amin otransferase activity and liver hydroxyproline content, was not differ ent among the 4 dietary groups; however, the FO diet lowered the liver triacylglycerol (TG) level when compared with the ET and SO diets. Th e FO diet group exhibited a significantly higher level of thiobarbitur ic acid-reactive substances (TBARS) in the liver when compared with th e three other dietary groups. Chronic CCl4 treatment decreased the pro portion of eicosanoid precursors (arachidonate and eicosapentaenoate) rather than that of DHA, with the highest peroxidizability among major fatty acids in liver, and did not enhance TBARS formation in any of t he dietary groups. The protein carbonyl content in the liver was simil ar among the 4 dietary groups but was decreased following CCl4 treatme nt. Liver alpha-tocopherol contents were affected both by diet and CCl 4 treatment, and a positive correlation was observed between alpha-toc opherol and TG contents. These results indicate that increasing the au toxidizability of dietary fatty acids or the chronic CCl4 treatment di d not synergistically enhance liver injury or the accumulation of oxid ation products in mice.