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Carvedilol inhibits the mitochondrial permeability transition by an antioxidant mechanism

Paulo J Oliveira1, Telma Esteves, Anabela P Rolo

  • 1Center for Neurosciences and Cellular Biology of Coimbra, Department of Zoology, University of Coimbra, Coimbra, Portugal. pauloliv@ci.uc.pt

Cardiovascular Toxicology
|March 23, 2004
PubMed

Insights

Carvedilol

Area of Science:

  • Biochemistry
  • Cardiology
  • Pharmacology

Background:

  • Carvedilol, a beta-adrenergic antagonist, possesses antioxidant properties.
  • Previous studies indicated carvedilol inhibits mitochondrial permeability transition (MPT).

Purpose of the Study:

  • To investigate if carvedilol's inhibition of MPT is solely due to its antioxidant effects.
  • To determine the role of antioxidant properties in carvedilol's MPT inhibition.

Main Methods:

  • Utilized three distinct MPT inducers: calcium plus phosphate, calcium plus t-butylhydroperoxide, and calcium plus carboxyatractyloside.
  • Assessed MPT-associated events and thiol group oxidation.
  • Compared carvedilol's effects with cyclosporin-A, a known MPT inhibitor.

Main Results:

  • Carvedilol inhibited mitochondrial swelling and thiol oxidation with calcium plus phosphate and calcium plus t-butylhydroperoxide.
  • Carvedilol did not inhibit MPT induced by calcium plus carboxyatractyloside.
  • Cyclosporin-A provided full protection against calcium plus carboxyatractyloside-induced MPT.

Conclusions:

  • Carvedilol's MPT inhibitory effect is dependent on the induction of oxidative stress.
  • The antioxidant properties of carvedilol are critical for its MPT-inhibiting action.
  • Carvedilol may be beneficial in cardiac conditions marked by increased oxidative stress.

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