Flashcards in Copper Deck (26)
Is copper supplementation necessary?
No. Trace minerals generally do not need supplementation.
Cuprous and Cupric Copper
+1 reduced (absorbable)
Use chaperones so they're not unnecessarily used within the body.
What can reduce copper or keep it reduced?
Only occurs when copper is in excess.
DMT (divalent metal transporter)
Regulated by iron status. Can transport iron as well.
50% absorbed via DMT
Ctr1 (copper transporter 1)
Regulated based on copper status.
Amino acid carriers
Minor copper transporter.
Which vitamins compete with copper absorption?
Antacids reduce absorption because it lowers pH.
Zinc regulates metallothionine.
Copper binds better than zinc.
If excess zinc, Cu can't leave enterocyte because it's bound to metallothionine
Stored for 2-3 days.
Protein that helps copper leave enterocyte.
Binds to albumin
Binds to ceruloplasmin. Oxidizes iron. Antioxidant.
90% of copper is bound to ceruloplasmin.
Copper deficiency can lead to anemia because most copper is bound to ceruloplasmin which oxidizes iron.
Iron binds to transferrin to be transported to bone marrow to make hemoglobin.
Copper is chaperoned on proteins to prevent oxidation reactions.
Glutathione, Atox1, Cox17
Liver has complete control of copper.
Storage: Copper stored in metallothionine.
Transport: Ceruloplasmin is produced in liver, binds to copper, released into systemic blood.
Excretion: ATP7B puts copper in bile to be excreted.
Genetic defect not polymorphism.
Cannot make protein ATP7A. Cannot absorb copper.
Children die in infancy.
Copper treatment does not expand lifespan.
Cannot excrete copper.
Copper toxicity in muscles and liver. Iris.
Chelation. Zinc. Low copper diet.
RDA: .9 mg
Best: liver, organ meats
Typical: nuts, cashews, potato, whole grains
Increases when Cu status is low
Serum copper (static)
Serum ceruloplasmin activity (functional)
Coenzyme. Enzymes that need a reduced metal.
Ceruloplasmin: antioxidant, oxidizes iron (ferroxidase)
Cytochrome c Oxidase: used in ETC to transport e-
At risk if using antacids and zinc supplements (40mg/d).
Hypochromic anemia: most Cu is bound to ceruloplasmin which transfers Fe to transferrin to bone marrow to make blood
Leukopenia: impaired immune function
Hypopigmentation: depigmentation of hair
Zinc toxicity makes copper deficiency because metallothionine is upregulated and Cu binds to it.
Iron toxicity makes Cu deficiency because DMT1 is down regulated which absorbs 50% of Cu
Nausea, vomiting, diarrhea, kidney and liver damage.
Copper toxicity. Ring around the eye.
Cytochrome c Oxidase
Last step in ETC.
Contain 3 Cu atoms on 2 subunits:
The first subunit contains 2 Cu atoms that receive e from cytochrome c.
Transfer to second subunit to reduce oxygen.
Iron: low Cu that leads to low ceruloplasmin which traps iron in the cells. Secondary iron deficiency anemia.
Molybdenum: enhances copper excretion.
Within the hepatocyte, transfers Cu to bile to be excreted.