Abstract: Abstract: Cardiac contractile dysfunction and arrhythmic genesis result from disturbed intracellular Na+ and Ca2+ handling in condition of oxidation stress. Stress-induced intracellular signaling regulation mechanisms in which many activated stress kinases, such cAMP-dependent protein kinase A, protein kinase C and Ca/calmodulin-dependent protein kinase Ⅱ as classical pathways, are known involved. However, it is becoming increasingly evidence that reactive oxygen species may directly oxidize these kinases, Na+ and Ca2+ channel protein and transports, leading to alter the intracellular Na+ and Ca2+ accumulation, to trigger arrhythmias.

Key words: Oxidation stress, reactive oxygen species, Na+ and Ca2+ handling, redox system, arrhythmias