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Biochem BLOCK 3 > Nucleotide Metabolism > Flashcards

Nucleotide Metabolism Flashcards

1
Q

Nucleotides functions

A
  • structural component of DNA and RNA
  • carriers of activated intermediates (UDP-glucose formation)
  • secondary messengers in signal transduction (cAMP, cGMP)
  • energy currency of the cell (ATP)
  • regulators of many pathways
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2
Q

Nucleotide structural components of coenzymes

A
  • CoA
  • NAD+
  • FAD
  • NADP+
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3
Q

Main structural features of nucleotides

A
  • Nitrogenous base

- sugar (can have phosphate associated)

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4
Q

Types of nitrogenous bases

A
  • purines

- pyrimidines

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5
Q

Purines

A
  • nitrogenous base
  • adenine and guanine
  • dicyclic
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6
Q

Pyrimidines

A
  • nitrogenous base
  • cytosine, thiamine (DNA), uracil (RNA
  • unicyclic
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7
Q

Sugar of a nucleotide

A
  • ribose in RNA

- deoxyribose in DNA (missing O)

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8
Q

What links the 2nd and 3rd phosphate on a nucleoside triphosphate (ATP)?

A

Anhydride bonds, high energy bonds driving many biochemical reactions
-this is why we can use them as energy source

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9
Q

Nucleoside

A

Nitrogenous base + sugar (no phosphate)

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10
Q

Nucleotide

A

-nucleoside + 1-3 phosphate groups

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11
Q

Where is the ribose 5-phosphate from in purine synthesis

A

HMP shunt

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12
Q

Purine synthesis

A
  • dicyclic so they are bigger and more complicated

- we are essentially building base on a sugar molecule

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13
Q

Step 1 of purine nucleotide synthesis

A

-PRPP synthetase catalyzes the formation of the activated pentose

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14
Q

PRPP synthetase

A
  • in step 1 of purine synthesis

- catalyzes the formation of the activates pentose

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15
Q

PRPP activator

A

Inorganic phosphate

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16
Q

PRPP inhibitor

A

Purine ribonucleotides

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17
Q

Where is the pyrophosphate attached in purine synthesis?

A

1’ carbon, which is where the nitrogenous base will be attached

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18
Q

PUrine nucleotide synthesis default

A

Production of ribonucleotides

-if deoxyribonucleotides are needed, further steps will be taken

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19
Q

Is the rate limiting step the first step of purine synthesis?

A

No

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20
Q

Rate limiting step of purine synthesis

A
  • catalyze by PRPP amidotransferase

- committed step

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21
Q

After PRPP amidotransferase catalyzes purine synthesis…

A

The following steps are basically just modifying your base to get your purine
-amino acids become part of the nitrogenous bases

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22
Q

Folate

A

Required for purine synthsis, required for subsequent steps as a carbon donor

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23
Q

What form does folate need to be in to be activated?

A

THF

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24
Q

Dihydrofolate reductase

A

Required to make THF, the form in which folate is used

  • have to have this enzyme to continue pathway.
  • obtained from diet
  • bacteria synthesize there own
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25
Q

PRPP amidotransferase inhibited by

A

Purine nucleotides (end products)

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26
Q

PRP amidotransferase reductase activated by

A

PRPP (substrate)

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27
Q

IMP can be utilized as…

A

AMP and GMP

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28
Q

What is the rate limiting and committed step in purine synthesis catalyzes by?

A

PRPP amidotransferase

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29
Q

6-Mercaptopurine

A
  • purine analog
  • acts like IMP, GMP, and AMP
  • inhibits the PRPP amidotransferase
  • cancer treatment
  • can be misincorporated into the synthesis of purines and script the structure
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30
Q

What drug inhibits PRPP amidotransferase?

A

6-Mercaptopurine

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31
Q

Methotrexate

A
  • folic acid analog
  • anti-tumor
  • inhibits dihydrofolate reductase
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32
Q

How does methotrexate affect dihydrofolate reductase?

A
  • inhibits nucleotide biosynthesis
  • inhibiting rapidly dividing cells selectively
  • specific to mammalian cells
33
Q

What is a drug that inhibits dihydrofolate reductase?

A

Methotrexate

34
Q

Sulfonamides is the analog to…

A

PABA

35
Q

What does sulfonamides do

A

Competitive inhibit of bacterial production of folic acid

-bacterial purine synthesis inhibited

36
Q

What do sulfa drugs act as?

A

Antibiotics

37
Q

What do sulfa drugs do in bacteria?

A

-binds to enzyme that produces folate, inhibits THF, can’t produce purines

38
Q

CPS II (Carbamoyl phosphate synthetase II)

A

-rate limiting, committed step in pyrimidine synthesis

39
Q

What is the rate limiting, committed step in pyrimidine synthesis?

A

CPS II

40
Q

What is CPS II activated by?

