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Additionally, ROS promote arrhythmias by disrupting potassium channel function, inducing endoplasmic reticulum and mitochondrial dysfunction, and causing electrical conduction disturbances between endothelial cells and cardiomyocytes [329]

This self-perpetuating loop drains the cells glutathione reserves, as the antioxidant is rapidly consumed in a desperate attempt to neutralize the surging ROS

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