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DMPS and N-acetylcysteine induced renal toxicity in mice exposed to mercury.
Biometals. 2006 Aug; 19(4):389-98.B

Abstract

Acute effects of mercuric chloride (HgCl2) were evaluated on mice. Mice received a single dose of HgCl2 (4.6 mg/kg, subcutaneously) for three consecutive days. Thirty minutes after the last injection with HgCl2, mice received one single injection of 2,3-dimercapto-1-propanesulfonic acid (DMPS) or N-acetylcysteine (NAC) or diphenyl diselenide (PhSe)2. DMPS, NAC and (PhSe)2 were utilized as therapy against mercury exposure. At 24 h after the last HgCl2 injection, blood, liver and kidney samples were collected. delta-Aminolevulinate dehydratase (delta-ALA-D) and Na+, K- (+) ATPase activities, thiobarbituric acid-reactive substances (TBARS), non-protein thiols (NPSH) and ascorbic acid concentrations were evaluated. Plasma aspartate (AST) and alanine (ALT) aminotransferase activities, as well as urea and creatinine levels were determined. The group of mice exposed to Hg + (PhSe)2 presented 100% of lethality. Exposure with HgCl2 caused a decrease on the body weight gain and treatments did not modify this parameter. delta-ALA-D, AST and ALT activities, TBARS, ascorbic acid levels and NPSH (hepatic and erythrocytic) levels were not changed after HgCl2 exposure. HgCl2 caused an increase in renal NPSH content and therapies did not modify these levels. Mice treated with (PhSe)2, Hg + NAC and Hg + DMPS presented a reduction in plasma NPSH levels. Creatinine and urea levels were increased in mice exposed to Hg + NAC, while Hg + DMPS group presented an increase only in urea level. Na+, K- (+) ATPase activity was inhibited in mice exposed to Hg + DMPS and Hg + NAC. In conclusion, therapies with (PhSe)2, DMPS and NAC following mercury exposure must be better studied because the formation of more toxic complexes with mercury, which can mainly damage renal tissue.

Authors+Show Affiliations

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

16841248

Citation

Brandão, Ricardo, et al. "DMPS and N-acetylcysteine Induced Renal Toxicity in Mice Exposed to Mercury." Biometals : an International Journal On the Role of Metal Ions in Biology, Biochemistry, and Medicine, vol. 19, no. 4, 2006, pp. 389-98.
Brandão R, Santos FW, Zeni G, et al. DMPS and N-acetylcysteine induced renal toxicity in mice exposed to mercury. Biometals. 2006;19(4):389-98.
Brandão, R., Santos, F. W., Zeni, G., Rocha, J. B., & Nogueira, C. W. (2006). DMPS and N-acetylcysteine induced renal toxicity in mice exposed to mercury. Biometals : an International Journal On the Role of Metal Ions in Biology, Biochemistry, and Medicine, 19(4), 389-98.
Brandão R, et al. DMPS and N-acetylcysteine Induced Renal Toxicity in Mice Exposed to Mercury. Biometals. 2006;19(4):389-98. PubMed PMID: 16841248.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - DMPS and N-acetylcysteine induced renal toxicity in mice exposed to mercury. AU - Brandão,Ricardo, AU - Santos,Francielli W, AU - Zeni,Gilson, AU - Rocha,João B T, AU - Nogueira,Cristina W, PY - 2005/09/19/received PY - 2005/10/12/accepted PY - 2006/7/15/pubmed PY - 2006/9/27/medline PY - 2006/7/15/entrez SP - 389 EP - 98 JF - Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine JO - Biometals VL - 19 IS - 4 N2 - Acute effects of mercuric chloride (HgCl2) were evaluated on mice. Mice received a single dose of HgCl2 (4.6 mg/kg, subcutaneously) for three consecutive days. Thirty minutes after the last injection with HgCl2, mice received one single injection of 2,3-dimercapto-1-propanesulfonic acid (DMPS) or N-acetylcysteine (NAC) or diphenyl diselenide (PhSe)2. DMPS, NAC and (PhSe)2 were utilized as therapy against mercury exposure. At 24 h after the last HgCl2 injection, blood, liver and kidney samples were collected. delta-Aminolevulinate dehydratase (delta-ALA-D) and Na+, K- (+) ATPase activities, thiobarbituric acid-reactive substances (TBARS), non-protein thiols (NPSH) and ascorbic acid concentrations were evaluated. Plasma aspartate (AST) and alanine (ALT) aminotransferase activities, as well as urea and creatinine levels were determined. The group of mice exposed to Hg + (PhSe)2 presented 100% of lethality. Exposure with HgCl2 caused a decrease on the body weight gain and treatments did not modify this parameter. delta-ALA-D, AST and ALT activities, TBARS, ascorbic acid levels and NPSH (hepatic and erythrocytic) levels were not changed after HgCl2 exposure. HgCl2 caused an increase in renal NPSH content and therapies did not modify these levels. Mice treated with (PhSe)2, Hg + NAC and Hg + DMPS presented a reduction in plasma NPSH levels. Creatinine and urea levels were increased in mice exposed to Hg + NAC, while Hg + DMPS group presented an increase only in urea level. Na+, K- (+) ATPase activity was inhibited in mice exposed to Hg + DMPS and Hg + NAC. In conclusion, therapies with (PhSe)2, DMPS and NAC following mercury exposure must be better studied because the formation of more toxic complexes with mercury, which can mainly damage renal tissue. SN - 0966-0844 UR - https://www.unboundmedicine.com/medline/citation/16841248/DMPS_and_N_acetylcysteine_induced_renal_toxicity_in_mice_exposed_to_mercury_ L2 - https://doi.org/10.1007/s10534-005-4020-3 DB - PRIME DP - Unbound Medicine ER -