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MHG - Exam I > Lecture 8-Nucleotide Metabolism II (Nakai) > Flashcards

Lecture 8-Nucleotide Metabolism II (Nakai) Flashcards

1
Q

What converts dUTP –> dUMP?

A

dUTPase

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2
Q

What converts dUMP –> dTMP?

A

thymidilate synthase

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3
Q

What are the 2 causes of gout?

A
  • difficulties in excretion of uric acid

- purines being overproduced

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4
Q

ADA deficiency results in _______

A

SCID

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5
Q

HGRTase deficiency results in _____

A

Lesch-Nyhan syndrome

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6
Q

allopurinol

A
  • analog of hypoxanthene that inhibits xanthine oxidase
  • used to treat gout
  • hypoxanthine and xanthine build up from deficient xanthine oxidase activity and can be excreted by the kidneys
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7
Q

azaserine/acivicin

A
  • gln analogs used as chemotherapeutic agents–they would disrupt glutamine amidotransferases ( remember! gln PRPP amidotransferase!)
  • not used as much due to toxic side effects since
  • Gln is involved in: purine biosynthesis, N metablism and Gln (?) is used as a CNS NT
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8
Q

Hydroxyurea

A

ribonucleotide reductase inhibitor

- used as a chemotherapeutic agent and it inhibits DNA synthesis specifically with little effect on RNA synthesis

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9
Q

fluorouracil; what kind of inhibition does it use?

A
  • analog of thymine that’s readily converted to FdUMP which inhibits thymidylate synthase (dUMP –> dTMP)
  • its a SUICIDE INHIBITOR
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10
Q

Methotrexate and trimethorpim

A
  • folate analogs that competitively and directly inhibit dihydrofolate reductase
  • prevent regeneration of THF and therefore the methylating agent (N5,N10 methylene THF)
  • this is used as a cofactor in the reaction with thymidylate synthase
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11
Q

What will ultimately reoxidize ribonucleotide reductase so it itself can oxidize another NTP?

A

NADPH

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12
Q

When dCTP binds the secondary site of ribonucleotide reductase what does it promote to bind?

A

nothing!

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13
Q

When dTTP binds to the secondary site of ribonucleotide reductase what does it promote to bind? What does it inhibit?

A
  • GDP

- dCTP/dCDP; dUDP/dTTP

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14
Q

What is ATP’s effect when it binds the primary site of ribnoucleotide reductase? dATP?

A
  • turns RNR on

- turns RNR off

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15
Q

Why does DNA Pol need equal levels of all nucleotides in the cell?

A
  • it has a low Km and high Vmax
  • increasing one dNTP will cause it to have a higher Km for that nucleotide and the chance that it will be incorrectly incorporated is very high
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16
Q

Why are there differing affinities for each of the nucleotides at the secondary site of RNR?

A

The affinities are based on the levels naturally occurring within the cell and this aims to balance them out.

17
Q

Thymidilate synthase is the target of _______.

A

Many chemotherapies

–REMEMBER: dUMP–>dTMP

18
Q

Thymidilate synthase mediates what kind of reaction? Using what?

A
  • 1 C transfer

- N5, N10 methylene THF

19
Q

What converts dihydrofolate from thymidilate synthase reaction back to N5, N10 methylene THF

A
  • dihydrofolate reductase + NADPH

- Ser hydroxymethyltransferase + PLP + Ser

20
Q

Dihydrofolate reductase is targeted for _____

A

chemotherapeutic agents

21
Q

Catabolism of purines is especially high where?

A
  • liver
22
Q

What is usually the 1st step of nucleotide catabolism?

A
  • dephosphorylation
23
Q

adenosine deaminase

A

deaminates adenosine to inosine

24
Q

Inosine has a _____ base

A

hypoxanthine

25
Q

How do you get uric acid from hypoxanthine?

A
  • hypoxanthine –> xanthine –> uric acid

- each of these reactions use xanthine oxidase

26
Q

What are the only cofactors used in purine catabolism?

A

H2O

27
Q

What does guanine get converted too (i.e., where does it meet up with the AMP degradation)?

A
  • xanthine
28
Q

Why can uric acid build up in joints?

A
  • pKa 5.7 and therefore low solubility in aqueous solution
29
Q

What happens when uric acid builds up in joints?

A
  • WBCs (PMNLs) eat up the crystals
  • release hydrolytic enzymes
  • causes inflammation, pain
30
Q

What is the basic salvaging reaction?

A

adenine + PRPP –> AMP + PPi

- adenosine phosphoribosyl transferase

31
Q

HRGTase mediates what 2 reactions?

A
  • hypoxanthine + PRPP –> IMP + PPi

- guanine + PRPP –> GMP + PPi

32
Q

Where is HRGTase esp important in why?

A
  • neural cells

- dont have the energy to do purine synthesis

33
Q

Why does HRGTase deficiency result in LN syndrome? What is LN characterized by?

A
  • brain is esp dependent on HRGTase because it doesn’t want to use its energy stores on nucleotide synthesis
  • brain forced to use de novo pathway and gets an ATP deficiency
  • Characterized by: - you get an accumulation of PRPP because of the enzyme deficiency
  • high PRPP signals liver to pump out purines at a very high rate
  • high purines = high uric acid

MHG - Exam I (11 decks)

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