Abnormal iron accumulation in human tissues and oxidative damage are emerging issues in the medical field (1,2). The most commonly recognized type of pathological accumulation has been associated with the general appearance of plasma non-transferrin bound iron (NTBI) (3-16) and particularly with a labile iron component that can infiltrate cells in an unregulated manner (17-19). A major consequence of excess iron accumulation is a rise in cellular labile iron (LCI) (4,8,10) that can promote the formation of reactive oxygenspecies (ROS) from physiological oxygenintermediates (ROI), overriding the cellular antioxidant machineries and causing oxidative damage...
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Cabantchik et al. (2013) studied this question.
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