Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2004 May;9(3):111-7.
doi: 10.1007/BF02898069.

Inhibitory effect of α-tocopherol on methylmercury-induced oxidative steress

Affiliations

Inhibitory effect of α-tocopherol on methylmercury-induced oxidative steress

Taro Yamashita et al. Environ Health Prev Med. 2004 May.

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.

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.

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 NO(2) (-) and NO(3) (-) 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.

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.

Keywords: cerebellar degeneration; lipid peroxidation; methylmercury; oxidative stress; vitamin E.

PubMed Disclaimer

References

    1. None
    2. Hunter D Bomford RR, Russell DS. Poisoning by methyl mercury compounds. Quart. J. Med. 1940; 9: 193–213.
    1. {'text': '', 'ref_index': 1, 'ids': [{'type': 'DOI', 'value': '10.1136/jnnp.17.4.235', 'is_inner': False, 'url': 'https://doi.org/10.1136/jnnp.17.4.235'}, {'type': 'PMC', 'value': 'PMC503192', 'is_inner': False, 'url': 'https://pmc.ncbi.nlm.nih.gov/articles/PMC503192/'}, {'type': 'PubMed', 'value': '13212411', 'is_inner': True, 'url': 'https://pubmed.ncbi.nlm.nih.gov/13212411/'}]}
    2. Hunter D, Russell DS. Focal cerebral and cerebellar atrophy in a human subject due to orgnanic mercury compounds. J. Neurol. Neurosurg. Psychiat. 1954; 17: 235–241. - PMC - PubMed
    1. None
    2. Takeuchi T. Pathology of Minamata disease. In Study Group of Minamata disease, Kumamoto University (ed. Kutsuna, M.) Shuhan Publisher, Tokyo, Japan. 1968. pp. 141–228.
    1. {'text': '', 'ref_index': 1, 'ids': [{'type': 'PubMed', 'value': '6765001', 'is_inner': True, 'url': 'https://pubmed.ncbi.nlm.nih.gov/6765001/'}]}
    2. Takeuchi T. Pathology of Minamata disease. With special reference to its pathogenesis. Acta. Pathol. Jpn., 1982; 32: Suppl 1: 73–99. - PubMed
    1. {'text': '', 'ref_index': 1, 'ids': [{'type': 'PubMed', 'value': '9437808', 'is_inner': True, 'url': 'https://pubmed.ncbi.nlm.nih.gov/9437808/'}]}
    2. Nagashima KA. Review of experimental methylmercury toxicity in rats: neuropathology and evidence for apoptosis. Toxicol. Pathol. 1997; 25: 624–631. - PubMed