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• W2012171863 startingPage "313" @default.
• W2012171863 abstract "Iron and copper are essential nutrients, excesses or deficiencies of which cause impaired cellular functions and eventually cell death. The metabolic fates of copper and iron are intimately related. Systemic copper deficiency generates cellular iron deficiency, which in humans results in diminished work capacity, reduced intellectual capacity, diminished growth, alterations in bone mineralization, and diminished immune response. Copper is required for the function of over 30 proteins, including superoxide dismutase, ceruloplasmin, lysyl oxidase, cytochrome c oxidase, tyrosinase and dopamine-beta-hydroxylase. Iron is similarly required in numerous essential proteins, such as the heme-containing proteins, electron transport chain and microsomal electron transport proteins, and iron-sulfur proteins and enzymes such as ribonucleotide reductase, prolyl hydroxylase phenylalanine hydroxylase, tyrosine hydroxylase and aconitase. The essentiality of iron and copper resides in their capacity to participate in one-electron exchange reactions. However, the same property that makes them essential also generates free radicals that can be seriously deleterious to cells. Thus, these seemingly paradoxical properties of iron and copper demand a concerted regulation of cellular copper and iron levels. Here we review the most salient characteristics of their homeostasis." @default.
• W2012171863 created "2016-06-24" @default.
• W2012171863 creator A5001975069 @default.
• W2012171863 creator A5011854092 @default.
• W2012171863 date "2005-08-01" @default.
• W2012171863 modified "2023-10-14" @default.
• W2012171863 title "Iron and copper metabolism" @default.
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• W2012171863 doi "https://doi.org/10.1016/j.mam.2005.07.010" @default.
• W2012171863 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/16112186" @default.
• W2012171863 hasPublicationYear "2005" @default.
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