Abstract
Background: Reactive oxygen species are endogenously generated as by-products of the mitochondrial electron transport chain, and play important roles in the regulation of cell growth, neurotransmission, and the immune system. In elevated levels however, ROS ultimately lead to oxidation of DNA, proteins, and cell membranes. The resulting oxidative stress underlies the pathogenesis of numerous disease states, including cardiovascular disease, and chemotherapy-induced cardiotoxicity. Despite their widespread pathological importance, there is currently no means of non-invasively detecting elevated ROS levels in humans.
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