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Assessment of Mitochondrial Functions and Cell Viability in Renal Cells Overexpressing Protein Kinase C Isozymes
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Mitochondrial NOS upregulation during renal I/R causes apoptosis in a peroxynitrite-dependent manner

J L Viñas1, A Sola, G Hotter

  • 1Department of Experimental Pathology, Instituto de Investigaciones Biomédicas, IIBB-CSIC, IDIBAPS, Barcelona, Spain.

Kidney International
|March 25, 2006
PubMed

Insights

Mitochondrial nitric oxide synthase (mNOS) upregulation promotes kidney apoptosis during ischemia-reperfusion injury. Increased nitric oxide leads to peroxynitrite formation, cytochrome c release, and cell death.

Area of Science:

  • Mitochondrial biochemistry
  • Renal pathophysiology
  • Cellular apoptosis

Background:

  • Mitochondrial nitric oxide synthase (mNOS) produces nitric oxide in various models.
  • The role of mNOS in renal ischemia-reperfusion (I/R) injury and apoptosis remains unclear.

Purpose of the Study:

  • To investigate the role of mNOS in promoting apoptosis during rat kidney I/R injury.
  • To explore the direct implications of mNOS in isolated kidney mitochondria under hypoxia/reoxygenation.

Main Methods:

  • Analysis of neuronal NOS (nNOS) in rat kidney mitochondria during I/R.
  • Measurement of nitric oxide production and peroxynitrite formation.
  • Assessment of cytochrome c release and apoptosis induction.

Main Results:

  • Neuronal NOS is upregulated in the inner mitochondrial membrane during renal I/R.
  • Increased nitric oxide production correlates with upregulation.
  • This leads to intramitochondrial peroxynitrite generation, cytochrome c release, and apoptosis.

Conclusions:

  • mNOS plays a significant role in promoting apoptosis during renal I/R injury.
  • Nitric oxide produced by mNOS contributes to kidney damage via peroxynitrite formation and cytochrome c release.

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