MitoQ administration prevents endotoxin-induced cardiac dysfunction

American Journal of Physiology - Regulatory Integrative and Comparative Physiology

Volumn 297, Issue 4, 2009, Pages

  Supinski, G S ^a,c   Murphy, M P ^b   Callahan, L A ^a  

^a UNIVERSITY OF KENTUCKY   (United States)

^b UNIVERSITY OF CAMBRIDGE   (United Kingdom)

^c UNIVERSITY OF KENTUCKY   (United States)

Author keywords

Caspase; Proteolysis

Indexed keywords

10 (6 UBIQUINONYL)DECYLTRIPHENYLPHOSPHONIUM; ADENOSINE TRIPHOSPHATE; ANTIOXIDANT; CASPASE 3; CASPASE 9; ENDOTOXIN; SODIUM CHLORIDE; UNCLASSIFIED DRUG;

ANIMAL EXPERIMENT; ANIMAL TISSUE; ARTICLE; CONTROLLED STUDY; DIASTOLIC BLOOD PRESSURE; ENZYME ACTIVATION; HEART DISEASE; HEART MITOCHONDRION; HEART MUSCLE CONTRACTILITY; HEART VENTRICLE PRESSURE; MOUSE; NONHUMAN; POLAROGRAPHY; PRIORITY JOURNAL; RAT; RESPIRATION CONTROL; SYSTOLIC BLOOD PRESSURE;

ADENOSINE TRIPHOSPHATE; ANIMALS; ANTIOXIDANTS; CASPASE 3; CASPASE 9; CELL RESPIRATION; DISEASE MODELS, ANIMAL; DRUG ADMINISTRATION SCHEDULE; ENDOTOXEMIA; ENZYME ACTIVATION; HEART DISEASES; MICE; MITOCHONDRIA, HEART; MYOCARDIAL CONTRACTION; MYOCARDIUM; ORGANOPHOSPHORUS COMPOUNDS; PROTEIN CARBONYLATION; RATS; TUMOR NECROSIS FACTOR-ALPHA; UBIQUINONE; VENTRICULAR FUNCTION, LEFT; VENTRICULAR PRESSURE;

EID: 70349627246     PISSN: 03636119     EISSN: 15221490     Source Type: Journal    
DOI: 10.1152/ajpregu.90902.2008     Document Type: Article

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