Memetabolsim of nuclotides-pyrimidne and purine Flashcards

1
Q

what are the atoms of pruine ring contributed by

A

aas (asparatate, glycine and glutamine)

CO2

n10-formyltetrahydrofolate

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2
Q

where is the purine ring constructed

A

in liver by series that add the carbons and nitrogens to ribose-5-phospgate

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3
Q

act and inhi of PRPP SYNTHASE

A

act: inorganic phosphate
inhi: pruine nuclotides

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4
Q

act and inhi GPAT

A

inihi: amp and gmp

act: controlled by intracellular concentration of PRPP

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5
Q

what inginit adenosine and guanosine monophospahte synthesis

A

by end product of that pathway

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6
Q

inhibitor of imp dehydrogenase and adenylosuccinate synthetase

A

revrsible inhibitor, mycophenolic acid

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7
Q

what is lesch nyhan syndrome

A
  • xlinked disorder
    deficiency of HGPRT –>result in inability to salvage hypoxanthine of G form which excessive amounts of uric acid is produced.

+ cause increased PRPP lvl and decreased IMP and GMP levels

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8
Q

what is regulative step in purine synthesis

A

GPAT

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9
Q

what is lesch nyhan a cause of and what does it resykt form

A

. The combination of decreased purine reutilization
and increased purine synthesis results in increased
degradation of purines and the production of large amounts
of uric acid, making HGPRT deficiency an inherited cause of
hyperuricemia

rsult in formation of uric acid stones in kidneys adn urate crustals in joints and soft tissues.

characteri: motor dysfunction, cognitive deficits, behavioral disturbances

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10
Q

what inhibit and act ribonucleotide reductase

A

inhi: dATP, hydroxyurea
act: ATP

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11
Q

where does purine nucleotide degradation occur

A

small intestine, where pancreatic nucleases hydrolyze them to nuclotides

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12
Q

what is gout initiated by + treatment

A

high levels of uric acid in blood (hyperuricemia) as result of either overproduction or underexcretion of uric acid

treatment: allopurinol inhibits xanthine oxidase, resulting in accumulation of hypoxanthine

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13
Q

what can hyperuricemia lead to

A

monosodium uraye crystals in joints

inflammatory response to cyrstals

uric acid stones in kidney

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14
Q

hyperuricemia-result fo

A
  • decreased salvage of hypoxanthine and G and the subsequent increased availability of PRPP
  • consequence of increased availability of purines

unrelated metabolic diseases, such as von Gierke disease or hereditary fructose
intolerance

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15
Q

what is the regualting step in pyrimidine synthesis

ihibiton and act

A

mammalian cellS: Synthesis of carbamoyl phosphate form GLUTAMINE AND CO2, catalyzed by CPSII.

inhi: UTP
act: PRPP

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16
Q

difference between CPSI(urea) and CPSII(pyrimidine)

A

CPS1:
-located in mitrochondria
- involved in ura cucle
- source is ammonia (nitrogen source)
- regualtors: act is N-acetylglutamate

CPSII:
- in cytosol
-pyrimidine synthesis
- Y-amide group of glutamine (nitrogen source)
- regulators: act is PRPP, inh is UTP

17
Q

when is the pyrimidine ring closed and what is redced here

A
  • dihyroorotase
  • dihydroorotate–>orotic acid = FMN is reduced
18
Q

what is the ribose 5 phos donor in pyrimidien

A

PRPP

19
Q

what are inhibitors of thymylate syntahse

A

t analogs like 5-flurouracil

20
Q

dhf reductase inhibbtiors

A

folate aalogs like methotrexate