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Ischemic preconditioning enhances fatty acid-dependent mitochondrial uncoupling.

Raquel S Carreira1, Sayuri Miyamoto, Paolo Di Mascio

  • 1Departamento de Bioquímica, Instituto de Química, Universidade de São Paulo, Av. Prof. Lineu Prestes 748, Cidade Universitária, 05508-900 São Paulo, São Paulo, Brazil.

Journal of Bioenergetics and Biomembranes
|October 6, 2007
PubMed
Summary

Ischemic preconditioning (IP) enhances fatty acid transport and mild mitochondrial uncoupling by activating the adenine nucleotide translocator. This process involves thiol oxidation, affecting ATP production and mitochondrial function.

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Area of Science:

  • Biochemistry
  • Mitochondrial Physiology
  • Cardiovascular Research

Background:

  • Ischemic preconditioning (IP) is a phenomenon where brief periods of ischemia protect tissues from subsequent longer ischemic insults.
  • The precise molecular mechanisms underlying IP remain incompletely understood, particularly concerning mitochondrial function.
  • Fatty acids (FA) play a critical role in cellular energy metabolism and can influence mitochondrial respiration and oxidative phosphorylation.

Purpose of the Study:

  • To investigate whether ischemic preconditioning (IP) alters the uncoupling between mitochondrial respiration and oxidative phosphorylation in a fatty acid (FA)-dependent manner.
  • To elucidate the molecular pathways involved in IP-induced changes in mitochondrial function related to FA metabolism.

Main Methods:

  • Mitochondrial membrane potential measurements in the presence and absence of fatty acids.
  • Assessment of fatty acid levels and mitochondrial membrane integrity.
  • Experiments utilizing fatty acid hydroperoxides, guanosine triphosphate (GTP), thiol reductants, and atractyloside (an adenine nucleotide translocator inhibitor).

Main Results:

  • IP did not affect mitochondrial membrane integrity or overall FA levels.
  • IP enhanced mitochondrial membrane potential decreases in the presence of FA, in an ATP-sensitive manner.
  • The effects of FA hydroperoxides were similar in control and preconditioned mitochondria, and GTP did not abolish the IP effect, ruling out uncoupling proteins.
  • Thiol reductants and atractyloside eliminated the differential response to FA between control and preconditioned mitochondria.

Conclusions:

  • Ischemic preconditioning (IP) induces thiol oxidation and activates the adenine nucleotide translocator.
  • This activation enhances fatty acid transport into mitochondria.
  • The enhanced FA transport leads to mild mitochondrial uncoupling, impacting cellular energy production.