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Nicorandil Affects Mitochondrial Respiratory Chain Function by Increasing Complex III Activity and ROS Production in

E Sánchez-Duarte1, C Cortés-Rojo2, L A Sánchez-Briones2

  • 1Departamento de Ciencias Aplicadas al Trabajo, Universidad de Guanajuato Campus León, Eugenio Garza Sada 572, Lomas del Campestre Sección 2, 37150, León, Guanajuato, Mexico.

The Journal of Membrane Biology
|July 5, 2020
PubMed
Summary

Adenosine triphosphate-dependent potassium channel openers like nicorandil may not activate mitochondrial KATP channels. Instead, nicorandil increases mitochondrial reactive oxygen species production, suggesting non-specific effects.

Keywords:
MitochondriaNicorandilReactive oxygen speciesSkeletal musclemitoKATP channel

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Area of Science:

  • Mitochondrial physiology
  • Cardiovascular research
  • Skeletal muscle metabolism

Background:

  • Adenosine triphosphate-dependent potassium channels (KATP) openers protect skeletal muscle via mitochondrial KATP (mitoKATP) channels.
  • Modulators of mitoKATP channels may have off-target effects on isolated mitochondria.

Purpose of the Study:

  • Investigate if nicorandil, a KATP opener, exerts protective effects through non-specific mitochondrial actions.
  • Determine the impact of nicorandil on mitochondrial respiration, electron transport chain (ETC) activity, and reactive oxygen species (ROS) production.

Main Methods:

  • Isolated chicken muscle mitochondria were used.
  • Mitochondrial respiration measured polarographically.
  • ETC complex activities (I-IV) assessed spectrophotometrically.
  • ROS levels and lipid peroxidation quantified via flow cytometry and thiobarbituric acid assay, respectively.

Main Results:

  • Both nicorandil and 5-hydroxydecanoate (5-HD) reduced mitochondrial respiration.
  • Nicorandil enhanced Complex III activity and inhibited Complex IV activity; 5-HD antagonized Complex III effects.
  • Nicorandil increased ROS production, an effect reversed by 5-HD or MPG.
  • Lipid peroxidation remained unaffected by the tested drugs.

Conclusions:

  • Nicorandil increases mitochondrial ROS production, likely from Complex III.
  • This occurs due to partial Complex IV inhibition, favoring a more reduced state of electron carriers.
  • Findings suggest nicorandil and potentially other mitoKATP openers may not act primarily through mitoKATP channel activation.