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Diphenyl diselenide potentiates nephrotoxicity induced by mercuric chloride in mice.
J Appl Toxicol. 2011 Nov; 31(8):773-82.JA

Abstract

Following our long-standing interest in the mechanisms involved in selenium toxicity, the aim of this work was to extend our previous studies to gain a better understanding of mercuric chloride (HgCl₂) + diphenyl diselenide (PhSe)₂ toxicity. Mice received one daily dose of HgCl₂ (4.6 mg kg(-1) , subcutaneously) for three consecutive days. Thirty minutes after the last injection of HgCl₂, mice received a single dose of (PhSe)₂ (31.2 mg kg(-1) , subcutaneously). Five hours after (PhSe)₂ administration, mice were euthanized and δ-aminolevulinate dehydratase, catalase (CAT), glutathione S-transferase (GST) and Na(+) , K(+) -ATPase activities as well as thiobarbituric acid-reactive substances (TBARS), ascorbic acid and mercury levels were determined in kidney and liver. Parameters in plasma (urea, creatinine, protein and erythropoietin), whole blood (hematocrit and hemoglobin) and urine (protein) were also investigated. HgCl₂ + (PhSe)₂ exposure caused a decrease in renal GST and Na(+) , K(+) -ATPase activities and an increase in renal ascorbic acid and TBARS concentrations when compared with the HgCl₂ group. (PhSe)₂ potentiated the increase in plasma urea caused by HgCl₂. HgCl₂ + (PhSe)₂ exposure caused a reduction in plasma protein levels and an increase in hemoglobin and hematocrit contents when compared with the HgCl₂ group. There was a significant reduction in hepatic CAT activity and an increase in TBARS levels in mice exposed to HgCl₂ + (PhSe)₂ when compared with the HgCl₂ group. The results demonstrated that (PhSe)₂ did not modify mercury levels in mice. In conclusion, (PhSe)₂ potentiated damage caused by HgCl₂ affecting mainly the renal tissue.

Authors+Show Affiliations

Departamento de Análises Clínicas e Toxicológicas, Centro de Ciências da Saúde, Universidade Federal de Santa Maria, CEP 97105-900, Santa Maria, RS, Brazil. ricardo_br79@yahoo.com.brNo 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

21259295

Citation

Brandão, Ricardo, et al. "Diphenyl Diselenide Potentiates Nephrotoxicity Induced By Mercuric Chloride in Mice." Journal of Applied Toxicology : JAT, vol. 31, no. 8, 2011, pp. 773-82.
Brandão R, Moresco RN, Bellé LP, et al. Diphenyl diselenide potentiates nephrotoxicity induced by mercuric chloride in mice. J Appl Toxicol. 2011;31(8):773-82.
Brandão, R., Moresco, R. N., Bellé, L. P., Leite, M. R., de Freitas, M. L., Bianchini, A., & Nogueira, C. W. (2011). Diphenyl diselenide potentiates nephrotoxicity induced by mercuric chloride in mice. Journal of Applied Toxicology : JAT, 31(8), 773-82. https://doi.org/10.1002/jat.1631
Brandão R, et al. Diphenyl Diselenide Potentiates Nephrotoxicity Induced By Mercuric Chloride in Mice. J Appl Toxicol. 2011;31(8):773-82. PubMed PMID: 21259295.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Diphenyl diselenide potentiates nephrotoxicity induced by mercuric chloride in mice. AU - Brandão,Ricardo, AU - Moresco,Rafael N, AU - Bellé,Luziane P, AU - Leite,Marlon R, AU - de Freitas,Mayara L, AU - Bianchini,Adalto, AU - Nogueira,Cristina W, Y1 - 2011/01/24/ PY - 2010/07/19/received PY - 2010/10/27/revised PY - 2010/10/27/accepted PY - 2011/1/25/entrez PY - 2011/1/25/pubmed PY - 2012/3/20/medline SP - 773 EP - 82 JF - Journal of applied toxicology : JAT JO - J Appl Toxicol VL - 31 IS - 8 N2 - Following our long-standing interest in the mechanisms involved in selenium toxicity, the aim of this work was to extend our previous studies to gain a better understanding of mercuric chloride (HgCl₂) + diphenyl diselenide (PhSe)₂ toxicity. Mice received one daily dose of HgCl₂ (4.6 mg kg(-1) , subcutaneously) for three consecutive days. Thirty minutes after the last injection of HgCl₂, mice received a single dose of (PhSe)₂ (31.2 mg kg(-1) , subcutaneously). Five hours after (PhSe)₂ administration, mice were euthanized and δ-aminolevulinate dehydratase, catalase (CAT), glutathione S-transferase (GST) and Na(+) , K(+) -ATPase activities as well as thiobarbituric acid-reactive substances (TBARS), ascorbic acid and mercury levels were determined in kidney and liver. Parameters in plasma (urea, creatinine, protein and erythropoietin), whole blood (hematocrit and hemoglobin) and urine (protein) were also investigated. HgCl₂ + (PhSe)₂ exposure caused a decrease in renal GST and Na(+) , K(+) -ATPase activities and an increase in renal ascorbic acid and TBARS concentrations when compared with the HgCl₂ group. (PhSe)₂ potentiated the increase in plasma urea caused by HgCl₂. HgCl₂ + (PhSe)₂ exposure caused a reduction in plasma protein levels and an increase in hemoglobin and hematocrit contents when compared with the HgCl₂ group. There was a significant reduction in hepatic CAT activity and an increase in TBARS levels in mice exposed to HgCl₂ + (PhSe)₂ when compared with the HgCl₂ group. The results demonstrated that (PhSe)₂ did not modify mercury levels in mice. In conclusion, (PhSe)₂ potentiated damage caused by HgCl₂ affecting mainly the renal tissue. SN - 1099-1263 UR - https://www.unboundmedicine.com/medline/citation/21259295/Diphenyl_diselenide_potentiates_nephrotoxicity_induced_by_mercuric_chloride_in_mice_ L2 - https://doi.org/10.1002/jat.1631 DB - PRIME DP - Unbound Medicine ER -