Diphenyl diselenide potentiates nephrotoxicity induced by mercuric chloride in mice.
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.
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.br
Ricardo
R
Brandão
Rafael N
RN
Moresco
Luziane P
LP
Bellé
Marlon R
MR
Leite
Mayara L
ML
de Freitas
Adalto
A
Bianchini
Cristina W
CW
Nogueira
D058186:Acute Kidney Injury / Q000139:chemically induced / Q000473:pathology*; D000818:Animals; D001205:Ascorbic Acid / Q000378:metabolism; D001555:Benzene Derivatives / Q000633:toxicity*; D002374:Catalase / Q000378:metabolism; D003404:Creatinine / Q000097:blood; D004921:Erythropoietin / Q000097:blood; D005982:Glutathione Transferase / Q000378:metabolism; D007668:Kidney / Q000187:drug effects* / Q000378:metabolism; D008099:Liver / Q000187:drug effects / Q000378:metabolism; D008297:Male; D008627:Mercuric Chloride / Q000633:toxicity*; D008628:Mercury / Q000032:analysis; D051379:Mice; D016566:Organoselenium Compounds / Q000633:toxicity*; D018384:Oxidative Stress / Q000187:drug effects; D000623:Porphobilinogen Synthase / Q000378:metabolism; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism; D014508:Urea / Q000097:blood
D001555:Benzene Derivatives; D016566:Organoselenium Compounds; D017392:Thiobarbituric Acid Reactive Substances; D004921:Erythropoietin; C061132:diphenyldiselenide; D008627:Mercuric Chloride; D014508:Urea; D003404:Creatinine; D002374:Catalase; D005982:Glutathione Transferase; D000623:Porphobilinogen Synthase; D008628:Mercury; D001205:Ascorbic Acid