Related Experiment Video

Updated: Jul 18, 2026

Application of Genetically Encoded Fluorescent Nitric Oxide (NO•) Probes, the geNOps, for Real-time Imaging of NO• Signals in Single Cells
08:32

Application of Genetically Encoded Fluorescent Nitric Oxide (NO•) Probes, the geNOps, for Real-time Imaging of NO• Signals in Single Cells

Published on: March 16, 2017

Nitric oxide and mitochondria

Guy C Brown1

  • 1Department of Biochemistry, University of Cambridge, Tennis Court Road, Cambridge CB2 1QW, United Kingdom. gcb@mole.bio.cam.ac.uk

Frontiers in Bioscience : a Journal and Virtual Library
|November 28, 2006
PubMed

Insights

Nitric oxide (NO) impacts mitochondria by stimulating biogenesis and inhibiting respiration. While NO can induce cell death through oxidative stress or energy depletion, it also offers protective mechanisms against mitochondrial dysfunction.

Area of Science:

  • Mitochondrial biology
  • Cellular signaling
  • Biochemistry

Background:

  • Nitric oxide (NO) and reactive nitrogen species (RNS) play complex roles in cellular processes.
  • Mitochondria are central to cellular energy production and apoptosis.
  • The interplay between NO/RNS and mitochondria is crucial for cell fate.

Purpose of the Study:

  • To elucidate the multifaceted effects of nitric oxide (NO) on mitochondrial function.
  • To investigate NO's influence on mitochondrial biogenesis, respiration, and cell death pathways.
  • To understand the dual role of NO as both a modulator and potential protector of mitochondria.

Main Methods:

  • Review of existing literature on nitric oxide and mitochondrial interactions.
  • Analysis of NO's effects on mitochondrial respiration, biogenesis, and signaling pathways.
  • Examination of NO's role in inducing or preventing apoptosis and necrosis via mitochondrial mechanisms.

Main Results:

  • NO stimulates mitochondrial biogenesis, partly through cGMP-dependent pathways.
  • NO acutely inhibits cytochrome oxidase and irreversibly affects other respiratory sites via RNS.
  • Mitochondria produce reactive oxygen and nitrogen species influenced by NO.
  • NO can induce apoptosis (oxidative stress) and necrosis (energy depletion).
  • RNS can activate the mitochondrial permeability transition pore, leading to cell death.

Conclusions:

  • Nitric oxide exerts complex, dose-dependent effects on mitochondria.
  • NO can promote mitochondrial biogenesis and respiration under certain conditions.
  • NO signaling can lead to both cell death and cell survival, highlighting its dual role in mitochondrial regulation.

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