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30 Cards in this Set

  • Front
  • Back
componants in nucleotides
base- purine or pyrimidinne
nucleoside- base + sugar
nucleotide- + phosphate (mono, di, or tri)

eg. ATP, adenosine, adenine
functions of nucleotides (& sides & bases)
make DNA/RNA
signaling (cAMP)
metabolism (NAD)
DeNovo synthesis of purines
R5P to base then add P's

PRPP is "holder"
C-1 groups from THF
N donors are glycine, aspartate, glutamine

make PRPP
then ring (5 ATP)
IMP then AMP (via adenylosuccinate) & GMP (via XMP glutamine amidotransferase)

kinases add P's (ATP)
regulation of purine synthesis

feedback inhibition
ADP (low energy) inhibs PRPP synthetase
AMP, GMP, IMP (product) inhib amidiotransferase
AMP inhibs IMP to AMP
GMP inhibs IMP to GMP
enzymes for denovo synth of purines
PRPP synthetase (inhib by ADP)
Glutamine-PRPP amidotransferase (inhib by AMP, IMP, GMP)
DeNovo synthesis of pyrimidines
aspartate & carbamoyl P (urea cycle)


make deoxy b4 making TMP
Thimidine monophosphate synthesis
comes from CDP or UDP
must be deoxy first (ribonucleotide reductase)
then add P (nside diphosphate kinase)
dCTP to cUTP (deaminase)
to dUMP (dUTPase)
to dTMP (thymidylate synthase)
thymidylate synthase
last step in converting CDP & UDP to dTMP (thru dCTP, dUTP, dUMP, dTMP)
regulation of pyrmidine synthesis
feedback inhibition

especially dATP for dTMP
ribonucleotide reductase
pyrmidine synthesis (denovo)
gives deoxy form
(only way to get dTMP)
storage of nucleotides
very little
nucleotide synthesis is good med target
degredation of nucleotides
use up leftovers
nucleotidase (tide to side)
-gives MP

hydrolyze off ribose
or phosphorylyze off R1P
degredation of pyrmidines
easily broken down to water soluble products
degredation of purines
xanthine oxidase
-Hypoxanthine to xan(hypoxanthine from AMP)
-xanthine to uric acid
(from Hypox or guanine)
Salvage pathway of nucleotides
saves N
only for purines (gout)
enzymes for purine salvage
Requires PRPP

-adenine & PRPP to AMP + PPi

-hypoxan (or guanine) + PRPP to IMP (or GMP) to PPi
diseases associated w/nucleotide metabolism
ADA defic (SCID)
PNP defic (Ts prefd)
Lesh Nyan (salvage)
Gout (purine deg or synth)
bubble boy disease
ADA deficiency
AMP builds up
100 fold increase in dATP
inhibits ribonucleotide reductase

get deficient in ALL deoxy's
No T's or B's
ribonucleotide reductase inhibited by
high dATP
(found in ADA defic)
low ADA
low deoxy's
T's & B's deficient
ADA deficiency
PNP deficiency
less severe than ADA
only effects T's
clutzy child with neuro def's
self destructive
Lesch-Nyan Syndrome
deficient HGPRT (aka HPRT)
clutzy child with neuro def's
no self destructive
Lesch-Nyan Syndrome
Lesch-Nyan Syndrome
mutation in HGPRT (aka HPRT)
excess PRPP

feed forward activation & less feedback inhibition leads to high levels AMP/GMP & Uric acid

(die from kidney damage)
high PRPP

high AMP/GMP & uric acid
lesch nyans
causes of gout
excess purine synth
-increased PRPP (overactive synthetase)
-G6Ptase defic- increases PRPP via HMP (von Gierke)

or impaired degredation
-defic APRT or HGPRT

or high levels purines
- cell destriction (chemo)
-kidney dysf
-diet (liver, dried beans)
MOA allopurinol
inhibits xanthine oxidase
(decreases uric acid & H2O2)
(pee out hypoxan & xan)
characteristics of gout
high levels uric acid
increased H2O2
Tophi- deposits
deposits of monosodium urate
big bump on toe
drugs using nucleotide metabolism pathway
flurourasil-binds thymidylate synthase
methotrexate- inhibits DHF reductase (suicide)
trimethoprim- binds BACTERIAL DHF reductase