title: Fatty acid composition and arachidonate metabolites in the livers of ethanol-treated rats fed an arachidonate-supplemented diet: effect of dietary fat.
abstract: The effects of 1% arachidonic acid ethyl ester (AA) administration on the liver prostanoid metabolites and on serum and liver lipids in 3 g/kg ethanol-administered rats fed 10% lard or corn oil were studied. The rats were divided into 6 groups: lard-sucrose (Lard-Suc); lard-ethanol without AA (Lard-Et); lard-ethanol with AA (Lard-EtAA); corn oil-sucrose (Corn-Suc); corn oil-ethanol without AA (Corn-Et); and corn oil-ethanol with AA (Corn-EtAA). Liver triglyceride increased in Corn-EtAA compared with Corn-Et. Arachidonic acid (20: 4n-6) levels in liver phospholipid were significantly decreased in Corn-Et, but elevated in Lard-Et. The levels of 20:4n-6 were significantly increased with AA administration in both ethanol groups. Liver 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) in Corn-Suc (24.7 +/- 5.1 pg/mg protein) was markedly higher than in Lard-Suc (4.5 +/- 1.2 pg/mg protein), and the 6-keto-PGF1 alpha lowered significantly with the addition of ethanol (9.3 +/- 0.9 pg/mg protein), but it increased with AA administration (21.6 +/- 4.9 pg/mg protein). In Lard-EtAA, a significant increase in 6-keto-PGF1 alpha was observed compared with Lard-Suc. The liver leukotriene B4 (LTB4) level in Lard-Suc was significantly lower than that of Corn-Suc. In the corn oil group, ethanol feeding was associated with a significant increase in liver LTB4. AA administration to Corn-Et suppressed the elevated LTB4. Serum thiobarbituric acid-reactive substance (TBARS) concentrations in the corn oil group were higher than in the lard group, and these concentrations were not altered by AA administration. From these results, we concluded that the administration of AA in rats treated with ethanol increased 20:4n-6 in liver phospholipid and liver PGI2 levels, irrespective of dietary fat, and may protect against alcoholic liver injury. AA with a diet rich in linoleic acid (18:2n-6), however, may increase fat in the alcoholic liver.
authors: Department of Nutritional Science, Faculty of Health and Welfare Science, Okayama Prefectural University, Soja, Japan.
authors: M
authors: M
authors: Okita
authors: T
authors: T
authors: Sasagawa
authors: K
authors: K
authors: Suzuki
authors: A
authors: A
authors: Miyamoto
authors: H
authors: H
authors: Wakabayashi
authors: A
authors: A
authors: Watanabe
mesh_terms: D000410:Alanine Transaminase / Q000378:metabolism; D000818:Animals; D016718:Arachidonic Acid / Q000008:administration & dosage* / Q000378:metabolism*; D004032:Diet; D004041:Dietary Fats / Q000494:pharmacology*; D000431:Ethanol / Q000494:pharmacology*; D005227:Fatty Acids / Q000032:analysis*; D015289:Leukotrienes / Q000032:analysis; D008099:Liver / Q000737:chemistry / Q000187:drug effects / Q000378:metabolism*; D008297:Male; D009929:Organ Size; D010743:Phospholipids / Q000032:analysis; D011453:Prostaglandins / Q000032:analysis; D051381:Rats; D017207:Rats, Sprague-Dawley; D017392:Thiobarbituric Acid Reactive Substances / Q000032:analysis; D014280:Triglycerides / Q000032:analysis
chemical_list: D004041:Dietary Fats; D005227:Fatty Acids; D015289:Leukotrienes; D010743:Phospholipids; D011453:Prostaglandins; D017392:Thiobarbituric Acid Reactive Substances; D014280:Triglycerides; D016718:Arachidonic Acid; D000431:Ethanol; D000410:Alanine Transaminase