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Involvement of glutamate and reactive oxygen species in methylmercury neurotoxicity
Aschner, M; Syversen, T; Souza, D. O; Rocha, J. B. T; Farina, M.
  • Aschner, M; Vanderbilt University Medical Center. Departments of Pediatrics and Pharmacology, and the Kennedy Center. Nashville. US
  • Syversen, T; Norwegian University of Science and Technology. Department of Clinical Neuroscience. Trondheim. NO
  • Souza, D. O; Universidade Federal de Santa Maria. Centro de Ciências da Saúde. Departamento de Análises Clínicas e Toxicológicas. Santa Maria. BR
  • Rocha, J. B. T; Universidade Federal do Rio Grande do Sul. Instituto de Ciências Básicas da Saúde. Departamento de Bioquímica. Porto Alegre. BR
  • Farina, M; Universidade Federal de Santa Catarina. Centro de Ciências Biológicas. Departamento de Bioquímica. Florianópolis. BR
Braz. j. med. biol. res ; 40(3): 285-291, Mar. 2007. ilus
Article in English | LILACS | ID: lil-441772
ABSTRACT
This review addresses the mechanisms of methylmercury (MeHg)-induced neurotoxicity, specifically examining the role of oxidative stress in mediating neuronal damage. A number of critical findings point to a central role for astrocytes in mediating MeHg-induced neurotoxicity as evidenced by the following observations a) MeHg preferentially accumulates in astrocytes; b) MeHg specifically inhibits glutamate uptake in astrocytes; c) neuronal dysfunction is secondary to disturbances in astrocytes. The generation of reactive oxygen species (ROS) by MeHg has been observed in various experimental paradigms. For example, MeHg enhances ROS formation both in vivo (rodent cerebellum) and in vitro (isolated rat brain synaptosomes), as well as in neuronal and mixed reaggregating cell cultures. Antioxidants, including selenocompounds, can rescue astrocytes from MeHg-induced cytotoxicity by reducing ROS formation. We emphasize that oxidative stress plays a significant role in mediating MeHg-induced neurotoxic damage with active involvement of the mitochondria in this process. Furthermore, we provide a mechanistic overview on oxidative stress induced by MeHg that is triggered by a series of molecular events such as activation of various kinases, stress proteins and other immediate early genes culminating in cell damage.
Subject(s)

Full text: Available Index: LILACS (Americas) Main subject: Astrocytes / Oxidative Stress / Glutamic Acid / Mercury Poisoning, Nervous System / Methylmercury Compounds / Neurons Type of study: Prognostic study Limits: Animals Language: English Journal: Braz. j. med. biol. res Journal subject: Biology / Medicine Year: 2007 Type: Article / Project document Affiliation country: Brazil / Norway / United States Institution/Affiliation country: Norwegian University of Science and Technology/NO / Universidade Federal de Santa Catarina/BR / Universidade Federal de Santa Maria/BR / Universidade Federal do Rio Grande do Sul/BR / Vanderbilt University Medical Center/US

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Full text: Available Index: LILACS (Americas) Main subject: Astrocytes / Oxidative Stress / Glutamic Acid / Mercury Poisoning, Nervous System / Methylmercury Compounds / Neurons Type of study: Prognostic study Limits: Animals Language: English Journal: Braz. j. med. biol. res Journal subject: Biology / Medicine Year: 2007 Type: Article / Project document Affiliation country: Brazil / Norway / United States Institution/Affiliation country: Norwegian University of Science and Technology/NO / Universidade Federal de Santa Catarina/BR / Universidade Federal de Santa Maria/BR / Universidade Federal do Rio Grande do Sul/BR / Vanderbilt University Medical Center/US