Diphenyl diselenide potentiates nephrotoxicity induced by mercuric chloride in mice Journal Articles uri icon

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abstract

  • ABSTRACTFollowing 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. Copyright © 2011 John Wiley & Sons, Ltd.

authors

  • Brandão, Ricardo
  • Moresco, Rafael N
  • Bellé, Luziane P
  • Leite, Marlon R
  • de Freitas, Mayara L
  • Bianchini, Adalto
  • Nogueira, Cristina W

publication date

  • November 2011

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