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MCBM > Nucleotide Metabolism > Flashcards

Nucleotide Metabolism Flashcards

1
Q

What are critical functions of nucleotides

A
  1. storage and flow of genetic info: key structural comp on DNA and RNA
  2. storage and source of energy: energy rich phosphodiester bonds in ATP & GTP
  3. Component of key cofactors: NAD, FAD, coenzyme A, S- adensoylmethionine
  4. form activated intermediates: UDP glucose in glycogen synthesis, CDP= diacylglycerol in phospholipid synthesis
  5. Metabolic regulators: cAMP, cGMP are cellular second messengers.
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2
Q

What are three principal components nucleotides have

A
  1. nitrogenous base
  2. pentose sugar
  3. one/more phosphate groups
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3
Q

what are the two types of nitrogenous bases

A
  1. pyrimidine (little structure)
  2. purine (big structure)
    (nitrogen and carbon in ring)
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4
Q

What include the pyrimidines

A
  1. Cytosine
  2. Thymine
  3. Uracil
    “cut the pyramid”
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5
Q

what are the purines

A
  1. adenine
  2. guanine
    “Pure As Gold”
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6
Q

what are the pentose sugars

A
  1. ribose (OH is on the bottom)

2. deoxyribose (just H on the bottom)

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7
Q

What are nucleosides formed by

A

attachment of nitrogenous base to sugar. Attachment is always to C-1 on sugar, N-9 of purine, ad N-1 of pyrimidine

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8
Q

How are nucleotides formed

A

by attachment of phosphate to sugar in nucleoside. Phosphates are never attached to base. Phosphates can be added to sugar.

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9
Q

adenine + sugar =

when it has all three component =

A

adenose; adenylate

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10
Q

What are two types of pathways of nucleotides

A
  1. De novo (from new): synthesis from metabolic precursors (aa, ribose - 5- phosphate, CO2, NH3) Energy expensive!
  2. salvage: recycle free bases and nucleosides released from nucleic acid breakdown. Energy economical! Do this a lot with purines!
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11
Q

which methyl group is primarily used

A

tetrahydrafolate

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12
Q

What

A

Build oratate first then attach it.

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13
Q

What are the precursors for purines and pyrimidines

A

inosine 5- monophosphate and orotidine 5’ monophosphate

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14
Q

Synthesis of common nucleotides DOES NOT proceed via their free bases: precursor is always coupled to:

A

ribose

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15
Q

5 phosphoribosyl-1 pyrophosphate (PRPP) is a key activated ____ intermediate which activates C1 on ribose. It is a key substrate in both purine and pyrimidine synthesis

A

sugar

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16
Q

The purine ring precursor ____ (a nitrogenous base) is synthesized stepwise directly on the ribose C-1

A

hypoxanthine

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17
Q

The pyrimidine ring precursor ____ is synthesized stepwise THEN attached to the ribose C-1.

A

orotate

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18
Q

where do you get ribose 5 - phosphate from

A

PPP; pentose phosphate pathway

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19
Q

How are purines synthesized

A
  1. assemble 5 member ring on C-1 of PRPP

2. complete 6 member ring

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20
Q

what aa are used to make purines

A
  1. 2 glutamine
  2. 1 glycine
  3. 1 aspartate
  4. 2 formate from tetrahydroflate
  5. 1 CO2- from bicarbonate
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21
Q

The nucleotide is called ____. The base is called ____

A

inosinate (IMP) -the base, phosphate and sugar; hypoxanthine.

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22
Q

You can convert inosinate to

A

Can convert it to AMP or GMP by adding nitrogen groups to two spots

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23
Q

How do you make the 5 membered ring

A
  1. Directly attach the N group of glutamine
  2. Add 2 glycine (C–C-N)
  3. Add 2 C via formate
  4. Add C02 from bicarbonate
  5. Add N from aspartate and then close the ring
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24
Q

what is the committed step

A

adding first N group on PRPP via glutamine PRPP amidotransferase

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25
Q

what is glutamine PRPP admidotransferase inhibited by

A

azaerine, acivian. This is a good target for chemotherapy

26
Q

How many ATP are made from making inosinate

A

7 ATP

27
Q

AMP uses ___as the N donor. GMP uses _____ as N donor.

