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IHN BIOCHEMISTRY FINAL > FINAL: copper > Flashcards

FINAL: copper Flashcards

1
Q

acute ingestion of copper leads to

A

epigastric pain
anorexia
vomiting
diarrhea

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2
Q

food source copper

A

oysters
crab
liver
legumes
nuts

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3
Q

biological form of copper

A

Cu2+

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4
Q

brush border transporters of copper

A
  1. Ctr1: transports Cu1+ (reduced, cuprous)
  2. DCT1: transports Cu1+, Cu2+, Fe2+
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5
Q

key chaperone for Cu

A

Atox1

transports Cu from Ctr1 to ATP7A in trans-Golgi network
ATP7A then expels Cu into circulation

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6
Q

main IC Cu transporter

A

ATP7A

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7
Q

role of ATP7A, what is it dependent on

A

role: extrude Cu into portal blood
ATP7A is dependent on ATP

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8
Q

__% Cu absorption

A

12-60% Cu absorption

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9
Q

Cu absorption __ with increased intake

A

Cu absorption decreases with increased intake

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10
Q

Cu absorption

A
  1. Cu bound to food broken down to Cu2+
  2. reductases (Steap2 + DcytB) turn Cu2+ to Cu1+
  3. Cu1+ enters via Ctr1 (DCT1 may also help)
  4. Cu1+ bound by chaperone (Atox1) which takes Cu1+ to ATP7A
  5. Cu1+ leaves cell –> proteins bind in blood (mainly albumin)
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11
Q

storage and distribution of Cu
normal Cu intake =
excess Cu intake =

A

storage and distribution of Cu
normal Cu intake = ceruloplasmin formed
excess Cu intake = excreted in feces

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12
Q

enhancers of Cu absorption

A
  1. some amino acids
  2. decreased pH
  3. glutathione
  4. acids
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13
Q

inhbitors of Cu absorption

A
  1. increased pH
  2. phytic acid
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14
Q

Cu path to bile

A
  1. Cu enters via Ctr1
  2. Atox1 takes Cu to TGN to make ceruloplasmin (CP)
  3. CP brings Cu to extrahepatic tissue
  4. with excess Cu, ATP7B picks up Cu
  5. ATP7B brings Cu to bile
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15
Q

__% Cu lost in feces

A

>95% Cu lost in feces

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16
Q

__ controls secretion of Cu to bile

A

ATP7B controls secretion of Cu to bile

17
Q

Cu dependent proteins (5)

A
  1. ceruloplasmin (hephaestin, DcytB)
  2. superoxide dismutase (SOD)
  3. dopamine monooxigenase (dopamine –> norepinephrine)
  4. lysyl oxidase (stablizes connective tissue: collagen)
  5. cytochrome c oxidase (mitochondrial electron transport: energy!)
18
Q

superoxide dismutase is essential for __ protection

A

superoxide dismutase is essential for free radical protection

19
Q

__ or __ SOD in cytosol
__ SOD in mitochondria

A

Cu or Zn SOD in cytosol
Mn SOD in mitochondria

20
Q

what does SOD NEED to work

A

Cu, Mn, AND Zn

21
Q

decreased SOD in tissues =

A

more labile to damage by ROS

22
Q

assessing Cu, best to use

A

multiple markers

23
Q

4 options for assessing Cu

A
  1. serum, plasma, RBC (common, but variable)
  2. plasma CP (good for early manifestation)
  3. Cu-dependent enzymes (SOD, sensitive to long-term deficiency)
  4. urinary excretion (falls once deficiency is already established
24
Q

is primary Cu deficiency common?

A

no, it is rare

25
Q

at risk populations for primary Cu deficiency

A
  1. excess Zn consumption (MT)
  2. chronic kidney failure
  3. patients on dialysis
  4. malabsorption (GI resection, Crohn’s)
  5. genetic alterations that affect abspt and transport (Wilson’s disease, Menkes disease)
26
Q

Cu deficiency symptoms

A
  1. hypochromic microcytic anemia (impaired CP mediated oxidation of iron)
  2. leukopenia
  3. hypopigmentation of hair and skin
  4. alterations in connective tissue
  5. neurological abnormalities (in fetal and neonatal deprivation)
27
Q

Wilson’s disease

A
  1. defect in ATP7B (Cu storage disease)
  2. Cu can’t get to bile, stays in cell
  3. damaged mitochondria: autophagy of mito –> lysosomes
28
Q

Menkes disease

A

more severe
1. X-linked neurodegenerative disease (ATP7A mutation)
2. low serum copper = accumulation in intestinal cells and other cells
3. death by 3 years of life

IHN BIOCHEMISTRY FINAL (15 decks)

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