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Diphenyl diselenide, a simple organoselenium compound, decreases methylmercury-induced cerebral, hepatic and renal oxidative stress and mercury deposition in adult mice.
Brain Res Bull. 2009 Apr 06; 79(1):77-84.BR

Abstract

Oxidative stress has been pointed out as an important molecular mechanism in methylmercury (MeHg) intoxication. At low doses, diphenyl diselenide ((PhSe)2), a structurally simple organoselenium compound, has been shown to possess antioxidant and neuroprotective properties. Here we have examined the possible in vivo protective effect of diphenyl diselenide against the potential pro-oxidative effects of MeHg in mouse liver, kidney, cerebrum and cerebellum. The effects of MeHg exposure (2 mg/(kg day) of methylmercury chloride 10 ml/kg, p.o.), as well as the possible antagonist effect of diphenyl diselenide (1 and 0.4 mg/(kg day); s.c.) on body weight gain and on hepatic, cerebellar, cerebral and renal levels of thiobarbituric acid reactive substances (TBARS), non-protein thiols (NPSH), ascorbic acid content, mercury concentrations and activities of antioxidant enzymes (glutathione peroxidase (GPx), catalase (CAT) and superoxide dismutase (SOD)) were evaluated after 35 days of treatment. MeHg caused an increase in TBARS and decreased NPSH levels in all tissues. MeHg also induced a decrease in hepatic ascorbic acid content and in renal GPx and CAT activities. Diphenyl diselenide (1 mg/kg) conferred protection against MeHg-induced hepatic and renal lipid peroxidation and at both doses prevented the reduction in hepatic NPSH levels. Diphenyl diselenide also conferred a partial protection against MeHg-induced oxidative stress (TBARS and NPSH) in liver and cerebellum. Of particular importance, diphenyl diselenide decreased the deposition of Hg in cerebrum, cerebellum, kidney and liver. The present results indicate that diphenyl diselenide can protect against some toxic effects of MeHg in mice. This protection may be related to its antioxidant properties and its ability to reduce Hg body burden. We posit that formation of a selenol intermediate, which possesses high nucleophilicity and high affinity for MeHg, accounts for the ability of diphenyl diselenide to ameliorate MeHg-induced toxicity.

Authors+Show Affiliations

Departamento de Química, Centro de Ciências Naturais e Exatas, Universidade Federal de Santa Maria, Santa Maria, CEP 97105-900 RS, Brazil.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

19047014

Citation

de Freitas, Andressa Sausen, et al. "Diphenyl Diselenide, a Simple Organoselenium Compound, Decreases Methylmercury-induced Cerebral, Hepatic and Renal Oxidative Stress and Mercury Deposition in Adult Mice." Brain Research Bulletin, vol. 79, no. 1, 2009, pp. 77-84.
de Freitas AS, Funck VR, Rotta Mdos S, et al. Diphenyl diselenide, a simple organoselenium compound, decreases methylmercury-induced cerebral, hepatic and renal oxidative stress and mercury deposition in adult mice. Brain Res Bull. 2009;79(1):77-84.
de Freitas, A. S., Funck, V. R., Rotta, M. d. o. s. . S., Bohrer, D., Mörschbächer, V., Puntel, R. L., Nogueira, C. W., Farina, M., Aschner, M., & Rocha, J. B. (2009). Diphenyl diselenide, a simple organoselenium compound, decreases methylmercury-induced cerebral, hepatic and renal oxidative stress and mercury deposition in adult mice. Brain Research Bulletin, 79(1), 77-84. https://doi.org/10.1016/j.brainresbull.2008.11.001
de Freitas AS, et al. Diphenyl Diselenide, a Simple Organoselenium Compound, Decreases Methylmercury-induced Cerebral, Hepatic and Renal Oxidative Stress and Mercury Deposition in Adult Mice. Brain Res Bull. 2009 Apr 6;79(1):77-84. PubMed PMID: 19047014.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Diphenyl diselenide, a simple organoselenium compound, decreases methylmercury-induced cerebral, hepatic and renal oxidative stress and mercury deposition in adult mice. AU - de Freitas,Andressa Sausen, AU - Funck,Vinícius Rafael, AU - Rotta,Mariana dos Santos, AU - Bohrer,Denise, AU - Mörschbächer,Vanessa, AU - Puntel,Robson Luís, AU - Nogueira,Cristina Wayne, AU - Farina,Marcelo, AU - Aschner,Michael, AU - Rocha,João Batista Teixeira, Y1 - 2008/11/29/ PY - 2008/10/30/received PY - 2008/11/04/accepted PY - 2008/12/3/pubmed PY - 2009/5/13/medline PY - 2008/12/3/entrez SP - 77 EP - 84 JF - Brain research bulletin JO - Brain Res Bull VL - 79 IS - 1 N2 - Oxidative stress has been pointed out as an important molecular mechanism in methylmercury (MeHg) intoxication. At low doses, diphenyl diselenide ((PhSe)2), a structurally simple organoselenium compound, has been shown to possess antioxidant and neuroprotective properties. Here we have examined the possible in vivo protective effect of diphenyl diselenide against the potential pro-oxidative effects of MeHg in mouse liver, kidney, cerebrum and cerebellum. The effects of MeHg exposure (2 mg/(kg day) of methylmercury chloride 10 ml/kg, p.o.), as well as the possible antagonist effect of diphenyl diselenide (1 and 0.4 mg/(kg day); s.c.) on body weight gain and on hepatic, cerebellar, cerebral and renal levels of thiobarbituric acid reactive substances (TBARS), non-protein thiols (NPSH), ascorbic acid content, mercury concentrations and activities of antioxidant enzymes (glutathione peroxidase (GPx), catalase (CAT) and superoxide dismutase (SOD)) were evaluated after 35 days of treatment. MeHg caused an increase in TBARS and decreased NPSH levels in all tissues. MeHg also induced a decrease in hepatic ascorbic acid content and in renal GPx and CAT activities. Diphenyl diselenide (1 mg/kg) conferred protection against MeHg-induced hepatic and renal lipid peroxidation and at both doses prevented the reduction in hepatic NPSH levels. Diphenyl diselenide also conferred a partial protection against MeHg-induced oxidative stress (TBARS and NPSH) in liver and cerebellum. Of particular importance, diphenyl diselenide decreased the deposition of Hg in cerebrum, cerebellum, kidney and liver. The present results indicate that diphenyl diselenide can protect against some toxic effects of MeHg in mice. This protection may be related to its antioxidant properties and its ability to reduce Hg body burden. We posit that formation of a selenol intermediate, which possesses high nucleophilicity and high affinity for MeHg, accounts for the ability of diphenyl diselenide to ameliorate MeHg-induced toxicity. SN - 1873-2747 UR - https://www.unboundmedicine.com/medline/citation/19047014/Diphenyl_diselenide_a_simple_organoselenium_compound_decreases_methylmercury_induced_cerebral_hepatic_and_renal_oxidative_stress_and_mercury_deposition_in_adult_mice_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0361-9230(08)00377-8 DB - PRIME DP - Unbound Medicine ER -