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Cited by 177Cardiac Ischemia and ReperfusionMitochondrial Function and PathologyAutophagy in Disease and Therapy

The DOI matches its Crossref record; 29 of the 29 references it cites were found in a registry or an index.

Mitochondrial Generation of Oxygen Radicals During Reoxygenation of Ischemic Tissues

Turrens, Julio F., Beconi, Martha, Barilla, Jean, Chavez, Ulises B., McCord, Joe M.·1991·Free Radical Research Communications
DOI 10.3109/10715769109145847
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Abstract

Ischemia and reperfusion causes severe mitochondrial damage, including swelling and deposits of hydroxyapatite crystals in the mitochondrial matrix. These crystals are indicative of a massive influx of Ca2+ into the mitochondrial matrix occurring during reoxygenation. We have observed that mitochondria isolated from rat hearts after 90 minutes of anoxia followed by reoxygenation, show a specific inhibition in the electron transport chain between NADH dehydrogenase and ubiquinone in addition to becoming uncoupled (unable to generate ATP). This inhibition is associated with an increased H2O2 formation at the NADH dehydrogenase level in the presence of NADH dependent substrates. Control rat mitochondria exposed for 15 minutes to high Ca2+ (200 nmol/mg protein) also become uncoupled and electron transport inhibited between NADH dehydrogenase and ubiquinone, a lesion similar to that observed in post-ischemic mitochondria. This Ca(2+)-dependent effect is time dependent and may be partially prevented by albumin, suggesting that it may be due to phospholipase A2 activation, releasing fatty acids, leading to both inhibition of electron transport and uncoupling. Addition of arachidonic or linoleic acids to control rat heart mitochondria, inhibits electron transport between Complex I and III. These results are consistent with the following hypothesis: during ischemia, the intracellular energy content drops severely, affecting the cytoplasic concentration of ions such as Na+ and Ca2+. Upon reoxygenation, the mitochondrion is the only organelle capable of eliminating the excess cytoplasmic Ca2+ through an electrogenic process requiring oxygen (the low ATP concentration makes other ATP-dependent Ca2+ transport systems non-operational).(ABSTRACT TRUNCATED AT 250 WORDS)

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Crossref · 10.3109/10715769109145847

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Research works printed but not linked: 3

  1. Downey J., 1986, Circulation., 74, 372
  2. Eddy L. J., 1987, American Journal of Physiology., 253, H709
  3. Wikstrom M., 1984, Bioenergetics., 49

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Metadata

Authors
Turrens, J. F., Beconi, M., Barilla, J., Chavez, U. B., & McCord, J. M.
Affiliations
University of South Alabama (US)
ORCID
McCord, Joe M.
Venue
Free Radical Research Communications
Publisher
Informa UK Limited
Published
1991-01
Volume
13
Issue
1
Pages
681-689
ISSN
8755-0199 (ISSN-L)
DOI
10.3109/10715769109145847
OpenAlex
W2113144597
Cited by
177
References
29
Citations by year
2026: 2 · 2024: 1 · 2023: 1 · 2021: 6 · 2020: 1 · 2019: 1 · 2018: 3 · 2017: 7 · 2016: 3 · 2015: 6 · 2014: 3 · 2013: 4 · 2012: 6
FWCI
10.60
Type
journal article
Language
en
Open access
closed
Locations
  • Free Radical Research Communications (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • American Heart Association
  • Universidad de Buenos Aires
Topics
  • Health Sciences › Medicine › Cardiology and Cardiovascular 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 › Cell Biology › Autophagy in Disease and Therapy
Keywords
ischemia-reperfusion injury, reoxygenation, hydroxyapatite crystals, mitochondrial calcium overload, electron transport inhibition, NADH dehydrogenase, coenzyme Q10, mitochondrial uncoupling, hydrogen peroxide, phospholipase A2, arachidonic acid, linoleic acid, albumin, heart mitochondria
MeSH terms
Animals, Fatty Acids, Free Radicals, Hydrogen Peroxide, Mitochondria, Heart, Oxygen, Oxygen Consumption, Rabbits, Myocardial Reperfusion Injury, Rats, In Vitro Techniques

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