A

aspartate; glutamine

28
Q

Inosinate in ____

A

tRNA

29
Q

How is purine regulated

A

almost exclusively via feed back inhibition of

  1. PRPP synthetase by end products
  2. committed step by end products
  3. branches by each end product
  4. reciprocal use of GTP and ATP in AMP, GMP pathways
30
Q

How do you make pyrimidines

A

glutamine + bicarbonate to make carbamoyl phosphate
then add aspartate to make orotate and hook it up to PRPP. (making ring first and then adding it to the sugar) The first ring we’re making is UMP.
* this can happen in cytosol

31
Q

How many ATPs does it take to make pyrimidine

A

2

32
Q

what makes a pyrimidine

A
  1. glutamine
  2. 1 aspartate
  3. 1 CO2
  4. 2 ATP
33
Q

where does pyramdine synthesis get N from

A

directly from glutamine

34
Q

what is the committed step in making pyrymidines. what is it feedback inhibited by?

A

aspartate transcarbamoylase. Inhibited by CTP

35
Q

Common nucleotides already have ____added. PRPP is key to both purine and pyrmidine synthesis.

A

sugar

36
Q

What happens after you have UMP?

A

UTP –> animate it to CTP (by using glutamine as a N group donor)

37
Q

Nucleoside monophosphate kinase uses ATP as source of phosphate and:

A

we can swap phosphate groups among all of our bases.

38
Q

what enzyme gives you deoxyribonucleotides

A

ribonucleotide reductase; makes internal disulfide bond. Donates H and e- from enzyme to form disulfide bond.

39
Q

Process of re reducing requires

A

glutathione (GSH) and NADPH

40
Q

How can thymidine (dTMP) can be synthesized

A

From deoxy precursors:

  1. CDP –>deoxy CDP –>deaminated dUTP –> dUMP–>dTMP
  2. UDP–>dUDP–>dUTP –>dUMP–> dTMP
41
Q

what enzyme is precursor for thymidine synthesis

A

dUMP

42
Q

what enzyme converts dUMP to dTMP

A

thymidylate synthase

43
Q

what is thymidylate synthase a good target for

A

chemotherapy; if you cant make T to go into DNA; DNA synthesis will slow down

44
Q

what is a good agent for chemotherapy or what inhibits thymidylate synthase

A

flourouracil

45
Q

what is difference bet dTMP and dUMP

A

methyl group; it

46
Q

what donates a methyl group to make TMP

A

N10 tetrahydrofolate; it has to be regenerated.

47
Q

what converts dihydrofolate to tetrahydrofolate

A

dihydrofolate reductase

48
Q

what is dihydrofolate reducatase a good target for

A

chemotheraupetic agents and some classes of antibiotics.

49
Q

what is dihydrofolate reductase inhibited by

A

methotrexate, aminopterin, & trimethoprim

50
Q

what are breakdown products of pyrimidine

A

free ammonia (goes to urea) and succinate (goes to TCA cycle); so we mainly say breakdown product is UREA

51
Q

what is breakdown product of purines

A

URATE; a lot recycled in salvage pathway

52
Q

what enzyme is used to make purine, adenine via the salvage pathway

A

adenosine phosphoribosyltransferase (APRT)

53
Q

what enzyme is used to make purine, guanine

A

HGPRT

54
Q

What is the nucleotide catabolism for purines like

A

takes N group back off and forms inosine–> take sugar off and maky hypothanxine –> xanthine–> urate

55
Q

What does SCID stand for

A

severe combined immuno deficient; complete lack of immune system; there is a deficiency in adenosine deaminada (ADA). T and B lymphocytes do not dev properly

56
Q

what converts hypoxanthine to xanthine

A

xanthine oxidase; generating peroxide in our body.

57
Q

what converts adenosine to inosine

A

adenosine deaminase

58
Q

too much uric acid:

A

starts to precipitate and can cause gout. Therefore We inhibit enzymes: adenosime deaminase, & xanthine oxidase with inhibitor drugs

59
Q

whats gout

A

heritable leading to elev uric acid in blood; can cause damage to kidneys

60
Q

which mechanisms can lead to elevated serum urate:

A
  1. Hyperactive PRPP synthetase:excess PRPP accelerates purine biosynthesis
  2. Partial lack of HGPRT: reduced salvage pathway; leads to excess PRPP, and accelerated purine biosynthesis
61
Q

how do you treat gout

A

allopurinol; enters salvage pathway and forms ribonucleotide; uses up PRPP which reduces purine biosynthesis. Other drugs include probenecid and febuxostat

62
Q

what is Lesch-Nyhan Syndrome

A

complete genetic lack of HGPRT; X linked recessive (males) manifests early; mental retardation, poor coordination, self destructive, self mutilating, gout

MCBM (59 decks)

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