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Effects of cadmium and monensin on renal and cardiac functions of mice subjected to subacute cadmium intoxication
Cadmium (Cd) is a well-known nephrotoxic agent. Cd-induced renal dysfunction has been considered as one of the causes leading to the development of hypertension. The correlation between Cd concentration in blood and urine and cardiovascular diseases has been discussed in many epidemiological studies...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Slovak Toxicology Society SETOX
2014
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4427723/ https://www.ncbi.nlm.nih.gov/pubmed/26109887 http://dx.doi.org/10.2478/intox-2014-0015 |
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author | Ivanova, Juliana Gluhcheva, Yordanka Arpadjan, Sonja Mitewa, Mariana |
author_facet | Ivanova, Juliana Gluhcheva, Yordanka Arpadjan, Sonja Mitewa, Mariana |
author_sort | Ivanova, Juliana |
collection | PubMed |
description | Cadmium (Cd) is a well-known nephrotoxic agent. Cd-induced renal dysfunction has been considered as one of the causes leading to the development of hypertension. The correlation between Cd concentration in blood and urine and cardiovascular diseases has been discussed in many epidemiological studies. A therapy with chelating agents is utilized for the treatment of toxic metal intoxication. Herein we present novel information indicating that monensin (applied as tetraethylammonium salt) is a promising chelating agent for the treatment of Cd-induced renal and cardiac dysfunction. The study was performed using the ICR mouse model. Adult ICR male mice were divided into three groups with six animals in each group: control (received distilled water and food ad libitum for 28 days); Cd-intoxicated (treated orally with 20 mg/kg b.w. Cd(II) acetate from day 1 to day 14 of the experimental protocol), and monensin treated group (intoxicated with Cd(II) acetate as described for the Cd-intoxicated group followed by oral treatment with 16 mg/kg b.w. tetraethylammonium salt of monensic acid for 2 weeks). Cd intoxication of the animals resulted in an increase of the organ weight/body weight indexes. Cd elevated significantly creatinine and glucose level in serum. Monensin treatment improved the organ weight/body weight ratios. The therapy of the Cd-intoxicated animals with monensin ameliorated the creatinine and glucose level in serum and decreased the concentration of the toxic metal ions in the heart and kidneys by 54% and 64%, respectively. |
format | Online Article Text |
id | pubmed-4427723 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | Slovak Toxicology Society SETOX |
record_format | MEDLINE/PubMed |
spelling | pubmed-44277232015-06-24 Effects of cadmium and monensin on renal and cardiac functions of mice subjected to subacute cadmium intoxication Ivanova, Juliana Gluhcheva, Yordanka Arpadjan, Sonja Mitewa, Mariana Interdiscip Toxicol Original Article Cadmium (Cd) is a well-known nephrotoxic agent. Cd-induced renal dysfunction has been considered as one of the causes leading to the development of hypertension. The correlation between Cd concentration in blood and urine and cardiovascular diseases has been discussed in many epidemiological studies. A therapy with chelating agents is utilized for the treatment of toxic metal intoxication. Herein we present novel information indicating that monensin (applied as tetraethylammonium salt) is a promising chelating agent for the treatment of Cd-induced renal and cardiac dysfunction. The study was performed using the ICR mouse model. Adult ICR male mice were divided into three groups with six animals in each group: control (received distilled water and food ad libitum for 28 days); Cd-intoxicated (treated orally with 20 mg/kg b.w. Cd(II) acetate from day 1 to day 14 of the experimental protocol), and monensin treated group (intoxicated with Cd(II) acetate as described for the Cd-intoxicated group followed by oral treatment with 16 mg/kg b.w. tetraethylammonium salt of monensic acid for 2 weeks). Cd intoxication of the animals resulted in an increase of the organ weight/body weight indexes. Cd elevated significantly creatinine and glucose level in serum. Monensin treatment improved the organ weight/body weight ratios. The therapy of the Cd-intoxicated animals with monensin ameliorated the creatinine and glucose level in serum and decreased the concentration of the toxic metal ions in the heart and kidneys by 54% and 64%, respectively. Slovak Toxicology Society SETOX 2014-06 2014-11-15 /pmc/articles/PMC4427723/ /pubmed/26109887 http://dx.doi.org/10.2478/intox-2014-0015 Text en Copyright © 2014 SETOX & Institute of Experimental Pharmacology and Toxicology, SASc. http://creativecommons.org/licenses/by/2.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Article Ivanova, Juliana Gluhcheva, Yordanka Arpadjan, Sonja Mitewa, Mariana Effects of cadmium and monensin on renal and cardiac functions of mice subjected to subacute cadmium intoxication |
title | Effects of cadmium and monensin on renal and cardiac functions of mice subjected to subacute cadmium intoxication |
title_full | Effects of cadmium and monensin on renal and cardiac functions of mice subjected to subacute cadmium intoxication |
title_fullStr | Effects of cadmium and monensin on renal and cardiac functions of mice subjected to subacute cadmium intoxication |
title_full_unstemmed | Effects of cadmium and monensin on renal and cardiac functions of mice subjected to subacute cadmium intoxication |
title_short | Effects of cadmium and monensin on renal and cardiac functions of mice subjected to subacute cadmium intoxication |
title_sort | effects of cadmium and monensin on renal and cardiac functions of mice subjected to subacute cadmium intoxication |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4427723/ https://www.ncbi.nlm.nih.gov/pubmed/26109887 http://dx.doi.org/10.2478/intox-2014-0015 |
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