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Exam 3 > Skildlum- Nucelotide Metabolism > Flashcards

Skildlum- Nucelotide Metabolism Flashcards

1
Q

Which bases are purines?

A

GA

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2
Q

Which bases are pyrimidines?

A

CT U

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3
Q

What are hypoxanthine and inosine?

A

Intermediates when nucleotides are being converted to fuel sources

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4
Q

What are nucleotide functions?

A
  1. To make DNA and RNA
  2. Handles“Handles” for enzyme cofactors:
    CoASH
    NAD+
    FAD
    Adenosylcobalamin
  3. Energizing substrates–prepares them for reactions
    UDP-glucose
    CDP-choline
  4. Second messengers
    cAMP
  5. Allosteric activators
    AMP, ADP, ATP
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5
Q

What is PRPP?

A
  1. An activated ribose sugar

2. Created by the transfer of pyrophospahte to ribose 5 phosphate by PRPP synthetase

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6
Q

What inhibits PRPP synthetase?

A

GDP and ADP

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7
Q

What is the first step in purine synthesis?

A

The transfer of an amine from glutamine by the glutamine phosphoribosyl amidotransferase.

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8
Q

What is the second step in purine synthesis?

A

Addition of glycine to make glycinamide ribosyl 5-Phosphate.

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9
Q

How do you make IMP (inosine monophosphate)?

A
  1. Add C and N from tetrahydrofolate
  2. Add CO2
  3. Add glutamine
  4. Add aspartate
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10
Q

What happens in the conversion of IMP to AMP?

A
  1. Aspartate bonds to IMP to make adenylosuccinate (hydrolysis of GTP)
  2. Fumarate is cleaved off to make AMP
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11
Q

How do you form GMP?

A
  1. IMP is oxidized to xanthine monophosphate

2. Amine group is transferred from glutamine (using ATP hydrolysis to power reaction)

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12
Q

What happen to AMP and GMP?

A
  1. Phosphorylated to diphosphates
    THEN
  2. ADP and GDP can be phosphorylated again and: hydrolyzed for energy/incorporated into RNA
    OR
  3. Ribose sugar of ADP and GDP can be reduced to make dADP and GDP
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13
Q

What is thioredoxin?

A

A protein redox cofactor, like glutathione, that can exist in reduced or oxidized states depending on cysteine side chain sulfur atom.

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14
Q

What happens in purine salvage?

A

Cells expend a lot of energy to make nucleotides. To conserve this energy, there are different pathways to recycle nucleosides and bases in the cell

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15
Q

What can adenosine kinase do that is special? What must the other purine nucleosides do?

A
  1. It directly phosphorylates Adenosine to AMP

2. Have their ribose sugars removed, then added back from PRPP, to make monophosphate nucleosides.

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16
Q

What causes Lesch Nyhan Syndrome?

A

An inherited deficiency in hypoxanthine-guanine phophoribosyltransferase

17
Q

What causes SCID (Severe combined immunodeficiency)?

A

An inherited deficiency in adenosine deaminase

18
Q

What cause CID (Combined immunodeficiency)?

A

An inherited deficiency in purine nucleoside phosphorylase (PNP)

19
Q

What does PNP deficiency cause and what are the symptoms?

A
  1. Combined immunodeficiency

2. Low but not absent T cells, chronic infection, FTT, neurological symptoms

20
Q

What is the second most common cause of autosomal recessive SCID?

A

ADA deficiency

21
Q

What does ADA deficiency lead to? What are the symptoms? What is the treatment?

A
  1. Accumulation of 2 deoxyadenosine in the blood. This is toxic to lymphocytes.
  2. Symptoms: Lymphocytes < 500 / mm3 (normal 3,000 – 9,000/mm3 for children), Costrochondral junction dysplasia (skeletal abnormalities)
  3. Treatment: Bone marrow transplant, +/- chemotherapy
22
Q

What is Lesh Nhyan Disease? What are the symptoms?

A

HGPRT–He’s got purine recylcing trouble

  1. A rare X linked syndrome due to inherited deficiency in hypoxanthine-guanine phosphoribosyltransferase.
  2. Symptoms: Self injury (biting of the fingers and lips), Elevated uric acid in urine, mental retardation, dystonia, recurrent vomiting
23
Q

What do patients with LND often die from?

A

Renal failure in their 30s. Can be prevented with drugs (allipurinol) that reduce uric acid.

24
Q

What is the cause of self mutilation in LND?

A

Disturbance in dopamine signaling

25
Q

In purine metabolism, GMP and AMP are degraded to xanthine, which is oxidized to uric acid by what enzyme?

A

xanthine oxidase

26
Q

What is gout?

A

The precipitation of uric acid in distal joints, caused by purine degradation.

**If you eat a lot of organ meat, you get a lot of nucleotides coming in that get degraded to uric acid. Xanthine oxidase makes uric acid, which is the normal rout of excretion for excess nucleotides.
Treatment is a COMPETITOR of xanthine oxidase.

27
Q

How do purines and pyrimidines differ in synthesis/assembly?

A
  1. Purines: assembled on ribose sugar

2. Pyrimidines: assembled than transferred to ribose sugar

28
Q

What does CPS II do?

A

Uses glutamine as an amine donor to form carbamoyl phosphate.
2. Allosterically inhibited by: UTP, activated by PRPP

29
Q

How do you make UMP?

A
  1. Carbamoyl phosphate bonds to aspartate to make carbamoyl aspartate.
  2. This is cyclized to ORotATE
  3. Orotate combines with PRPP to make a nucleotide, which is then decarboxylated to form UMP

**Carbamoyl phosphate is used in urea cycle, but it is also a substrate for pyrimidine synthesis

30
Q

What is characteristic of urea cycle disorders downstream of CPS I?

A

Elevated urinary orotic acid

31
Q

What happens in pyrimidine degradation?

A

Cytosine > uracil > CO2, NH4+, and b-alanine

Thymine > CO2, NH4+, and b-aminoisobutyrate

**Accumulation of pyrmidine metabolites is not associated with pathology

Exam 3 (12 decks)

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