Cited by 721Cardiac Ischemia and ReperfusionCell death mechanisms and regulationMitochondrial Function and Pathology

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Reactive Oxygen Species Released from Mitochondria during Brief Hypoxia Induce Preconditioning in Cardiomyocytes

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Vanden Hoek, Terry L., Becker, Lance B., Shao, Zuohui, Li, Changqing, Schumacker, Paul T.·1998·Journal of Biological Chemistry

DOI 10.1074/jbc.273.29.18092

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Abstract

Reactive oxygen species (ROS) have been proposed to participate in the induction of cardiac preconditioning. However, their source and mechanism of induction are unclear. We tested whether brief hypoxia induces preconditioning by augmenting mitochondrial generation of ROS in chick cardiomyocytes. Cells were preconditioned with 10 min of hypoxia, followed by 1 h of simulated ischemia and 3 h of reperfusion. Preconditioning decreased cell death from 47 +/- 3% to 14 +/- 2%. Return of contraction was observed in 3/3 preconditioned versus 0/6 non-preconditioned experiments. During induction, ROS oxidation of the probe dichlorofluorescin (sensitive to H2O2) increased approximately 2.5-fold. As a substitute for hypoxia, the addition of H2O2 (15 micromol/liter) during normoxia also induced preconditioning-like protection. Conversely, the ROS signal during hypoxia was attenuated with the thiol reductant 2-mercaptopropionyl glycine, the cytosolic Cu,Zn-superoxide dismutase inhibitor diethyldithiocarbamic acid, and the anion channel inhibitor 4,4'-diisothiocyanato-stilbene-2,2'-disulfonate, all of which also abrogated protection. ROS generation during hypoxia was attenuated by myxothiazol, but not by diphenyleneiodonium or the nitric-oxide synthase inhibitor L-nitroarginine. We conclude that hypoxia increases mitochondrial superoxide generation which initiates preconditioning protection. Furthermore, mitochondrial anion channels and cytosolic dismutation to H2O2 may be important steps for oxidant induction of hypoxic preconditioning.

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Authors: Vanden Hoek, T. L., Becker, L. B., Shao, Z., Li, C., & Schumacker, P. T.
Affiliations: University of Chicago (US)
Corresponding author: Schumacker, Paul T.
ORCID: Becker, Lance B.
Li, Changqing
Schumacker, Paul T.
Venue: Journal of Biological Chemistry
Publisher: Elsevier BV
Published: 1998-07
Volume: 273
Issue: 29
Pages: 18092-18098
ISSN: 0021-9258 (ISSN-L)
DOI: 10.1074/jbc.273.29.18092
OpenAlex: W2145047965
Cited by: 721
References: 40
Citations by year: 2026: 5 · 2025: 5 · 2024: 7 · 2023: 4 · 2022: 4 · 2021: 15 · 2020: 10 · 2019: 8 · 2018: 11 · 2017: 8 · 2016: 29 · 2015: 16 · 2014: 31 · 2013: 33 · 2012: 26
FWCI: 20.19
Type: journal article
Language: en
Open access: hybrid
doi.org
Licence: cc-by
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
creativecommons.org/licenses/by/4.0/ (vor, 8147 d)
Locations: Journal of Biological Chemistry (publishedVersion, cc-by)
PubMed (publishedVersion)
Funders: National Institutes of Health (5k08hl003779-02, HL35440)
National Heart, Lung, and Blood Institute (HL 32646, HL-03779, R01HL035440, HL35440)
Topics: Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Ischemia and Reperfusion
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
Keywords: reactive oxygen species, mitochondrial superoxide, hypoxia, cardioprotection, preconditioning, cardiomyocytes, ischemia-reperfusion injury, hydrogen peroxide, superoxide dismutase, DIDS, myxothiazol, nitric oxide synthase, cell death
MeSH terms: Animals, Cells, Cultured, Chick Embryo, Cytosol, Ditiocarb, Enzyme Inhibitors, Hydrogen Peroxide, Tiopronin, Methacrylates, Mitochondria, Heart, Myocardial Contraction, Onium Compounds, Superoxide Dismutase, Thiazoles, Cell Hypoxia, Cell Death, Reactive Oxygen Species, Nitric Oxide Synthase, Ischemic Preconditioning, Myocardial

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Reactive Oxygen Species Released from Mitochondria during Brief Hypoxia Induce Preconditioning in Cardiomyocytes

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