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Flashcards in Copper Deck (26)
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1

Is copper supplementation necessary?

No. Trace minerals generally do not need supplementation.

2

Cuprous and Cupric Copper

+1 reduced (absorbable)
+2 oxidized

Use chaperones so they're not unnecessarily used within the body.

3

What can reduce copper or keep it reduced?

Amino acids
Organic acids
Vitamin C
Cytochrome B

4

Passive diffusion

Only occurs when copper is in excess.

5

DMT (divalent metal transporter)

Active transporter.

Regulated by iron status. Can transport iron as well.

50% absorbed via DMT

6

Ctr1 (copper transporter 1)

Regulated based on copper status.

50-80% absorption

7

Amino acid carriers

Minor copper transporter.

8

Which vitamins compete with copper absorption?

Zinc
Iron
Calcium
Phytates

Antacids reduce absorption because it lowers pH.

9

Metallothionine

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.

10

ATP7A

Protein that helps copper leave enterocyte.
Active transport.

11

Portal blood
Systemic blood

Binds to albumin

Binds to ceruloplasmin. Oxidizes iron. Antioxidant.

90% of copper is bound to ceruloplasmin.

12

Anemia

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.

13

Chaperones

Copper is chaperoned on proteins to prevent oxidation reactions.

Glutathione, Atox1, Cox17

14

Liver has complete control of copper.
Storage
Transport
Excretion


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.

15

Menke's Disease

Genetic defect not polymorphism.

Cannot make protein ATP7A. Cannot absorb copper.

Children die in infancy.

Copper treatment does not expand lifespan.

16

Wilson's Disease

Cannot excrete copper.
Copper toxicity in muscles and liver. Iris.

Chelation. Zinc. Low copper diet.

17

Sources

RDA: .9 mg

Best: liver, organ meats

Typical: nuts, cashews, potato, whole grains

Bioavailability 50-80%
Increases when Cu status is low



18

Biochemical Assessment

Serum copper (static)

Serum ceruloplasmin activity (functional)

19

Functions

Coenzyme. Enzymes that need a reduced metal.

Ceruloplasmin: antioxidant, oxidizes iron (ferroxidase)

Cytochrome c Oxidase: used in ETC to transport e-

20

Deficiency

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

21

Toxicity

10 mg/day

Nausea, vomiting, diarrhea, kidney and liver damage.

22

Kayser-Fleischer Ring

Wilson's Disease

Copper toxicity. Ring around the eye.

23

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.

Creates ATP.

24

Nutrient interactions

Iron: low Cu that leads to low ceruloplasmin which traps iron in the cells. Secondary iron deficiency anemia.

Molybdenum: enhances copper excretion.

25

ATP7B

Within the hepatocyte, transfers Cu to bile to be excreted.

26

Ceruloplasmin

Synthesized in liver.

90% of copper bound in systemic blood

Functional measure of copper status.

Oxidizes iron so it can get on to transferrin to make blood.

Antioxidant.