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Oxidative stress mediates renal endothelial cell damage in trichloroethylene-sensitized mice

Bodong Li1, Haibo Xie1,2, Xian Wang1

  • 1Department of Occupational Health and Environmental Health, School of Public Health, Anhui Medical University, China.

The Journal of Toxicological Sciences
|May 10, 2019
PubMed

Insights

Trichloroethylene (TCE) exposure causes immune kidney damage linked to oxidative stress in renal endothelial cells. The antioxidant Tempol partially mitigated this damage, suggesting oxidative stress is a key factor in TCE-induced kidney injury.

Area of Science:

  • Nephrology
  • Toxicology
  • Immunology

Background:

  • Trichloroethylene (TCE) is a common environmental pollutant linked to kidney damage.
  • Immune-mediated kidney injury is a significant health concern.
  • The role of oxidative stress in TCE-induced renal pathology requires further elucidation.

Purpose of the Study:

  • To investigate the association between renal endothelial cell injury and oxidative stress in TCE-induced immune kidney damage.
  • To explore the protective effects of the antioxidant Tempol in a mouse model of TCE sensitization.
  • To analyze key markers of kidney function, oxidative stress, and endothelial activation.

Main Methods:

  • A mouse model of skin sensitization to TCE was established.
  • Kidney function was assessed via blood urea nitrogen (BUN) and creatinine (Cre) levels, and histological examination.
  • Oxidative stress markers (nitric oxide, nitric oxide synthase, superoxide dismutase, malondialdehyde) and endothelial adhesion molecules (eNOS, E-selectin, VCAM-1, ICAM-1) were quantified.

Main Results:

  • TCE sensitization increased BUN and Cre levels, accompanied by renal tubule damage.
  • Oxidative stress markers showed an imbalance: decreased NO, NOS, SOD, eNOS and increased MDA.
  • Elevated levels of adhesion molecules (E-selectin, VCAM-1, ICAM-1) were observed in TCE-exposed mice.
  • Tempol treatment attenuated the TCE-induced changes in oxidative stress and adhesion molecule expression.

Conclusions:

  • TCE-induced immune kidney injury in mice is significantly associated with oxidative stress in renal endothelial cells.
  • The antioxidant Tempol demonstrates a protective effect by mitigating oxidative stress and endothelial activation.
  • These findings highlight the critical role of oxidative stress in the pathogenesis of TCE nephrotoxicity.
Keywords:
Adhesion moleculesEndothelial cellsKidneyOxidative stressTrichloroethylene

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