title: Galactosamine-induced acute liver injury in rats reduces hepatic alpha-tocopherol transfer protein production.
abstract: The liver plays the main role in the secretion of food-derived alpha-tocopherol into the circulation through the functioning of alpha-tocopherol transfer protein (alpha-TTP). However, the effect of liver disease on alpha-TTP level and alpha-tocopherol metabolism has not been clarified. We examined the amount of liver alpha-TTP and its effect on serum alpha-tocopherol concentration in liver injury. Male Wistar rats were injected intraperitoneally with D-galactosamine at 800 mg/kg body weight, and liver and serum lipid concentrations, alpha-tocopherol concentrations, and hepatic alpha-TTP mRNA and protein levels were measured at 24, 48, and 72 h after injection. On the basis of body weight changes and serum transaminase activities, the livers were found to be in an injured state 24 and 48 h after galactosamine injection but had recovered by 72 h. The hepatic alpha-TTP mRNA level was reduced throughout the experimental period, and at 48 h after injection the alpha-TTP protein level had begun to decrease. Lipid and alpha-tocopherol concentrations in the serum were decreased at 24 and 48 h after injection and increased at 72 h. Liver lipid concentrations were increased at 24 and 48 h after injection, but the liver alpha-tocopherol concentration was unchanged. These results show that galactosamine-induced liver injury decreases hepatic alpha-TTP synthesis in rats. Serum alpha-tocopherol concentration was not directly affected by the acute change in hepatic alpha-TTP level, suggesting that the chronic changes in alpha-TTP activity would be necessary to regulate serum alpha-tocopherol concentration.
authors.affiliation: Department of Bioresource Engineering, Faculty of Agriculture, Yamagata University, Yamagata, Japan. takenaka@isc.meiji.ac.jp
authors.forename: Asako
authors.initials: A
authors.lastname: Takenaka
authors.forename: Akiko
authors.initials: A
authors.lastname: Kita
authors.forename: Masafumi
authors.initials: M
authors.lastname: Ikeya
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Arai
authors.forename: Kiharu
authors.initials: K
authors.lastname: Igarashi
mesh_terms: D000410:Alanine Transaminase / Q000097:blood; D000818:Animals; D001219:Aspartate Aminotransferases / Q000097:blood; D015153:Blotting, Western; D002352:Carrier Proteins / Q000096:biosynthesis* / Q000097:blood / Q000235:genetics; D056486:Chemical and Drug Induced Liver Injury; D002784:Cholesterol / Q000097:blood; D004195:Disease Models, Animal; D005688:Galactosamine; D007770:L-Lactate Dehydrogenase / Q000097:blood; D008107:Liver Diseases / Q000201:enzymology / Q000235:genetics / Q000378:metabolism*; D008297:Male; D010743:Phospholipids / Q000097:blood; D012333:RNA, Messenger / Q000096:biosynthesis / Q000235:genetics; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D020133:Reverse Transcriptase Polymerase Chain Reaction; D014280:Triglycerides / Q000097:blood; D024502:alpha-Tocopherol / Q000097:blood / Q000378:metabolism
chemical_list: D002352:Carrier Proteins; D010743:Phospholipids; D012333:RNA, Messenger; D014280:Triglycerides; C017763:alpha-tocopherol transfer protein; D005688:Galactosamine; D002784:Cholesterol; D007770:L-Lactate Dehydrogenase; D001219:Aspartate Aminotransferases; D000410:Alanine Transaminase; D024502:alpha-Tocopherol