Iron not only functions as a cofactor for various enzymes, but it is also a source of potentially cytotoxic molecules produced through interactions with certain reactive intermediates of oxygen (ROI) and nitrogen (RNI). Protection from such iron-mediated damage results in large part from homeostatic mechanisms that regulate the sequestration of iron. Perturbations in iron homeostasis can result in an array of adverse cellular manifestations including oxidative and nitrosative stress, enhanced production of free radicals, macromolecular damage, and cell death. This brief review focuses on some of the potentially adverse reactions of iron with ROI and RNI.
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