Cited by 73Cardiac Ischemia and ReperfusionMitochondrial Function and PathologyCell death mechanisms and regulation

Ischemic preconditioning inhibits mitochondrial respiration, increases H2O2release, and enhances K+transport

da Silva, Mirian M., Sartori, Adriano, Belisle, Eduardo, Kowaltowski, Alicia J.·2003·American Journal of Physiology-Heart and Circulatory Physiology

Abstract

Ischemic preconditioning, or the protective effect of short ischemic episodes on a longer, potentially injurious, ischemic period, is prevented by antagonists of mitochondrial ATP-sensitive K+channels (mitoK ATP) and involves changes in mitochondrial energy metabolism and reactive oxygen release after ischemia. However, the effects of ischemic preconditioning itself on mitochondria are still poorly understood. We determined the effects of ischemic preconditioning on isolated heart mitochondria and found that two brief (5 min) ischemic episodes are sufficient to induce a small but significant decrease (∼25%) in mitochondrial NADH-supported respiration. Preconditioning also increased mitochondrial H 2 O 2 release, an effect related to respiratory inhibition, because it is not observed in the presence of succinate plus rotenone and can be mimicked by chemically inhibiting complex I in the presence of NADH-linked substrates. In addition, preconditioned mitochondria presented more substantial ATP-sensitive K+transport, indicative of higher mitoK ATP activity. Thus we directly demonstrate that preconditioning leads to mitochondrial respiratory inhibition in the presence of NADH-linked substrates, increased reactive oxygen release, and activation of mitoK ATP.

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Crossref · 10.1152/ajpheart.00955.2002

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57 of 57 references verified0 citation errors · 0 not checkable

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Authors
da Silva, M. M., Sartori, A., Belisle, E., & Kowaltowski, A. J.
Affiliations
  • Departamento de Bioquímica, Instituto de Química, Universidade de São Paulo, São Paulo SP 05508-900, Brazil
  • Universidade de São Paulo (BR)
Venue
American Journal of Physiology-Heart and Circulatory Physiology
Published
2003-07
Volume
285
Issue
1
Pages
H154-H162
ISSN
  • 0363-6135 (ISSN-L)
  • 1522-1539
OpenAlex
W2112944877
Cited by
73
References
57
Citations by year
2022: 2 · 2021: 3 · 2018: 3 · 2017: 1 · 2016: 3 · 2015: 1 · 2014: 4 · 2013: 7 · 2012: 4
FWCI
5.03
Type
journal article
Language
en
Open access
closed
Locations
  • American Journal of Physiology-Heart and Circulatory Physiology (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Pathology and Forensic Medicine › Cardiac Ischemia and Reperfusion
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
Keywords
ischemic preconditioning, mitochondrial respiration, hydrogen peroxide release, mitochondrial ATP-sensitive potassium channel, potassium transport, respiratory inhibition, mitochondrial complex I inhibition, reactive oxygen species, myocardial ischemia
MeSH terms
Adenosine Triphosphate, Animals, Biological Transport, Active, Cell Membrane, Hydrogen Peroxide, Male, Membrane Potentials, Mitochondria, Heart, Mitochondrial Swelling, Myocardium, NADP, Oxygen Consumption, Potassium, Rats, Sprague-Dawley, Reactive Oxygen Species, Ischemic Preconditioning, Rats, In Vitro Techniques

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