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Apoptotic pathways of oxidative damage to renal tubular epithelial cells

Alexei G Basnakian1, Gur P Kaushal, Sudhir V Shah

  • 1University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA.

Antioxidants & Redox Signaling
|February 8, 2003
PubMed

Insights

Reactive oxygen metabolites (ROM) cause kidney cell death in acute renal failure. Preventing ROM production and controlling cell death pathways may offer new treatments for human acute kidney injury.

Area of Science:

  • Nephrology
  • Cell Biology
  • Toxicology

Background:

  • Acute renal failure (ARF) can be induced by toxins (gentamicin, glycerol, cisplatin) or ischemia.
  • These insults lead to reactive oxygen metabolite (ROM) production in renal tubular epithelial cells.
  • ROM generation is a key factor in tubular cell death during ARF.

Purpose of the Study:

  • To investigate the role of ROM in the pathogenesis of ARF.
  • To explore the mechanisms of tubular epithelial cell death.
  • To identify potential therapeutic targets for ARF prevention and treatment.

Main Methods:

  • Induction of toxic and ischemic renal failure models in vivo.
  • Hypoxia/reoxygenation of tubular epithelial cells in vitro.
  • Assessment of reactive oxygen metabolite (ROM) production.
  • Evaluation of caspase and endonuclease activation and cell death.

Main Results:

  • Toxic and ischemic insults trigger significant ROM production.
  • ROM generation directly contributes to tubular epithelial cell death.
  • ROM are responsible for activating caspases and endonucleases.
  • Scavenging ROM prevents caspase/endonuclease activation and cell death.

Conclusions:

  • ROM play a critical role in the cell death pathways of acute renal failure.
  • Inhibiting ROM production is a potential therapeutic strategy.
  • Pharmacological targeting of caspase and endonuclease pathways offers promise for ARF treatment.
  • Combined inhibition of ROM and control of cell death pathways may prevent or treat human ARF.

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