Editing Homeostasis (section)

===Copper regulation===
{{Main |Copper in health#Homeostasis}}
Copper is absorbed, transported, distributed, stored, and excreted in the body according to complex [[homeostatic]] processes which ensure a constant and sufficient supply of the micronutrient while simultaneously avoiding excess levels.<ref>{{Citation |last1=Scheiber |first1=Ivo |title=Copper: Effects of Deficiency and Overload |date=2013 |work=Interrelations between Essential Metal Ions and Human Diseases |pages=359–387 |editor-last=Sigel |editor-first=Astrid |url=https://doi.org/10.1007/978-94-007-7500-8_11 |access-date=2024-08-11 |place=Dordrecht |publisher=Springer Netherlands |language=en |doi=10.1007/978-94-007-7500-8_11 |isbn=978-94-007-7500-8 |last2=Dringen |first2=Ralf |last3=Mercer |first3=Julian F. B. |volume=13 |pmid=24470097 |editor2-last=Sigel |editor2-first=Helmut |editor3-last=Sigel |editor3-first=Roland K.O.}}</ref> If an insufficient amount of copper is ingested for a short period of time, copper stores in the liver will be depleted. Should this depletion continue, a copper health deficiency condition may develop. If too much copper is ingested, an excess condition can result. Both of these conditions, deficiency and excess, can lead to tissue injury and disease. However, due to homeostatic regulation, the human body is capable of balancing a wide range of copper intakes for the needs of healthy individuals.<ref>{{Cite journal |last1=Burkhead |first1=Jason L. |last2=Gogolin Reynolds |first2=Kathryn A. |last3=Abdel-Ghany |first3=Salah E. |last4=Cohu |first4=Christopher M. |last5=Pilon |first5=Marinus |date=June 2009 |title=Copper homeostasis |url=https://nph.onlinelibrary.wiley.com/doi/10.1111/j.1469-8137.2009.02846.x |journal=New Phytologist |language=en |volume=182 |issue=4 |pages=799–816 |doi=10.1111/j.1469-8137.2009.02846.x |pmid=19402880 |bibcode=2009NewPh.182..799B |issn=0028-646X}}</ref>

Many aspects of copper homeostasis are known at the molecular level.<ref>{{Cite journal |last1=Stern |first1=Bonnie Ransom |last2=Solioz |first2=Marc |last3=Krewski |first3=Daniel |last4=Aggett |first4=Peter |last5=Aw |first5=Tar-Ching |last6=Baker |first6=Scott |last7=Crump |first7=Kenny |last8=Dourson |first8=Michael |last9=Haber |first9=Lynne |last10=Hertzberg |first10=Rick |last11=Keen |first11=Carl |last12=Meek |first12=Bette |last13=Rudenko |first13=Larisa |last14=Schoeny |first14=Rita |last15=Slob |first15=Wout |date=2007-04-03 |title=Copper and Human Health: Biochemistry, Genetics, and Strategies for Modeling Dose-response Relationships |url=http://www.tandfonline.com/doi/abs/10.1080/10937400600755911 |journal=Journal of Toxicology and Environmental Health, Part B |language=en |volume=10 |issue=3 |pages=157–222 |doi=10.1080/10937400600755911 |pmid=17454552 |bibcode=2007JTEHB..10..157S |issn=1093-7404}}</ref> Copper's essentiality is due to its ability to act as an electron donor or acceptor as its oxidation state fluxes between Cu<sup>1+</sup> ([[cuprous]]) and Cu<sup>2+</sup> ([[cupric]]). As a component of about a dozen [[cuproenzyme]]s, copper is involved in key [[redox]] (i.e., oxidation-reduction) reactions in essential metabolic processes such as [[mitochondria]]l respiration, synthesis of [[melanin]], and cross-linking of [[collagen]].<ref>{{Cite book |last1=Dameron |first1=C. |title=Cooper |last2=Howe |first2=Paul |date=1998 |publisher=World health organization |others=Programme international sur la sécurité des substances chimiques |isbn=978-92-4-157200-2 |series=Environmental health criteria |location=Geneva}}</ref> Copper is an integral part of the antioxidant enzyme copper-zinc superoxide dismutase, and has a role in iron homeostasis as a cofactor in ceruloplasmin.{{cn|date=March 2025}}