A

PRPP

41
Q

What is CPS II inhibited by?

A

UTP (End product)

42
Q

What two amino acids become part of the nitrogenous base structure of pyrimidines?

A
  • glutamine

- aspartate

43
Q

What provides the pentose for the pyrimidine?

A

PRPP

44
Q

Once the pyrimidine bases are produced, what happens?

A

They are attached to PRPP

45
Q

How do ribonucleotides get converted into deoxyribonucleotides?

A

Ribonucleotide reductase

46
Q

Hydroxyurea

A

-anti tumor drug that inhibits ribonucleotide reductase

47
Q

What drug inhibits ribonucleotide reductase?

A

Hydroxyurea

48
Q

Hydroxyurea in sickle cell anemia treatment

A

-increases the synthesis of fetal hemoglobin

49
Q

Thymidilate synthase

A

Plays a role in additional steps to convert dUMP into dTMP

50
Q

What is thmidylate synthase inhibited by?

A

5-FU

51
Q

What will affect the production of DNA, but not RNA?

A

Hydroxyurea and 5-FU

-are especially good at targeting rapidly dividing cells

52
Q

What is required for thymidylate synthesis?

A

Folate, which then requires dihydrofolate reductase

53
Q

What is dihydrofolate reductase inhibited by?

A

Methotrexate

54
Q

Trimethoprim

A

Class of antibiotics that is selective for the prokaryotic version of dihydrofolate reductase

55
Q

Class of antibiotics that is selective for the prokaryotic version of dihydrofolate reductase

A

Trimethoprim

56
Q

Sulfonamides

A
  • antibiotics

- target enzymes in bacteria that make folic acid

57
Q

What are sulfonamides selectively;y toxic for?

A

Prokaryotes

58
Q

What is the main mechanism of action of sulfonamides?

A

Inhibiting nucleotide metabolism in prokaryotes

59
Q

Pyrimidine salvaging

A
  • not salvaged to a significant degree

- no high yield diseases or enzymes are associated with their breakdown or salvage

60
Q

Which bases are more complex?

A

Purine

61
Q

Why are purines more complex than pyrimidines

A
  • dicyclic
  • many more steps involved
  • salvage pathway is more critical
62
Q

Salvage pathway for purines

A
  • nitrogenous base is recovered after removing phosphate and sugar moieties
  • yield hypoanthine or guanine which can be shuttled back into purine nucleotide synthesis
63
Q

What does the salvage pathway for purines yield

A

-hypoxanthine or guanine

64
Q

What happens to the hypoxanthine and guanine that is yielded from purine salvaging?

A

Shuttled back into purine nucleotide synthesis

65
Q

Adenosine delaminase deficiency

A

Causes severe combined immunodeficiency disease (SCID)

66
Q

SCID results from what deficiency?

A

-adenosine deaminase

67
Q

What happens in SCID

A
  • cells of the immune system are particularly affected by this deficiency
  • condition results in patients being susceptible to infection by almost any microorganism, requiring living in a sterile bubble
68
Q

What is the treatment for SCID?

A

Bone marrow transplant

69
Q

What happens to the nitrogenous base in the salvage/degradation pathway?

A

The base can be shuttled back into purine synthesis or can be degraded to Uric acid

70
Q

What enzyme does the excretion pathway of purine synthesis use?

A

Xanthine oxidase

71
Q

Xanthine oxidase

A
  • excretion
  • intermediate is xanthine
  • product is uric acid excreted in urine
72
Q

Gout is the result of what?

A
  • Hyperuricemia (elevated levels of uric blood
  • accumulation of uric acid crystals in the joints
  • leading to inflammation and gouty arthritis
73
Q

What can cause Gout?

A
  • underexcretion of uric acid (most common)
    • which can be caused by: poor kidney function, acid-base balance imbalance, certain drugs
  • overporduction of uric acid
74
Q

Overproduction of uric acid treatment

A

Allopurinol

75
Q

What does allopurinol do?

A

Treats gout in “overproducers” by inhibiting xanthine oxidase which produces uric acid

76
Q

Hyperuricemia as a secondary condition

A

Can be secondary to many conditions such as high cell turnover in cancer patients being treated with various anti tumor drugs

77
Q

Lesch-Nyah’s syndrome

A
  • deficiency in the purine salvage pathway
  • defect in HGPRT
  • deficit of purines
  • extreme hyperuricemia
78
Q

Symptom of Lesch-Nyhan

A
  • severe mental retardation
  • self destructive behavior
  • self mutilation

Chewing off lips and fingertips
Scratching/gouging eyes
Severe gout symptoms

79
Q

How can gout affect the eye?

A

Deposits tophi in

  • the conjunctiva
  • cornea
  • iris
  • sclera
  • lens
  • other eye tissue
  • the formation of transparent vesicles
  • bleeding in the subconjunctival space and vascular changes

Biochem BLOCK 3 (12 decks)

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