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Copper (Cu) is an essential element required as a structural component of numerous metalloenzymes, however, it poses distinct challenges when establishing regulatory guidelines because both dietary deficit, as well as excess, can produce adverse health consequences. Cu is able to change oxidation states between Cu(I) and Cu(II), thereby acting as an electron donor or recipient in biological systems. Excess dysregulated Cu may promote oxidative stress in vivo, contributing to pathology in a range of diseases, such as atherosclerosis and neurodegeneration.