Mitochondrial electron transport can become a significant source of oxidative injury in cardiomyocytes

Journal of Molecular and Cellular Cardiology

Volumn 29, Issue 9, 1997, Pages 2441-2450

  Vanden Hoek, Terry L ^a   Shao, Zuohui ^a   Li, Changqing ^a   Schumacker, Paul T ^a   Becker, Lance B ^a  

^a UNIVERSITY OF CHICAGO   (United States)

Author keywords

Antimycin; Cardiomyocytes; Cell survival; Chemical hypoxia; Contractile function; Cyanide; Electron transport inhibition; Reactive oxygen species; Rotenone

Indexed keywords

1,10 PHENANTHROLINE; ANTIOXIDANT; CITRININ; CYANIDE; FLUORESCENT DYE; OXYGEN; ROTENONE; TIOPRONIN; XANTHINE OXIDASE;

ANIMAL CELL; ARTICLE; CELL SURVIVAL; CELL VIABILITY; CHICK EMBRYO; CONTROLLED STUDY; ELECTRON TRANSPORT; EMBRYO; HEART MUSCLE CELL; HEART MUSCLE CONTRACTILITY; HEART MUSCLE ISCHEMIA; HEART MUSCLE REPERFUSION; MITOCHONDRION; NEUTROPHIL; NONHUMAN; OXIDATION; OXIDATION REDUCTION REACTION; PRIORITY JOURNAL; RESPIRATORY CHAIN;

ANIMALIA;

EID: 0031239721     PISSN: 00222828     EISSN: None     Source Type: Journal    
DOI: 10.1006/jmcc.1997.0481     Document Type: Article

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