title: Effect of vitamin E deficiency on inhibition of liver regeneration by long-term administration of alcohol.
abstract: The effects of vitamin E (VE) deficiency on liver regeneration suppressed by long-term administration of alcohol were studied. Male rats were divided into two groups: the alcohol group and the control group. In addition, each group was subdivided into two groups according to the presence or not of VE. Altogether, four groups were provided: a group maintained on the VE-deficient alcohol diet (group EA), a group maintained on the VE-deficient control diet (group EC), a group maintained on the ordinary alcohol diet (group A), and a group maintained on the ordinary control diet (group C). After pair-feeding for 6 weeks, partial hepatectomy was performed to determine the omithine decarboxylase (ODC) activity, polyamine levels, lipid peroxide levels, and DNA synthesis, DNA synthesis at 24 hr after partial hepatectomy was suppressed significantly in the alcohol administration group, regardless of the presence or not of VE DNA synthesis at 48 hr after partial hepatectomy tended to show low values in group EA, compared with group A. As for the hepatic ODC activity, group EA showed the lowest value at 4 hr after partial hepatectomy. Of polyamines, the putrescine level in group EA at 4 hr after partial hepatectomy was significantly low, compared with the other three groups. The levels of spermidine and spermine decreased by long-term administration of alcohol, but the effect of VE deficiency was not found. The lipid peroxide level increased significantly in the VE-deficient diet administration group, but the effect of alcohol administration was not found. These results suggested that the decrease in putrescine after ODC suppression by VE deficiency in addition to the decrease in spermidine and spermine caused by long-term alcohol administration were concerned with suppression of DNA synthesis later.
authors.affiliation: Department of Public Health, Osaka City University Medical School, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Tanaka
authors.forename: Y
authors.initials: Y
authors.lastname: Goto
authors.forename: M
authors.initials: M
authors.lastname: Imano
authors.forename: H
authors.initials: H
authors.lastname: Asai
authors.forename: T
authors.initials: T
authors.lastname: Yamada
authors.forename: S
authors.initials: S
authors.lastname: Kawai
authors.forename: S
authors.initials: S
authors.lastname: Kunitoh
authors.forename: K
authors.initials: K
authors.lastname: Kondo
authors.forename: T
authors.initials: T
authors.lastname: Yamashita
authors.forename: T
authors.initials: T
authors.lastname: Monna
authors.forename: S
authors.initials: S
authors.lastname: Nishiguchi
authors.forename: T
authors.initials: T
authors.lastname: Kuroki
authors.forename: S
authors.initials: S
authors.lastname: Otani
mesh_terms: D000818:Animals; D004261:DNA Replication / Q000187:drug effects / Q000502:physiology; D000431:Ethanol / Q000633:toxicity*; D006498:Hepatectomy; D015227:Lipid Peroxidation / Q000187:drug effects / Q000502:physiology; D008099:Liver / Q000187:drug effects / Q000473:pathology; D008108:Liver Diseases, Alcoholic / Q000473:pathology*; D008115:Liver Regeneration / Q000187:drug effects* / Q000502:physiology; D008297:Male; D009955:Ornithine Decarboxylase / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D013095:Spermidine / Q000378:metabolism; D013096:Spermine / Q000378:metabolism; D014811:Vitamin E Deficiency / Q000473:pathology*
chemical_list: D013096:Spermine; D000431:Ethanol; D009955:Ornithine Decarboxylase; D013095:Spermidine