Protective Effect of DPPD on Mercury Chloride-Induced Hepatorenal Toxicity in Rats

Mercury is a global environmental pollutant, accumulating mainly in the kidney and liver inducing hepatorenal toxicity, oxidative stress, and tissue damage. Oxidative stress is caused by an imbalance between free radicals’ production and cellular antioxidant defense systems. In the present study, we...

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Main Authors: Ahmed Nabil, Mohamed M. Elshemy, Medhat Asem, Heba F. Gomaa
Format: Article
Language:English
Published: Wiley 2020-01-01
Series:Journal of Toxicology
Online Access:http://dx.doi.org/10.1155/2020/4127284
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author Ahmed Nabil
Mohamed M. Elshemy
Medhat Asem
Heba F. Gomaa
author_facet Ahmed Nabil
Mohamed M. Elshemy
Medhat Asem
Heba F. Gomaa
author_sort Ahmed Nabil
collection DOAJ
description Mercury is a global environmental pollutant, accumulating mainly in the kidney and liver inducing hepatorenal toxicity, oxidative stress, and tissue damage. Oxidative stress is caused by an imbalance between free radicals’ production and cellular antioxidant defense systems. In the present study, we investigated the effect of N N′-diphenyl-1, 4-phenylenediamine (DPPD) antioxidant activity against mercury chloride- (HgCl2-) induced renal and hepatic toxicity. Thirty adult female Sprague Dawley rats were divided into three equal groups: the first group was injected with saline only and served as a control, the second group was injected with HgCl2, and the third group received DPPD + HgCl2 rats injected with HgCl2 without treatment showing a significant increase in alkaline phosphatase (ALP), aspartate aminotransferase (AST), alanine aminotransferase (ALT), urea, creatinine, and uric acids compared to control. Moreover, the second group showed a significant reduction in the activity of the antioxidant enzymes (superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH)) in addition to a marked increase in the malondialdehyde (MDA) content, histopathological alterations, collagen deposition, CD8%, CD4%, and TGF-β% in kidney and liver tissues compared with the control group. Treatment with DPPD showed significant recovery (p≤0.001) in all previous parameters and histopathological examination. In conclusion, we suggested that DPPD may have a promising antioxidant capacity, gives it the applicability to be used as a prophylactic agent against mercury-induced hepatorenal cytotoxicity in the future.
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spelling doaj-art-d2ec32b44760456eab8e41c77458f8472025-08-20T02:19:51ZengWileyJournal of Toxicology1687-81911687-82052020-01-01202010.1155/2020/41272844127284Protective Effect of DPPD on Mercury Chloride-Induced Hepatorenal Toxicity in RatsAhmed Nabil0Mohamed M. Elshemy1Medhat Asem2Heba F. Gomaa3Research Center for Functional Materials, National Institute for Materials Science (NIMS), 1-1 Namiki, Tsukuba, Ibaraki 305-0044, JapanFaculty of Science, Menoufia University, Menoufia, EgyptFaculty of Science, Menoufia University, Menoufia, EgyptZoology Department, Faculty of Science, Ain-Shams University, Cairo, EgyptMercury is a global environmental pollutant, accumulating mainly in the kidney and liver inducing hepatorenal toxicity, oxidative stress, and tissue damage. Oxidative stress is caused by an imbalance between free radicals’ production and cellular antioxidant defense systems. In the present study, we investigated the effect of N N′-diphenyl-1, 4-phenylenediamine (DPPD) antioxidant activity against mercury chloride- (HgCl2-) induced renal and hepatic toxicity. Thirty adult female Sprague Dawley rats were divided into three equal groups: the first group was injected with saline only and served as a control, the second group was injected with HgCl2, and the third group received DPPD + HgCl2 rats injected with HgCl2 without treatment showing a significant increase in alkaline phosphatase (ALP), aspartate aminotransferase (AST), alanine aminotransferase (ALT), urea, creatinine, and uric acids compared to control. Moreover, the second group showed a significant reduction in the activity of the antioxidant enzymes (superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH)) in addition to a marked increase in the malondialdehyde (MDA) content, histopathological alterations, collagen deposition, CD8%, CD4%, and TGF-β% in kidney and liver tissues compared with the control group. Treatment with DPPD showed significant recovery (p≤0.001) in all previous parameters and histopathological examination. In conclusion, we suggested that DPPD may have a promising antioxidant capacity, gives it the applicability to be used as a prophylactic agent against mercury-induced hepatorenal cytotoxicity in the future.http://dx.doi.org/10.1155/2020/4127284
spellingShingle Ahmed Nabil
Mohamed M. Elshemy
Medhat Asem
Heba F. Gomaa
Protective Effect of DPPD on Mercury Chloride-Induced Hepatorenal Toxicity in Rats
Journal of Toxicology
title Protective Effect of DPPD on Mercury Chloride-Induced Hepatorenal Toxicity in Rats
title_full Protective Effect of DPPD on Mercury Chloride-Induced Hepatorenal Toxicity in Rats
title_fullStr Protective Effect of DPPD on Mercury Chloride-Induced Hepatorenal Toxicity in Rats
title_full_unstemmed Protective Effect of DPPD on Mercury Chloride-Induced Hepatorenal Toxicity in Rats
title_short Protective Effect of DPPD on Mercury Chloride-Induced Hepatorenal Toxicity in Rats
title_sort protective effect of dppd on mercury chloride induced hepatorenal toxicity in rats
url http://dx.doi.org/10.1155/2020/4127284
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