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<p>Potassium dichromate (Cr) is a ubiquitous inorganic chemical reagent, most frequently employed as an oxidizing agent in variety of laboratory and industrial settings and can result in nephrotoxicity. The current study was done to explore the nephrotoxic effects of Cr with a specific focus on alterations in renal aquaporins (AQPs) expression, renal water channel protein, providing insights into how exposure to Cr may compromise renal water homeostasis in a dose-dependent pattern. Thirty-six Wistar albino male rats were assigned into 3 groups evenly; control rats received only distilled water daily, while Cr-Low and Cr-High groups received, 2.5&#xa0;mg/kg bw, and 7.5&#xa0;mg/kg bw of Cr i.p for 14 days, respectively. Blood and kidney samples were obtained. Cr induced nephrotoxicity in the current study in a dose-dependent manner, as exhibited by a remarkable deterioration of the renal parameters, oxidative status, histopathological and ultrastructural changes. Renal function registered a significant rise in urea and creatinine, as opposed to total protein and albumin, which decreased substantially. A significant dose dependent rise in malondialdehyde (MDA) level as well as dwindle in the antioxidant enzymes level. Furthermore, hematology divulged a notable reduction in hemoglobin concentration (Hb%) while significant upsurge in white blood cells (WBCs) in exposed groups. In addition, our study demonstrated that Cr, alters the expression level of AQP1 and AQP2 in renal tissue which are salutary for detecting the renal damage early. On the other hand, Cr boosted the upregulation of kidney injury molecule-1 (KIM-1) in kidney tissue confirming its disruption. Interestingly, gene expression of KIM-1, AQP1 and AQP2’s in renal membrane correlates well with creatine level, reinforcing their role as sensitive markers of tubular damage and reflect impaired tubular water handling. High exposure produced a severe nephrotoxic profile, distinctly different from controls and far more pronounced than the Cr-Low group.</p>

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Potassium dichromate induces dose-dependent nephrotoxicity through oxidative stress-mediated downregulation of renal aquaporins and upregulation of KIM-1

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年6月22日

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  • Hossam Shehab,
  • Ibrahim El Tantawy El Sayed,
  • Eman A. Badr,
  • Nuha Anajirih,
  • Afaf Abdelkader,
  • Eman E. ELwakeel,
  • Nagah E. Ali,
  • Enas M. Kasem,
  • Fatma Al-Zahraa N. Al-Shahed,
  • Madaniah O. Zakari,
  • Ekramy M. Elmorsy,
  • Samah F. Ibrahim,
  • Mustafa Shukry,
  • Eman M. El Nashar,
  • Areej M. Alshehri,
  • Ahmad F. Rawan,
  • Ahmed Abdeen

摘要

Potassium dichromate (Cr) is a ubiquitous inorganic chemical reagent, most frequently employed as an oxidizing agent in variety of laboratory and industrial settings and can result in nephrotoxicity. The current study was done to explore the nephrotoxic effects of Cr with a specific focus on alterations in renal aquaporins (AQPs) expression, renal water channel protein, providing insights into how exposure to Cr may compromise renal water homeostasis in a dose-dependent pattern. Thirty-six Wistar albino male rats were assigned into 3 groups evenly; control rats received only distilled water daily, while Cr-Low and Cr-High groups received, 2.5 mg/kg bw, and 7.5 mg/kg bw of Cr i.p for 14 days, respectively. Blood and kidney samples were obtained. Cr induced nephrotoxicity in the current study in a dose-dependent manner, as exhibited by a remarkable deterioration of the renal parameters, oxidative status, histopathological and ultrastructural changes. Renal function registered a significant rise in urea and creatinine, as opposed to total protein and albumin, which decreased substantially. A significant dose dependent rise in malondialdehyde (MDA) level as well as dwindle in the antioxidant enzymes level. Furthermore, hematology divulged a notable reduction in hemoglobin concentration (Hb%) while significant upsurge in white blood cells (WBCs) in exposed groups. In addition, our study demonstrated that Cr, alters the expression level of AQP1 and AQP2 in renal tissue which are salutary for detecting the renal damage early. On the other hand, Cr boosted the upregulation of kidney injury molecule-1 (KIM-1) in kidney tissue confirming its disruption. Interestingly, gene expression of KIM-1, AQP1 and AQP2’s in renal membrane correlates well with creatine level, reinforcing their role as sensitive markers of tubular damage and reflect impaired tubular water handling. High exposure produced a severe nephrotoxic profile, distinctly different from controls and far more pronounced than the Cr-Low group.