Inhibitory Effect of .ALPHA.-Tocopherol on Methylmercury-Induced Oxidative Steress

DOI 51 References
  • YAMASHITA Taro
    Department of Neurology, Graduate School of Medical Sciences, Kumamoto University
  • ANDO Yukio
    Department of Diagnostic Medicine, Graduate School of Medical Sciences, Kumamoto University
  • NAKAMURA Masaaki
    Department of Diagnostic Medicine, Graduate School of Medical Sciences, Kumamoto University
  • OBAYASHI Konen
    Department of Neurology, Graduate School of Medical Sciences, Kumamoto University
  • TERAZAKI Hisayasu
    Department of Gastroenterology and Hepatology, Graduate School of Medical Sciences, Kumamoto University
  • HARAOKA Katsuki
    Department of Gastroenterology and Hepatology, Graduate School of Medical Sciences, Kumamoto University
  • GUO Sun Xu
    Department of Diagnostic Medicine, Graduate School of Medical Sciences, Kumamoto University
  • UEDA Mitsuharu
    Department of Neurology, Graduate School of Medical Sciences, Kumamoto University
  • UCHINO Makoto
    Department of Neurology, Graduate School of Medical Sciences, Kumamoto University

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  • Inhibitory Effect of α-Tocopherol on Methylmercury-Induced Oxidative Steress

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Abstract

Objectives: The present study investigated the involvement of oxidative stress in the degeneration of the cerebellum during methylmercury (MeHg) intoxication and the protective effect of α-tocopherol (Vit E) against MeHg toxicity.<br> Methods: After 5 mg/kg of MeHg was administered to Wistar rats for 12 consecutive days, the cerebellum were examined histopathologically. In addition, the same amount of MeHg was administered to 3 different groups of Wistar rats: rats with a Vit E-deficient diet, rats fed 150 mg/kg of Vit E for 20 consecutive days after initial MeHg administration, and rats with an ordinary diet.<br> Results: Positive immunoreactivity against anti-hydroxynonenal (HNE), a marker of lipid peroxidation, was observed in the cerebellum after MeHg administration. Levels of thiobarbituric acid reactive substance (TBARS), another marker of lipid peroxidation, and those of protein carbonyl, a biomarker for protein oxidation, increased after MeHg administration. In the rats with MeHg and a Vit E-deficient diet, mortality and prevalence of piloerection significantly increased, and in the rats with MeHg and Vit E, mortality, piloerection, retracted and crossed hind leg, and ataxic gait significantly decreased, compared with the rats with MeHg alone. The levels of NO2− and NO3− in the serum significantly increased in the rats with MeHg alone 14 days after the initial MeHg administration, but were significantly suppressed by Vit E administration.<br> Conclusions: Oxidative stress, especially lipid peroxidation, may play an important role in the cerebellar degeneration process during MeHg intoxication and Vit E may play a protective role against MeHg toxicity as an effective antioxidant.<br>

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