Transient exposure to hydrogen peroxide causes an increase in mitochondria-derived superoxide as a result of sustained alteration in L-type Ca2+ channel function in the absence of apoptosis in ventricular myocytes

Circulation Research

Volumn 100, Issue 7, 2007, Pages 1036-1044

  Viola, Helena M ^b   Arthur, Peter G ^b   Hool, Livia C ^a  

^a UNIVERSITY OF WESTERN AUSTRALIA   (Australia)

^b NONE

Author keywords

Hydrogen peroxide; L type Ca2+ channel; Mitochondria

Indexed keywords

CALCIUM CHANNEL L TYPE; CALCIUM ION; CARBONYL CYANIDE 4 (TRIFLUOROMETHOXY)PHENYLHYDRAZONE; CASPASE 3; CATALASE; HYDROETHIDINE; HYDROGEN PEROXIDE; ISOPRENALINE; MYXOTHIAZOL; NISOLDIPINE; SUPEROXIDE;

ANIMAL CELL; APOPTOSIS; ARTICLE; BETA ADRENERGIC STIMULATION; CALCIUM CELL LEVEL; CALCIUM TRANSPORT; CELL DEATH; CONTROLLED STUDY; CYTOPATHOLOGY; HEART MITOCHONDRION; HEART VENTRICLE; MEMBRANE CHANNEL; MUSCLE CELL; NONHUMAN; OXIDATIVE STRESS; PRIORITY JOURNAL; RAT; SIGNAL TRANSDUCTION;

ANIMALS; APOPTOSIS; CALCIUM; CALCIUM CHANNELS, L-TYPE; ELECTRIC CONDUCTIVITY; ETHIDIUM; GUINEA PIGS; HEART VENTRICLES; HYDROGEN PEROXIDE; INTRACELLULAR MEMBRANES; MITOCHONDRIA, HEART; MYOCARDIAL CONTRACTION; MYOCYTES, CARDIAC; OXIDANTS; PATCH-CLAMP TECHNIQUES; SUPEROXIDES; TIME FACTORS;

EID: 34247146483     PISSN: 00097330     EISSN: None     Source Type: Journal    
DOI: 10.1161/01.RES.0000263010.19273.48     Document Type: Article

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