PMID- 9821808
OWN - NLM
STAT- MEDLINE
DCOM- 19990114
LR  - 20190719
IS  - 0918-6158 (Print)
IS  - 0918-6158 (Linking)
VI  - 21
IP  - 10
DP  - 1998 Oct
TI  - Effects of dietary unsaturated fatty acid and chronic carbon tetrachloride 
      treatment on the accumulation of oxidation products, alpha-tocopherol and liver 
      injury in mice.
PG  - 1050-6
AB  - 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 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 alpha-tocopherol contents were affected both by diet and CCl4 
      treatment, and a positive correlation was observed between alpha-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.
FAU - Yasuda, S
AU  - Yasuda S
AD  - Department of Biological Chemistry, Faculty of Pharmaceutical Sciences, Nagoya 
      City University, Nagoya, Japan.
FAU - Watanabe, S
AU  - Watanabe S
FAU - Kobayashi, T
AU  - Kobayashi T
FAU - Okuyama, H
AU  - Okuyama H
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Japan
TA  - Biol Pharm Bull
JT  - Biological & pharmaceutical bulletin
JID - 9311984
RN  - 0 (Fatty Acids, Unsaturated)
RN  - 0 (Phospholipids)
RN  - 0 (Proteins)
RN  - 0 (Thiobarbituric Acid Reactive Substances)
RN  - 0 (Triglycerides)
RN  - 1406-18-4 (Vitamin E)
RN  - CL2T97X0V0 (Carbon Tetrachloride)
RN  - EC 2.6.1.2 (Alanine Transaminase)
SB  - IM
MH  - Alanine Transaminase/blood
MH  - Animals
MH  - Carbon Tetrachloride/*toxicity
MH  - Diet
MH  - Drug Administration Schedule
MH  - Drug Interactions
MH  - Fatty Acids, Unsaturated/metabolism/*pharmacology
MH  - Fatty Liver/*chemically induced/*metabolism
MH  - Female
MH  - Lipid Peroxidation
MH  - Liver/drug effects/metabolism
MH  - Mice
MH  - Mice, Inbred ICR
MH  - Oxidation-Reduction
MH  - Phospholipids/metabolism
MH  - Proteins/metabolism
MH  - Thiobarbituric Acid Reactive Substances/metabolism
MH  - Triglycerides/metabolism
MH  - Vitamin E/*metabolism
EDAT- 1998/11/20 00:00
MHDA- 1998/11/20 00:01
CRDT- 1998/11/20 00:00
PHST- 1998/11/20 00:00 [pubmed]
PHST- 1998/11/20 00:01 [medline]
PHST- 1998/11/20 00:00 [entrez]
AID - 10.1248/bpb.21.1050 [doi]
PST - ppublish
SO  - Biol Pharm Bull. 1998 Oct;21(10):1050-6. doi: 10.1248/bpb.21.1050.