Cellular redox state protects acetaldehyde-induced alteration in cardiomyocyte function by modifying Ca2+ release from sarcoplasmic reticulum

American Journal of Physiology - Heart and Circulatory Physiology

Volumn 294, Issue 1, 2008, Pages

  Oba, Toshiharu ^a   Maeno, Yoshitaka ^a   Nagao, Masataka ^a   Sakuma, Nagahiko ^a   Murayama, Takashi ^b  

^a NAGOYA CITY UNIVERSITY GRADUATE SCHOOL OF MEDICAL SCIENCES   (Japan)

^b JUNTENDO UNIVERSITY SCHOOL OF MEDICINE   (Japan)

Author keywords

Ca2+ transient; Intracellular glutathione level; Intracellular redox state; Single ryanodine receptor type 2 channel activity

Indexed keywords

ACETALDEHYDE; CAFFEINE; CALCIUM; FK 506 BINDING PROTEIN; RYANODINE RECEPTOR 2;

ANIMAL TISSUE; ARTICLE; CELL PROTECTION; CONTROLLED STUDY; DOSE RESPONSE; DRUG EFFECT; HEART MUSCLE CELL; HEART VENTRICLE; NONHUMAN; OXIDATION REDUCTION POTENTIAL; OXIDATION REDUCTION STATE; PRIORITY JOURNAL; RAT; SARCOPLASMIC RETICULUM;

ACETALDEHYDE; ANIMALS; CALCIUM SIGNALING; CELLS, CULTURED; CYTOPLASM; DOSE-RESPONSE RELATIONSHIP, DRUG; GLUTATHIONE; ION CHANNEL GATING; MALE; MALEATES; MEMBRANE POTENTIALS; MICROSCOPY, CONFOCAL; MYOCYTES, CARDIAC; OXIDATION-REDUCTION; RABBITS; RATS; RATS, WISTAR; RYANODINE RECEPTOR CALCIUM RELEASE CHANNEL; SARCOPLASMIC RETICULUM; TIME FACTORS;

EID: 38149121331     PISSN: 03636135     EISSN: 15221539     Source Type: Journal    
DOI: 10.1152/ajpheart.00520.2007     Document Type: Article

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