Xanthine oxidase produces hydrogen peroxide which contributes to reperfusion injury of ischemic, isolated, perfused rat hearts.
Open accessAbstract
Three lines of investigation indicated that hydrogen peroxide (H2O2) from xanthine oxidase (XO) contributes to cardiac dysfunction during reperfusion after ischemia. First, addition of dimethylthiourea (DMTU), a highly permeant O2 metabolite scavenger (but not urea) simultaneously with reperfusion improved recovery of ventricular function as assessed by ventricular developed pressure (DP), contractility (+dP/dt), and relaxation rate (-dP/dt) in isolated Krebs-Henseleit-perfused rat hearts subjected to global normothermic ischemia. Second, hearts from rats fed tungsten or treated with allopurinol had negligible XO activities (less than 0.5 mU/g wet myocardium compared with greater than 6.0 mU/g in control hearts) and increased ventricular function after ischemia and reperfusion. Third, myocardial H2O2-dependent inactivation of catalase occurred after reperfusion following ischemia, but not after ischemia without reperfusion or perfusion without ischemia. In contrast, myocardial catalase did not decrease during reperfusion of ischemic hearts treated with DMTU, tungsten, or allopurinol.
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Various oxygenases, oxidases and peroxidases can directly produce reduced dioxygen forms in vivo, with H2O2 from xanthine oxidase especially implicated in ischaemia/reperfusion injury.
“Various other oxygenases, oxidases and peroxidases can also lead directly to the production of such 'reduced' forms of dioxygen in vivo (e.g. [46-48]), with H2O2 from xanthine oxidase being especially implicated in ischaemia/reperfusion injury (e.g. [47,49-54]).”
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References 20 · Cited by 137
Research works printed but not linked: 1
- Doring, H. J., and H. Dehvert. 1986. The isolated perfused warm-blooded heart according to Langendorff. In Biological Measure- ment Techniques. Vol. 5. 1-107.
- Authors
- Brown, J. M., Terada, L. S., Grosso, M. A., Whitmann, G. J., Velasco, S. E., Patt, A., Harken, A. H., & Repine, J. E.
- Affiliations
- University of Colorado Health (US)
- University of Colorado Denver (US)
- Venue
- Journal of Clinical Investigation
- Published
- 1988-04-01
- Volume
- 81
- Issue
- 4
- Pages
- 1297-1301
- ISSN
- 0021-9738 (ISSN-L)
- PMC
- PMC329662
- OpenAlex
- W2058919056
- Cited by
- 137
- References
- 20
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 1 · 2023: 1 · 2022: 2 · 2021: 2 · 2019: 1 · 2018: 1 · 2017: 2 · 2016: 1 · 2014: 2 · 2013: 6 · 2012: 2
- FWCI
- 8.15
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Clinical Investigation (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- American Heart Association
- National Institutes of Health (1p01am035098-01, 2r01hl028182-04, 1r01hl035378-01)
- National Heart, Lung, and Blood Institute (R01 HL-35378, R01 HL-28182)
- Topics
- Health Sciences › Medicine › Pathology and Forensic Medicine › Cardiac Ischemia and Reperfusion
- Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Keywords
- xanthine oxidase, hydrogen peroxide, ischemia-reperfusion injury, myocardial ischemia, dimethylthiourea, catalase inactivation, allopurinol, tungsten, ventricular function, oxidative stress, isolated perfused heart
- MeSH terms
- Allopurinol, Amitrole, Catalase, Coronary Disease, Hydrogen Peroxide, Myocardium, Perfusion, Thiourea, Tungsten, Urea, Xanthine Oxidase, In Vitro Techniques
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