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  • 标题:Effects of Dietary Unsaturated Fatty Acid and Chronic Carbon Tetrachloride Treatment on the Accumulation of Oxidation Products, α-Tocopherol and Liver Injury in Mice
  • 本地全文:下载
  • 作者:Satoshi YASUDA ; Shiro WATANABE ; TeTsuyuki KOBAYASHI
  • 期刊名称:Biological and Pharmaceutical Bulletin
  • 印刷版ISSN:0918-6158
  • 电子版ISSN:1347-5215
  • 出版年度:1998
  • 卷号:21
  • 期号:10
  • 页码:1050-1056
  • DOI:10.1248/bpb.21.1050
  • 出版社:The Pharmaceutical Society of Japan
  • 摘要:Mice, at weaning, were placed on a diet supplemented with beef tallow (BT), linoleic acid (18 : 2n-6)-rich saffower 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 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 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.
  • 关键词:carbon tetrachloride;dietary fatty acid;lipid peroxidation;liver injury
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