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Biochemistry 3 > Class 8: AA Metabolism/Urea > Flashcards

Class 8: AA Metabolism/Urea Flashcards

1
Q

Fate of AA,

Amino group and carbon skeleton:

A

Amino group is converted to urea and excreted

Carbon skeleton enters TCA and by gluconeogenesis can become glucose

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2
Q

Proteolytic enzyme in stomach that operates at low pH:

A

Pepsin

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3
Q

Proteins are marked for death with _________ covalently bound to lysine.

A

Ubiquitin linked by isopeptide bond

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4
Q

Steps in ubiquitination:

A
  1. Ubiquitin undergoes ATP hydrolysis.
  2. Activated w/ E1.
  3. Transferred to E2 conjugating enzyme.
  4. E2 acts as escort to E3 ligase
  5. E3 ligase enzyme is platform for protein and active E2 can meet and interact. E2 enzyme(s) can apply 4 ubiquitin molecules(polyubiquitin chain) to target protein substrate.
  6. Protein release from E3 and sent to proteosome
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5
Q

What dictates a proteins lifetime?

A

The N-terminus

short life: 2/3-30 min
Long: >20 hours

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6
Q

What is likely cause of protein accumulation

A

Defective E3

Common accumulation Dz: in Alzheimer’s, huntington’s, ALS

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7
Q

The executioner

4 subunits of 2 types (alpha beta-catalytic)

Fragments peptide making up protein and release ubiquitin from regulatory unit for reuse.

A

Proteosome

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8
Q

Fate of AA from proteolysis after going through proteosome:

A
  1. Left intact for biosynthesis
  2. Carbon skeletons for cellular respiration
  3. amino groups to be disposed of by urea cycle
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9
Q

Steps in the big picture:

A
  1. Aminotransferase
  2. Glutamate dehydrogenase
  3. urea cycle
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10
Q

Shuffling amino groups:

  1. alpha amino group transferred to an alpha ketoacid
  2. coupled reactions
  3. Enzymes called aminotransferases
A

Transamination

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11
Q

Reversible rxn’s

Directionality dictated by [ ]

Driven forward by removal of NH4

A

Transferase reactions.

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12
Q

Req’s pyridoxyl-5’-phosphate (PLP) - derivative of vitamin B-6

Derivatives of liver function tests:

A

Aminotransferases

Alanine transaminase (ALT)
Aspartate transaminase(AST)
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13
Q

How can NH4 go into the blood since it cant be sent directly? (Toxic)

A

Removed as GLN and ala

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14
Q

NH4 to caramoyl phosphate, irreversible?

This happens in mito.

A

Yes, b/c it hydrolyzes 2 ATP

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15
Q

How can urea leave the mito.

A

It must be converted to carbamoyl phosphate then to citrulline.

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16
Q

What connects urea cycle and cellular respiration?

A

Argininosuccinate

17
Q

What happens to carbon skeletons?

A

Transformed into glucose or a TCA cycle intermediate

18
Q

The 2 AA’s that only become acetyl CoA or acetoacetate (ketogenic)

A

Leucine and lysine

19
Q

The 5 AA’s that can be ketogenic or glucogenic:

A 
Isoleucine
Tryptophan
Phenylalanine
Tyrosine
Threonine
20
Q

The 13 AA’s that can only become glycogenic intermediates:

A 
Val
His
Arg
Asn
Gln
Glu 
Asp
Ala
Met
Gly
Pro
Ser
Cys
-----pyruvate or TCA cycle intermediates (OAA, alpha-ketoglutarate, succinyl CoA, fumarate)
21
Q

6 AA Metabolic fates:

A 
Pyruvate
OAA
Alpha-ketoglutarate
Succinyl CoA 
Acetyl CoA/acetoacetate
Fumarate
22
Q

Pyruvate as metabolic fate:

A

Entry point for the 3 carbon AAs

  • Alanine
  • serine
  • cysteine

Indirectly can become pyruvate:

  • Tryptophan
  • glycine
  • threonine
23
Q

Alanine becomes pyruvate by reacting w/ alpha-ketoglutarate.

Glutamate is formed w/ pyruvate.

A

Alanine transaminase (ALT)

24
Q

OAA as metabolic fate:

A

Entry point for:

  • Asp
  • Asn
25
Q

Aspartate combines w/ alpha-ketoglutarate to form OAA and glutamate

A

Aspartate aminotransferase (AST)

26
Q

Alpha-ketoglutarate as metabolic fate:

A

Entry point for several 5-carbon AAs by means of glutamate formation

Glutamine
Proline
Arginine 
Histidine
Glutamate
27
Q

Succinylcholine CoA as metabolic fate:

A

Entry point for several NONPOLAR AAs. This pathway is used for oxidation of FAs also

  • met
  • Val
  • isoleucine
28
Q

Acetyl Coa/ acetoacetate as metabolic fate:

29
Q

Fumarate/acetoacetate as metabolic fate:

A

Phenylalanine/tyrosine both break down to form fumarate AND acetoacetate

30
Q

Acetoacetate as metabolic fate:

A

Tryptophan

31
Q

Pyruvate: (6)

A 
Cys
Trp
Ala
Thr
Gly
Ser
32
Q

Succinyl CoA: (4)

A

Met
Thr
Val
Ile

33
Q

Alpha-ketoglutarate: (5)

A 
Gln
His
Arg
Pro
---> glutamate
34
Q

Fumarate (2):

35
Q

OAA (2):

36
Q

Screened at birth

Rapid decline

Regulated w/ diet only. No Rx available

A

IEM

Inborn error of metabolism

37
Q

Deficient dehydrogenase complex

Build-up of BRANCHED chain AA (Ile, Val, Leu)

Anorexia, anemia, vomiting, dehydration, lethargy, hypotonia, seizures, ketoacidosis, pancreatitis, rapid neurological decline, coma, cerebral edema

A

Maple syrup urine Disease

MSUD

38
Q

1:10,000 births

Absent/deficient phenylalanine hydroxylase

Untreated yields severe MR

“Musty” urine, seizures, hypopigmentation

Controlled dietarily

A

PKU

Phenylketonuria

Biochemistry 3 (13 decks)

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