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MCM > Purine and Pyrimidine Metabolism > Flashcards

Purine and Pyrimidine Metabolism Flashcards

1
Q

Purines, their nucleosides, and their nucleotide forms

A

Adenine
Adenosine
Adenosine X Phosphate (ATP, AMP, etc)

Guanine
Guanosine
Guanosine X phosphate (GMP, etc)

Hypoxanthine
Inosine
IMP

Xanthine
Xanthosine
XMP

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2
Q

Pyrimidines, their nucleosides, and their nucleotide forms

A

Cytosine
Cytodine
CMP

Thymine
Thymidine
TMP

Uracil
Uradine
UMP

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3
Q

Digestion of RNA/DNA

first step

A

DNA/RNA is broken into oligomers by

RNA: Ribonuclease
DNA: Deoxynuclease

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4
Q

Digestion of RNA/DNA

second step

A

Oligomers are separated into individual nucleotides by phosphodiesterase

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5
Q

Digestion of RNA/DNA

third step

A

phospho-ester bond is broke by nucleotidase

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6
Q

Digestion of RNA/DNA

fourth step

A

the base is removed from the sugar by nucleosidase

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7
Q

Rinonucleases/Deoxyribonucleases do what

A

convert RNA and DNA to short oligomers

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8
Q

Phosphodiesterases

A

convert these oligomers to nucleotide monophosphases (NMPs) or deoxynucleoside monophosphates (dNMPs)

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9
Q

Catabolism of GMP to Uric acid

A

GMP –> Guansosine —> Guanine –> Xanthine –> Uric acid

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10
Q

Catabolism of AMP to Uric acid

A

AMP -breaks down in two ways

  1. AMP— (adenosine monophosphate deaminase) –> IMP –> Inosine –> hypoxanthine – (xanthine oxidase)—> xanthine –(xanthine oxidase) –> uric acid
  2. AMP –> Adenosine –> (adenosine deaminase) –> inosine –> hypoxanthine —(xanthine oxidase)–> xanthine –uric acid
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11
Q

adenosine deaminase (ADA)

A

excessive production of ADA leads to hemolytic anaemia

underproduction of ADA lead to SCID

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12
Q

SCID

A

severe combined immune deficiency
defective T/B cells
second worst form caused by underproduction of ADA
X-linked: only impacts boys

deficiency of ADA leads to overproduction dATP, which blocks synthesis of dNDP/dNTPs.

impaired DNA synthesis and compromised immune system

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13
Q

Overproduction of adenosine deaminase (ADA) leads to

A

over-degradation of adenosine: depletes adenine nucleotide pool and triggers premature destruction of RBCs

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14
Q

Drug target for gout and drug

A

allopurinal targets xanthine oxidase

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15
Q

Xanthine oxidase

A

catalyzes oxidation of hyoxanthine to xanthine and xanthine to uric acid

has 2 FADs, 2 Mo atoms, and 8 Fe atoms per molecule of enzyme

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16
Q

Gout (general)

A

intensely painful/inflamed joints

most commonly affected area is big toe. (metatarsal pharangeal joint)

historically regarded as disease of the wealthy (too much wine, food, and sex)

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17
Q

Gour (details): primary, secondary

A

overproduction of uric acid = primary hyperuricemia
underexcretion of uric acid = secondary hyperuricemia

sodium-urate crystals build up in synovial fluid
MOs consume them, trigger acute inflammatory response

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18
Q

hyperuricemia

A

plasma levels of uric acid exceed ability to dissolve them

19
Q

What causes gout?

A

diet rich in purinesL MEAT and SEAFOOD, (beans, lentils, asparagus, spinach)

20
Q

gout =

A

excess purines

21
Q

treatments of gout (6)

A 
NSAIDs
steroids 
urate oxidase 
allopurinol 
colchicine 
probenecid
22
Q

colchicine

A

decreases granulocyte movement to site of affected area

23
Q

allopurinol

A

inhibits xanthine oxidase to form more soluble hypoxanthine

24
Q

probeneceid

A

increases excretion of uric acid

25
Q

serum uric levels
urinary uric levels
level indicating risk for gout

A

4-9 mg/dl men
3-6 mg/dl in women
26 mg/hr in urine

ABOVE 9 mg/dl increased risk of gout

26
Q

Pyrimidine catabolism: UMP, UDP, UTP

A

1) [UMP/DP/TP+dUMP/dDP/dTP]—-nucleotidase—-> Uridine/deoxyuridine –> Uridine/Deoxyuridine –> –> uracil –> melonyl Coa (ketogenic)

27
Q

Pyrimidine catabolism: CMP/DP/TP+dCMP/dCDP/dCTP

A

CMP/DP/TP+dCMP/DP/TP —-> neuclotidase –> Cytodine/Dcytodine –> deaminase rxn –> Uradine/deoxyuradine –> Uracil –> melonyl Co A

28
Q

Pyrimidine catabolism; deoxythymidine

A

dTDP/TTP –> nucleotidase –> Thymine –> Succinyl CoA

MethylMalonyl CoA

29
Q

which pyrimidines are converted to ketogenic compounds and what are they

A

Uracil and Cytosine

Melonyl co A

30
Q

which pyrimidines are converted to glucogenic compounds and what are they

A

thymine

succinyl co-a and methylmelonyl co a

31
Q

the “end” products of pyrimidine catabolism are insoluble or soluble?

A

water soluble

32
Q

Pyrimidine synthesis: committed step

A

committed step is the synthesis of phosphoribosyl amine

33
Q

phosphoribosyl amine =

A

first committed step in purine synthesis

this compound is either hypoxanthine ribose or

INOSINE MONOPHOSPHATE

34
Q

INOSINE MONOPHOSPHATE

A

the phosphoribosyl amine indicating the first committed step in purine synthesis

also called hypoxanthine ribose phosphate

inosine is the nucleoside of hypoxanthine (its base)

35
Q

Fate of inosine monophosphate

A

not used in DNA, so it is converted into adenosine and guanosine monophosphate

36
Q

Two salvage enzymes responsible for converting inosine monophosphate to AMP and GMP

first has four words in it.
second has 3 words in it

A

1) hypoxanthine guanine phosphoribosyl transferase

2) adenine phosphoribosyl transferase

37
Q

Purine synthesis: raw substrate molecules

A

CO2, Asp, Gln, Gly N-5, N-10-formyl THF

THF is the important one to remember

38
Q

Pyrimidine synthesis: raw substrate molecules

A

HCO3, Gln, Asp, N-5, N-10 methylene TH

THF, again, the important one

39
Q

THF

A

tetrahydrafolate

40
Q

PRPP

A

MUST be remembered

41
Q

the two essential substrates used in purines and pyrimidines (both)

A

THF and PRPP

42
Q

Purine vs Pyrimidine synthesis de novo: first step

A

unique because purine syn. begins with ribose and build ring structures on it

pyrimidines build ring structures and build on ribose

43
Q

De novo synthesis of purines: first step

A

PRPP synthase adds phosphate to ribose carbon 1 (From ATP) to make PRPP (ribose with two Ps)

inorganic phosphate is +FB
GMP, AMP, IMP are -FB

44
Q

De novo synthesis of purines: second step

A

d

MCM (22 decks)

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