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BioMed Research International
Volume 2013 (2013), Article ID 983821, 12 pages
Research Article

Effects of Diphenyl Diselenide on Methylmercury Toxicity in Rats

1Biochemistry and Molecular Biology Department, Graduation Program in Biological Sciences: Toxicological Biochemistry, Natural and Exact Sciences Center, Federal University of Santa Maria, 97105-900 Santa Maria, RS, Brazil
2Federal University of Pampa—Caçapava do Sul Campus, Avenida Pedro Anunciação, Vila Batista, 96570-000 Caçapava do Sul, RS, Brazil
3Higher Education Cenecista Institute of Santo Ângelo—IESA, Rua Dr. João Augusto Rodrigues 471, 98801-015 Santo Ângelo, RS, Brazil
4Regional University of Cariri, Pharmacology and Molecular Chemistry Laboratory, Rua Cel. Antônio Luís 1161, 63100-000 Crato, CE, Brazil
5Department of Pharmacology, Vanderbilt University Medical Center, Nashville, TN 37232, USA
6Department of Pediatrics, Vanderbilt University Medical Center, Nashville, TN 37232, USA

Received 19 September 2013; Revised 25 November 2013; Accepted 25 November 2013

Academic Editor: Fernando Barbosa Jr.

Copyright © 2013 Cristiane L. Dalla Corte et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


This study investigates the efficacy of diphenyl diselenide [(PhSe)2] in attenuating methylmercury- (MeHg-)induced toxicity in rats. Adult rats were treated with MeHg [5 mg/kg/day, intragastrically (i.g.)] and/ or (PhSe)2 [1 mg/kg/day, intraperitoneally (i.p.)] for 21 days. Body weight gain and motor deficits were evaluated prior to treatment, on treatment days 11 and 21. In addition, hepatic and cerebral mitochondrial function (reactive oxygen species (ROS) formation, total and nonprotein thiol levels, membrane potential ( ), metabolic function, and swelling), hepatic, cerebral, and muscular mercury levels, and hepatic, cerebral, and renal thioredoxin reductase (TrxR) activity were evaluated. MeHg caused hepatic and cerebral mitochondrial dysfunction and inhibited TrxR activity in liver (38,9%), brain (64,3%), and kidney (73,8%). Cotreatment with (PhSe)2 protected hepatic and cerebral mitochondrial thiols from depletion by MeHg but failed to completely reverse MeHg’s effect on hepatic and cerebral mitochondrial dysfunction or hepatic, cerebral, and renal inhibition of TrxR activity. Additionally, the cotreatment with (PhSe)2 increased Hg accumulation in the liver (50,5%) and brain (49,4%) and increased the MeHg-induced motor deficits and body-weight loss. In conclusion, these results indicate that (PhSe)2 can increase Hg body burden as well as the neurotoxic effects induced by MeHg exposure in rats.