Journal article
Hydrogen peroxide cytotoxicity in cultured cardiac myocytes is iron dependent
The American journal of physiology, Vol.266(1 Pt 2), pp.H121-H127
01/1994
DOI: 10.1152/ajpheart.1994.266.1.h121
PMID: 8304492
Abstract
Because of its potential importance in injury during myocardial ischemia and reperfusion, we assessed mechanisms of hydrogen peroxide (H2O2) cytotoxicity in cultured chick embryo cardiac myocytes. Injury was quantitated by release of lactate dehydrogenase (LDH) or 51Cr, both of which correlated with loss of cell viability assessed by trypan blue exclusion. The iron chelator deferoxamine (0.25-2 mM), but not equimolar iron-loaded deferoxamine, markedly reduced LDH and 51Cr release. Injury was also prevented or attenuated by the diffusible reactive oxygen metabolite scavengers dimethylthiourea (10-20 mM) and N-(2-mercaptopropionyl)-glycine (20 mM). The hydroxyl radical scavenger, dimethyl sulfoxide (200-400 mM), also reduced injury. Other scavengers that probably remained extracellular, superoxide dismutase and mannitol, were ineffective. Thus, with exposure of cardiac myocytes to H2O2, cytotoxicity requires reactions catalyzed by intracellular iron.
Details
- Title: Subtitle
- Hydrogen peroxide cytotoxicity in cultured cardiac myocytes is iron dependent
- Creators
- Richard M Byler - University of Colorado HealthNancy A Sherman - University of Colorado HealthJuliann S Wallner - University of Colorado HealthLawrence D Horwitz - University of Colorado Health
- Resource Type
- Journal article
- Publication Details
- The American journal of physiology, Vol.266(1 Pt 2), pp.H121-H127
- DOI
- 10.1152/ajpheart.1994.266.1.h121
- PMID
- 8304492
- NLM abbreviation
- Am J Physiol
- ISSN
- 0002-9513
- eISSN
- 2163-5773
- Grant note
- HL-48177 / NHLBI NIH HHS
- Language
- English
- Date published
- 01/1994
- Academic Unit
- Cardiovascular Medicine; Internal Medicine
- Record Identifier
- 9984656599002771
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