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Biomedical subjects

Edward D Harris

Publications and source records attributed to Edward D Harris.

28 records · Page 2Linked to original sources

Parallels and contrasts between iron and copper metabolism.

This paper reviews the Second International Workshop on Iron and Copper Homeostasis, held in Pucón, Chile 10-13 November, 2001. We cover the presentations and papers published (this issue) with the intent to point out parallels, contrasts and cutting edge areas rather than to say something about every paper. Iron and copper metabolism have been intertwined for nearly 150 years and the interrelationship is growing with advances in understanding the role of ceruloplasmin as one example and the probable role of hephaestin as another. The transporter DMT1 (divalent metal transporter 1) clearly plays a major part in iron uptake and trafficking. Emerging evidence suggests that it plays a lesser role in manganese, cadmium and copper transport; but it is still being evaluated there. Yet another interaction may come from the IRE/IRP (Iron Responsive Element/Iron Regulatory Protein) story where a paradigmatic role in iron homeostasis is well established, but interaction with copper is only now emerging. Parallels include the nutrient status of both metals based on their utility for redox reactions as well as their toxicity primarily via reactive oxygen species. The workshop also revealed that alternate splicing of pre-mRNAs for iron and copper related proteins and tissue specific responses are additional similarities. Regulation of gene expression and excretion offered contrasts between the two metals. The workshop also considered a series of continuing and emerging issues.

Animals↗

Basic and clinical aspects of copper.

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.

Adenosine Triphosphatases↗

Cellular transporters for zinc.

Nutritionally essential metals such as zinc are moved into and out of cells by a series of transport proteins or transporters. Their tri-fold purpose is to procure zinc from the environment, to protect cells against zinc toxicity, and maintain ample supplies of zinc for metabolic purposes. Two families of zinc transporters are known: the ZIP family that imports zinc and the ZnT family that functions in releasing zinc or sequestering zinc internally.

Biological Transport↗