title: Effects of inorganic selenium administration in methylmercury-induced neurotoxicity in mouse cerebral cortex.
abstract: Selenium can counteract methylmercury (MeHg) neurotoxicity. However, data about the neuroprotective effects of sodium selenite (Na(2)SeO(3)) on the activity of mitochondrial complexes and creatine kinase (mtCK) are scarce. Therefore, this study investigated the effects of the chronic exposure to Na(2)SeO(3) on brain energy metabolism and oxidative stress parameters in MeHg-poisoned mice. Adult male mice were orally treated with MeHg (40 mg L(-1) in drinking water, ad libitum) during 21 days and simultaneously administrated with daily subcutaneous injections of Na(2)SeO(3) (5 μmol kg(-1)), a potential neuroprotectant. Mitochondrial complexes I to IV and mtCK activities were measured in cerebral cortex mitochondria. The cerebro-cortical tissue was also used to evaluate the antioxidant enzymes glutathione peroxidase (GPx) and glutathione reductase (GR) activities, as well as lipid peroxidation. Metal deposition was followed autometalographically (AMG). Na(2)SeO(3) partially prevented MeHg-induced inhibition of complexes II-III, IV and mtCK activities; however, it was unable to prevent MeHg-induced complex I and II inhibition. MeHg increased lipid peroxidation, GR activity and decreased GPx activity in the cerebral cortex; however, Na(2)SeO(3) did not modify such events. Furthermore, Na(2)SeO(3)per se inhibited complexes I, II-III and IV and mtCK activities and increased GPx and GR activities and lipid peroxidation. These data show that inorganic selenium was ineffective in preventing most of the MeHg-induced brain biochemical alterations. However, the most prominent finding was the selenium-induced reduction of cells labelled for metal deposition. Although, the literature supports the beneficial effects of selenium against mercury toxicity, the toxic effects elicited by Na(2)SeO(3), alone or in combination with mercury, should be considered when this compound is proposed as a potential protective therapy for MeHg poisoning.
authors.affiliation: Laboratório de Bioenergética e Estresse Oxidativo, Departamento de Bioquímica, Centro de Ciências Biológicas, Universidade Federal de Santa Catarina, Florianópolis, SC, Brazil.
authors.forename: Viviane
authors.initials: V
authors.lastname: Glaser
authors.forename: Evelise Maria
authors.initials: EM
authors.lastname: Nazari
authors.forename: Yara Maria Rauh
authors.initials: YM
authors.lastname: Müller
authors.forename: Luciane
authors.initials: L
authors.lastname: Feksa
authors.forename: Clóvis Milton Duval
authors.initials: CM
authors.lastname: Wannmacher
authors.forename: João Batista Teixeira
authors.initials: JB
authors.lastname: Rocha
authors.forename: Andreza Fabro
authors.initials: AF
authors.lastname: de Bem
authors.forename: Marcelo
authors.initials: M
authors.lastname: Farina
authors.forename: Alexandra
authors.initials: A
authors.lastname: Latini
mesh_terms: D000818:Animals; D002540:Cerebral Cortex / Q000187:drug effects* / Q000378:metabolism; D004579:Electron Transport / Q000187:drug effects; D008297:Male; D008767:Methylmercury Compounds / Q000633:toxicity*; D051379:Mice; D020258:Neurotoxicity Syndromes / Q000378:metabolism*; D018384:Oxidative Stress / Q000187:drug effects; D018038:Sodium Selenite / Q000008:administration & dosage* / Q000494:pharmacology
chemical_list: D008767:Methylmercury Compounds; D018038:Sodium Selenite