Effect of Dietary Vitamin E Supplementation on Liver Oxidative Damage in Rats with Water-Immersion Restraint Stress

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  • OHTA Yoshiji
    Department of Chemistry, Fujita Health University School of Medicine
  • YASHIRO Koji
    Department of Chemistry, Fujita Health University School of Medicine
  • OHASHI Koji
    Department of Clinical Biochemistry, Faculty of Medical Technology, Fujita Health University School of Health Sciences
  • HORIKOSHI Yosuke
    Division of Medical Biochemistry, Department of Pathophysiological and Therapeutic Science, Tottori University
  • KUSUMOTO Chiaki
    Division of Medical Biochemistry, Department of Pathophysiological and Therapeutic Science, Tottori University
  • MATSURA Tatsuya
    Division of Medical Biochemistry, Department of Pathophysiological and Therapeutic Science, Tottori University
  • FUKUZAWA Kenji
    Faculty of Pharmacy, Yasuda Women’s University

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Abstract

We examined how dietary supplementation of vitamin E protects against liver oxidative damage in rats with water-immersion restraint stress (WIRS). Before WIRS exposure, rats received a normal diet (ND) or vitamin E-supplemented diet (VESD) (500 IU α-tocopherol/kg diet) at a mean dose of 15 g/animal/d for 4 wk. The two diet groups had serum transaminases and lactate dehydrogenase activities and adrenocorticotropic hormone, corticosterone, and glucose levels to a similar extent. VESD-fed rats had higher liver α-tocopherol concentrations and lower liver ascorbic acid, total coenzyme Q9 (CoQ9), reduced CoQ9, reduced CoQ10, and lipid peroxide (LPO) concentrations than ND-fed rats. When the two diet groups were exposed to 6 h of WIRS, the serum liver cell damage index enzyme activities increased more greatly in ND-fed rats than in VESD-fed rats but the serum stress marker levels increased to a similar extent. The WIRS exposure caused no change in liver LPO concentration with the further increase in liver α-tocopherol concentration in VESD-fed rats but increased liver LPO concentration without changing liver α-tocopherol concentration in ND-fed rats. Upon the WIRS exposure, liver reduced glutathione concentration decreased with the further decrease in liver ascorbic acid concentration in VESD-fed rats and those concentrations decreased in ND-fed rats. The WIRS exposure recovered the decreased liver total CoQ9 and reduced CoQ9 concentrations in VESD-fed rats but decreased liver total CoQ9, reduced CoQ9, and reduced CoQ10 concentrations in ND-fed rats. These results indicate that dietary vitamin E supplementation protects against liver oxidative damage without affecting the stress response in rats with WIRS.

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