The Effect of Selenium Against Cadmium-Induced Nephrotoxicity in Rats: The Role of the TRPM2 Channel

This study investigated the protective effect of selenium (Se) in a cadmium (Cd)-induced nephrotoxicity model in rats and the role of the TRPM2 channel in this mechanism. For this purpose, Cd (25 mg/kg orally), Se (0.5 mg/kg i.p.), and 2-aminoethoxydiphenyl borate (2-APB), a TRPM2 channel antagonist...

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Main Authors: Ömer Faruk Keleş, Mehmet Hafit Bayir, Hacı Ahmet Çiçek, Adem Ahlatcı, Kenan Yıldızhan
Format: Article
Language:English
Published: MDPI AG 2025-01-01
Series:Toxics
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Online Access:https://www.mdpi.com/2305-6304/13/2/87
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author Ömer Faruk Keleş
Mehmet Hafit Bayir
Hacı Ahmet Çiçek
Adem Ahlatcı
Kenan Yıldızhan
author_facet Ömer Faruk Keleş
Mehmet Hafit Bayir
Hacı Ahmet Çiçek
Adem Ahlatcı
Kenan Yıldızhan
author_sort Ömer Faruk Keleş
collection DOAJ
description This study investigated the protective effect of selenium (Se) in a cadmium (Cd)-induced nephrotoxicity model in rats and the role of the TRPM2 channel in this mechanism. For this purpose, Cd (25 mg/kg orally), Se (0.5 mg/kg i.p.), and 2-aminoethoxydiphenyl borate (2-APB), a TRPM2 channel antagonist, (3 mg/kg i.p.) were administered to rats every day for 5 days. At the end of the study, kidney tissues were analysed using histological and biochemical methods. A histopathological examination revealed congestion, tubular degeneration, necrosis, and glomerular adhesion in the Cd group. However, these lesions were significantly reduced in the Cd + Se and Cd + 2-APB groups, while the Cd + Se + 2-APB group showed a histological appearance similar to the control group. Immunohistochemical analysis revealed that Caspase-3, Bax, and TRPM2 expression was higher in the Cd group, while these levels were lower in the Se and 2-APB treatment groups (<i>p</i> < 0.05). Among the groups that received Cd, urea, creatinine, TOS, TNF-α, and IL-1β levels were at the highest level in the Cd group, while TAS level was at the lowest level (<i>p</i> < 0.05). The Se and 2-APB treatment modulated these parameters; however, Se + 2-APB treatment reduced urea, creatinine, TOS, TNF-α, and IL-1β levels to the lowest level compared to the Cd groups and brought the TAS level closer to the control group (<i>p</i> < 0.05). These findings indicated that targeting TRPM2 channel inactivation together with the selenium treatment could alleviate Cd-induced nephrotoxicity.
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publishDate 2025-01-01
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spelling doaj-art-c8a7bf18cf1c49ad9d83d19e61d8d8e32025-08-20T02:03:32ZengMDPI AGToxics2305-63042025-01-011328710.3390/toxics13020087The Effect of Selenium Against Cadmium-Induced Nephrotoxicity in Rats: The Role of the TRPM2 ChannelÖmer Faruk Keleş0Mehmet Hafit Bayir1Hacı Ahmet Çiçek2Adem Ahlatcı3Kenan Yıldızhan4Department of Pathology, Faculty of Veterinary Medicine, Van Yuzuncu Yil University, 65080 Van, TürkiyeDepartment of Histology, Faculty of Medicine, Van Yuzuncu Yil University, 65080 Van, TürkiyeDepartment of Pathology, Faculty of Veterinary Medicine, Van Yuzuncu Yil University, 65080 Van, TürkiyeVocational School of Health Services, Van Yuzuncu Yil University, 65080 Van, TürkiyeDepartment of Biophysics, Faculty of Medicine, Van Yuzuncu Yil University, 65080 Van, TürkiyeThis study investigated the protective effect of selenium (Se) in a cadmium (Cd)-induced nephrotoxicity model in rats and the role of the TRPM2 channel in this mechanism. For this purpose, Cd (25 mg/kg orally), Se (0.5 mg/kg i.p.), and 2-aminoethoxydiphenyl borate (2-APB), a TRPM2 channel antagonist, (3 mg/kg i.p.) were administered to rats every day for 5 days. At the end of the study, kidney tissues were analysed using histological and biochemical methods. A histopathological examination revealed congestion, tubular degeneration, necrosis, and glomerular adhesion in the Cd group. However, these lesions were significantly reduced in the Cd + Se and Cd + 2-APB groups, while the Cd + Se + 2-APB group showed a histological appearance similar to the control group. Immunohistochemical analysis revealed that Caspase-3, Bax, and TRPM2 expression was higher in the Cd group, while these levels were lower in the Se and 2-APB treatment groups (<i>p</i> < 0.05). Among the groups that received Cd, urea, creatinine, TOS, TNF-α, and IL-1β levels were at the highest level in the Cd group, while TAS level was at the lowest level (<i>p</i> < 0.05). The Se and 2-APB treatment modulated these parameters; however, Se + 2-APB treatment reduced urea, creatinine, TOS, TNF-α, and IL-1β levels to the lowest level compared to the Cd groups and brought the TAS level closer to the control group (<i>p</i> < 0.05). These findings indicated that targeting TRPM2 channel inactivation together with the selenium treatment could alleviate Cd-induced nephrotoxicity.https://www.mdpi.com/2305-6304/13/2/87cadmiumseleniumTRPM2 channelhistopathologyimmunohistochemicallyrat
spellingShingle Ömer Faruk Keleş
Mehmet Hafit Bayir
Hacı Ahmet Çiçek
Adem Ahlatcı
Kenan Yıldızhan
The Effect of Selenium Against Cadmium-Induced Nephrotoxicity in Rats: The Role of the TRPM2 Channel
Toxics
cadmium
selenium
TRPM2 channel
histopathology
immunohistochemically
rat
title The Effect of Selenium Against Cadmium-Induced Nephrotoxicity in Rats: The Role of the TRPM2 Channel
title_full The Effect of Selenium Against Cadmium-Induced Nephrotoxicity in Rats: The Role of the TRPM2 Channel
title_fullStr The Effect of Selenium Against Cadmium-Induced Nephrotoxicity in Rats: The Role of the TRPM2 Channel
title_full_unstemmed The Effect of Selenium Against Cadmium-Induced Nephrotoxicity in Rats: The Role of the TRPM2 Channel
title_short The Effect of Selenium Against Cadmium-Induced Nephrotoxicity in Rats: The Role of the TRPM2 Channel
title_sort effect of selenium against cadmium induced nephrotoxicity in rats the role of the trpm2 channel
topic cadmium
selenium
TRPM2 channel
histopathology
immunohistochemically
rat
url https://www.mdpi.com/2305-6304/13/2/87
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