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5 Written questions

5 Matching questions

  1. De nove purine biosynthesis is expensive, how much and what do we do
  2. Important Enzymes in Pyrimidine Biosynth
  3. Tx of Gout with Allopurinol
  4. Origins of Pyrimidine Ring Atoms
  5. Effects of Allopurinol Tx on LNS pts
  1. a CPS II = takes CO2 and Gln to Carbamoyl P
    ATCase, committed step = take Carbamoyl P and Aspartate to N-Carbamoyl aspartate
    CTPS = takes UTP to CTP
  2. b For AMP 8 high energy phosphates, 2 Gln, 1 Gly, 2 Asp

    For GMP 7 high energy phosphates, 3 Gln, 1 Gly, 1 Asp

    Thus we Regulate and use salvage pathways to recycle purines
  3. c N1, C4,5,6= all from Aspartate
    C2, N3 = all from Carbamoyl phosphate
  4. d Allopurinol is a suicide inhibitor of xanthine oxidase, because it is similar in configuration to hypoxanthine and it binds tightly to molybdenum in xanthine oxidase.

    Xanthine oxidase takes Hypoxanthine to xanthine and xanthine to uric acid
  5. e Reduces urate in LNS pts by blocking xanthine oxidase rxns

    Ineffective in reducing rate of de novo purine biosynthesis, since it cannot synthesize allopurinol ribonucleotide from allopurinal and PRPP, it requires HGPRT

    Can have neurological effects due to the brains reliace on salvage pathways for most purine nucleotide production and needs GTP for dopamine formation

5 Multiple choice questions

  1. Ring closure no ATP

    Forms Di hydroorotase

    after NAD+ forms to orotate
  2. rather than directly inhibiting Thymidylate Synthetase TS is inhibits the cyclical production of the methyl donor N5N10 methylene THF

    It does this by inhibiting the enzyme DHFR dihydrofolate reductase. Stopping the reduction of Dihydrofolate to THF, which is a needed substrate for N5N10 methylene THF
  3. PRA adds glycine, enzyme not important

    Methyl group added to N end of glycine with N10 formyl THF

    Glutamine adds N to replace carboxyl oxygen from glycine.

    First 5 point ring closes

    Biotin independent carboxylation with CO2

    Aspartate adds to carboxylated carbon with the N group first

    Fumarate leaves leaving N from Aspartate

    N10 formyl THF methylates lower N

    then there is low energy ring closure

    Makes IMP the base is called hypoxanthine
  4. Adenylate Kinase takes ATP and AMP to 2 ADPs

    nucleoside monophosphate kinases take G,C,UMPs plus ATP to ADP plus G,C,UDPs

    nucleoside diphosphate kinases take G,C,UDPs plus ATP to ADP plus G,C,UTPs

    oxidative phosphorylation takes ADP plus Pi to ATP
  5. IMP uses Aspartate and GTP to add N in place of carboxyl O at top

    Fumarate leaves leaving just NH2 and AMP is formed

5 True/False questions

  1. Ribonucleotid Reductase relates to SCIDS byRibonucleotide Reductase is a heterotatramer with 2 types of subunits

    There are 3 types of binding sites

    C= Catalytic site which binds to substrates A, U, G, CDP

    A= Activity Site, for allosterica regulation, this site regulates whether it is fast or slow. I only binds with ATP or dATP to slow the catalytic rate, high dATP is the stop signal

    S= Specificity Site for Allosteric regulation it binds
    -ATP or dATP to activate reduction of CDP and UDP
    -dTTP to activate reduction of GDP and inhibit production of CDP and UDP
    -dGTP to activate reduction of ADP and inhibit reduction of CDP and UDP

          

  2. HypoxanthineElevated levels of Uric Acid, chronic elevation of blood uric acid, hyperuricemia from xanthine overproduction and formation of uric acid

    Also called Gouty arthritis and uric acid nephrophathy

    Uric acid has limited water solubility and precipitates under acidic conditions like collecting ducts eg kidney stones, a can lead to sodium urate that is most likely to precipitate at neutral pH synovial fluid of jointe eg gouty arthritis

          

  3. Importance of adenosine DeaminaseSigns and Symptoms young with hematuria, megaloblastic anemia, hyperuricemia, crystals in urine, mental retardation, decreased gross motor function, and self mutilation, gout in early 20s

    is a Rare X linked disorder 1/400000 males, milder form = 8% kelly-seegmiller syndrome

    Cause = near total deficiency of HGPRT about 2% of activity

    biochemical consequenses
    Overproduction or urate
    Elevated PRPP concentrations
    Marked increase in rate of de novo purine biosynth

          

  4. Synthesis fo Thymine NucleotidesThymidylate Synthetase uses N5N10 Methylene THF as a methyl transfer group to turn dUMP to dTMP, then becomes DHF which must be recycled

          

  5. Anti neoplastics6 mercaptopurine
    6 thiaguanine
    These compounds compete with hypoxanthine and guanine for the salvage enzyme HGPRT.
    They are converted by HGPRT into respective ribonucleotides, they inhibit the committed step of de novo purine biosynthesis pathway catalyzed by Gln PRPP amidotransferase, an effect similar to allopurinol
    They are also incorporated into DNA and RNA