The molecular basis of copper and iron interactions.
Level 5 - mechanism / opinion, no new human data
Narrative review of mechanistic and animal data with no new clinical data.
PubMed 15831128 · doi:10.1079/pns2004386
What was done
This paper reviews the molecular mechanisms mediating the interaction between copper and iron metabolism, focusing on the roles of multi-copper ferroxidases (caeruloplasmin and hephaestin) and intestinal iron transporters (DMT1 and IREG1).
What was found
The abstract reports no numerical data. It describes that caeruloplasmin is required for iron mobilization from storage tissues, and copper deficiency impairs its ferroxidase activity, leading to anemia responsive to copper rather than iron. Hephaestin works with IREG1 to permit iron efflux from enterocytes, a process disrupted in sex-linked anemic mice bearing a truncated hephaestin mutation. Additionally, DMT1 functions as a physiologically relevant copper transporter and copper regulates both DMT1 and IREG1 expression.
Why it matters
The review clarifies the molecular pathways by which copper deficiency impairs iron homeostasis, explaining why some nutritional anemias require copper supplementation to resolve.
Limits
The abstract reports no quantitative measurements, statistical comparisons, or sample sizes. The underlying evidence relies on mechanistic reasoning and animal models such as the sla mouse rather than controlled clinical trials.
Cited by
- supports Copper helps regulate and protect iron in the body.