title: Vitamin E depletion enhances liver oxidative damage in rats with water-immersion restraint stress.
abstract: We examined the effect of vitamin E depletion on liver oxidative damage in rats with water-immersion restraint stress (WIRS). Male Wistar rats were fed a normal diet (N) or vitamin E-depleted diet (VE-D) for 4 wk. N- and VE-D-fed rats were exposed to WIRS for 6 h. The activities of serum transaminases and lactate dehydrogenase and serum ascorbic acid concentration were similar in both diet groups. WIRS exposure increased these serum enzyme activities and the serum ascorbic acid concentration in both diet groups but the ratios of these increases were higher in VE-D-fed rats than in N-fed rats. Serum and liver α-tocopherol concentrations in VE-D-rats were approximately 50% and 30% of those in N-fed rats, respectively. WIRS exposure reduced liver α-tocopherol concentration in VE-D-fed rats, but not in N-fed rats. Liver ascorbic acid and reduced glutathione concentrations were higher in the VE-D-fed group than in the N-fed group. WIRS exposure reduced liver ascorbic acid and reduced glutathione concentrations in both diet groups. There were no differences in liver concentrations of coenzyme Q9 or coenzyme Q10 in the reduced form between the N- and VE-D-fed groups. WIRS exposure reduced liver concentrations of coenzyme Q9 and coenzyme Q10 in the reduced form in both diet groups. Liver lipid peroxide concentration was higher in the VE-D-fed group than in the N-fed group. WIRS exposure raised liver lipid peroxide concentration more in the VE-D-fed group than in the N-fed group. These results indicate that vitamin E depletion enhances liver oxidative damage in rats with WIRS.
authors.affiliation: Department of Chemistry, Fujita Health University School of Medicine, Toyoake, Aichi, Japan. yohta@fujita-hu.ac.jp
authors.forename: Yoshiji
authors.initials: Y
authors.lastname: Ohta
authors.forename: Koji
authors.initials: K
authors.lastname: Yashiro
authors.forename: Koji
authors.initials: K
authors.lastname: Ohashi
authors.forename: Yoichiro
authors.initials: Y
authors.lastname: Imai
authors.forename: Chiaki
authors.initials: C
authors.lastname: Kusumoto
authors.forename: Tatsuya
authors.initials: T
authors.lastname: Matsura
authors.forename: Mayumi
authors.initials: M
authors.lastname: Hidaka
authors.forename: Kenji
authors.initials: K
authors.lastname: Fukuzawa
mesh_terms: D000818:Animals; D001205:Ascorbic Acid / Q000097:blood; D004032:Diet; D005978:Glutathione / Q000378:metabolism; D007770:L-Lactate Dehydrogenase / Q000097:blood; D008054:Lipid Peroxides / Q000378:metabolism; D008099:Liver / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D008297:Male; D018384:Oxidative Stress / Q000187:drug effects*; D051381:Rats; D017208:Rats, Wistar; D012149:Restraint, Physical; D013312:Stress, Physiological; D000637:Transaminases / Q000097:blood; D014451:Ubiquinone / Q000031:analogs & derivatives / Q000378:metabolism; D014810:Vitamin E / Q000097:blood*
chemical_list: D008054:Lipid Peroxides; D014451:Ubiquinone; D014810:Vitamin E; D007770:L-Lactate Dehydrogenase; D000637:Transaminases; C024989:coenzyme Q10; D005978:Glutathione; C030571:ubiquinone 9; D001205:Ascorbic Acid