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Renal tight junction proteins are decreased in cisplatin-induced nephrotoxicity in rats

Joyce Trujillo1, Eduardo Molina-Jijón, Omar Noel Medina-Campos

  • 1Department of Biology, Faculty of Chemistry, National Autonomous University of Mexico (UNAM) , University City, Mexico D.F. , Mexico .

Toxicology Mechanisms and Methods
|July 24, 2014
PubMed
Abstract

Insights

Cisplatin (CP) causes kidney damage by altering tight junction proteins, occludin and claudin-2, linked to oxidative stress. This study investigates these CP-induced nephrotoxicity effects in rats.

Area of Science:

  • Nephrology
  • Biochemistry
  • Cell Biology

Background:

  • Cisplatin (CP) is a widely used chemotherapy agent.
  • CP is known to induce significant nephrotoxicity and oxidative stress.
  • The impact of CP on renal tight junction (TJ) proteins remains largely uncharacterized.

Purpose of the Study:

  • To investigate the alterations in the expression and localization of key TJ proteins (occludin, claudin-2, claudin-5, ZO-1) in rat kidneys following CP administration.
  • To correlate these changes with markers of nephrotoxicity, oxidative stress, and nitrosative stress.

Main Methods:

  • Male Wistar rats were administered a single dose of CP (7.5 mg/kg) or saline.
  • Renal function was assessed using plasma and urinary biomarkers.
  • Histopathology, oxidative/nitrosative stress markers, and TJ protein levels (occludin, claudin-2, claudin-5, ZO-1) were evaluated via Western blot.

Main Results:

  • CP induced significant nephrotoxicity, evidenced by histological damage and altered kidney injury biomarkers.
  • Oxidative and nitrosative stress markers were elevated in CP-treated rats.
  • A significant decrease in the renal expression of occludin and claudin-2 was observed in the CP group.

Conclusions:

  • CP-induced nephrotoxicity in rats is associated with significant alterations in TJ protein expression, specifically a decrease in occludin and claudin-2.
  • These changes in the proximal tubule are linked to the observed oxidative and nitrosative stress.
  • Understanding these mechanisms may offer targets for mitigating CP-induced kidney damage.
Keywords:
Cisplatinclaudinsnitrotyrosineoccludinoxidative stresstight junction proteins

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