Abstract
An oxygen-rich atmosphere obligated living organisms to cope with reactive oxygen species (O2−, H2O2, OH·) that were the unavoidable by-products of cellular metabolism. As a redox cofactor Cu was selected as a co-catalyst for numerous biological processes, many involving the utilization of oxygen. Inadequate or excessive intake of Cu can be pathogenic and life-threatening. Mutations to genes that code for Cu-transporting ATPase enzymes are the molecular basis of Wilson and Menkes diseases and more recently Cu has been identified as a preemptory factor in amyloid and prion diseases. This review is dedicated to bringing historical and timely information on Cu transport, metabolism and homeostasis to the attention of those not familiar with this important mineral. Other comprehensive reviews are available to the interested readers.1−4
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