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Antioxidant enhanced spare capacity in cardiomyocytes as a protective response to oxidative stress induced by hypoxia and redox cycling agent
Author(s) -
Legmann Rachel,
melito Julie,
Ferrick David
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.887.8
Subject(s) - oxidative stress , antioxidant , chemistry , hypoxia (environmental) , reactive oxygen species , microbiology and biotechnology , oxidative phosphorylation , mitochondrion , ascorbic acid , glutathione , pharmacology , biophysics , biochemistry , oxygen , biology , organic chemistry , food science , enzyme
Increased reactive oxygen species (ROS) generation underlies many pathologies of the cardiovascular system. Strategies that enhance the cell's ability to cope with oxidative stress are being explored by many labs. The main objective of this work was to analyze the effect of antioxidant on cellular respiration in embryonic rat cardiac cells and their capability to cope with oxidative stress. The cells were adapted to hypoxia in the presence of the antioxidant, ascorbic acid, followed by exposure to the endogenous H 2 O 2 generator redox cycling agent, 2, 3‐dimethyloxy‐ 1, 4‐naphtoquinone (DMNQ). Mitochondrial function was measured in intact cells using an Extracellular Flux (XF) analyzer. The spare respiratory capacity of the cells decreased in a dose dependent manner following DMNQ treatment. Growing the cells in the presence of an antioxidant enhanced spare respiratory capacity and therefore protected from exposure to DMNQ both in hypoxic (Fig 1) and normoxic conditions. In conclusion, the admission of antioxidant to the cardiomyocytes, either in hypoxia or normoxia, enhanced significantly both their maximal respiration and spare respiratory capacity, enabling them to protect the mitochondria within the cell against oxidative damage. Boosting spare capacity should provide a means to counteract its decrease caused by environmental toxins, aging or the acute effects of disease.