Effects of inorganic selenium administration in methylmercury-induced neurotoxicity in mouse cerebral cortex

Selenium can counteract methylmercury (MeHg) neurotoxicity. However, data about the neuroprotective effects of sodium selenite (Na2SeO3) on the activity of mitochondrial complexes and creatine kinase (mtCK) are scarce. Therefore, this study investigated the effects of the chronic exposure to Na2SeO3 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 Na2SeO3 (5 mu mol 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 (AMC). Na2SeO3 partially prevented MeHg-induced inhibition of complexes 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, Na2SeO3 did not modify such events. Furthermore, Na2SeO3 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 Na2SeO3, alone or in combination with mercury, should be considered when this compound is proposed as a potential protective therapy for MeHg poisoning. (C) 2010 ISDN. Published by Elsevier Ltd. All rights reserved.