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Biochem Block 3 > Nucleotide Metabolism > Flashcards

Nucleotide Metabolism Flashcards

1
Q

Nucleotide functions

A
  1. Structural component of DNA AND RNA
  2. Carriers of activated intermediates (UDP-glucose)
  3. Structural components of coenzymes used in metabolism
  4. Secondary messengers in signal transduction (cAMP)
  5. Energy (ATP)
  6. Regulate pathways (using energy)
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2
Q

Structure of nucleotides

A

Nitrogenous base

Sugar

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3
Q

Purines

A
  • dicyclic

- adenine and guanine

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4
Q

Pyrimidines

A
  • monocyclic

- cytosine, thymine(DNA) and uracil(RNA)

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5
Q

Sugar is nucleotides

A

RNA:ribose
DNA: deoxyribose

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6
Q

Why is DNA more stab,e than RNA?

A

DAN uses deoxyribose which lacks an oxygen so it is more stable

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7
Q

Difference between nucleotides and nucleoside

A

Nucleoside: nitrogenous base and sugar
Nucleotides: nucleoside plus a phosphate group

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8
Q

What provides the energy to drive these reaction So?

A
  • anhydride bond links 2 and 3 phosphate on nucleotides
  • high energy bond that drives biochemical reactions
  • ATP AND GTP
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9
Q

Where does the ribose 5p come from for purine synthesis?

A

HMP shunt

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10
Q

What is a key difference in purine and pyramides metabolism?

A

Purines directly build the nitrogenous base ONTO the sugar

-pyramides build the base then attach it to the sugar

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11
Q

PRPP synthase in purine metabolism

A
  • catalyze so formation of the activated pentose

- uses energy

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12
Q

Regulation of PRPP SYNTHASE

A

Activator: inorganic phosphate
Inhibitor: purine ribonucleotides

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13
Q

What is the default of purine nucleotides synthesis?

A

-produces ribonucleotides(not deoxyribose

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14
Q

What is the rate limiting step of purine synthesis?

A

PRPP amidotransferase

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15
Q

PRPP AMIDOTRANSFERASE REGULATION

A

Activated: PRPP (substrate)
Inhibitors: purine nucleotides(end products)

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16
Q

What does folate do?

A
  • required for subsequent steps as a carbon donor

- active form is THF

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17
Q

What enzyme makes THF

A

-dihydrofolate reductase turns folate into THF

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18
Q

Who makes their own folate?

A

-bacteria make their own folate, we cant.

19
Q

What does THF turn into?

A
  • THF acts as a carbon donor and makes IMP

- IMP can then turn into AMP and GMP

20
Q

6-Mercaptopurine

A
  • purine analog that acts as a product inhibitor
  • inhibits PRPP amidotransferase
  • if base is formed, it will have mutations
21
Q

Methotrexate

A
  • folic acid analog
  • inhibits digydrofolate reductase so no THF can be made
  • works ONLY IN MAMMALS
  • selectively inhibits rapidly dividing cells
22
Q

Sulfonamides

A
  • structural analog of para-aminobenzoic acid (PABA)
  • competitive inhibitor of bacteria producing folic acid
  • bacteria purine synthesis inhibited
23
Q

What is the rate limiting enzyme for pyrimidine synthesis?

A

-CPS II

24
Q

Regulators of CPS II

A
  • activated by PRPP

- Inhibited by UTP(end product)

25
Q

What are the two amino acids used in nitrogenous base structure of pyrimidines?

A

-glutamine and aspartate

26
Q

What does PRPP provide for pyrimidine synthesis?

A

-pentose

27
Q

ribonucleotide reductase

A
  • ribonucleotides are converted into deoxyribonucleotides

- hydroxyurea inhibits it

28
Q

Hydroxyurea

A
  • inhibits ribonucleotide reductase

- also treats sickle cell by promoting fetal hemoglobin

29
Q

convert dUMP into dTMP

A

-use thymidylate synthase

30
Q

5-FU

A

-anti tumor drug that inhibits thymidylate synthase

31
Q

what do 5-FU and hydroxyurea target?

A
  • affect production of DNA, but not RNA

- so really good at targeting rapidly dividing cells

32
Q

Trimethoprim

A

-antibiotic that is selective for the prokaryotic version of dihydrofolate reductase

33
Q

Pyrimidine breakdown

A
  • they are not salvaged to a significant degree

- no high yield disease from breakdown so not important

34
Q

Why is it important to recycle purines?

A
  • purine bases are more complex than pyrimimdines
  • take more steps to make it
  • salvaging it is more important because it takes too much energy to make them
35
Q

salvage pathway of purine general

A
  • base is recovered by removing phosphate and sugar moieties
  • this yields hypoxanthine or guanine
  • those are shuttled back into synthesis
36
Q

adenosine deaminase deficiency

A
  • causes SCID
  • immune system(T and B cells) are primarily affected
  • patients are super susceptible to inflection (bubble)
  • it cannot be recycled, so youre excreting too much
37
Q

treatment of SCID

A

-bone marrow transplant or enzyme replacement

38
Q

Xanthine oxidase

A
  • excretion pathway of purines

- produces uric acid which is then excreted as urine

39
Q

Gout

A
  • result of hyperuricemia
  • accummulation of uric acid crystals in the joints
  • gouty arthritis
40
Q

What causes gout?

A
  • overproduction of uric acid

- problem with excretion

41
Q

Allopurinol

A
  • inhibits xanthine oxidase

- helps overproducers of uric acid stop making it

42
Q

Lesch-Nyhan syndrome

A
  • X linked
  • deficiency in purine salvage pathway
  • defect in HGPRT
  • you end up excreting like 90%
  • extreme hyperuricemia
43
Q

Gout and eyeballs

A
  • deposits of tophi in cornea, iris, sclera, lens
  • formation of transparent vesicles(metalic)
  • bleeding in subjunctiva

Biochem Block 3 (10 decks)

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