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GI > Nucleotide Metabolism I > Flashcards

Nucleotide Metabolism I Flashcards

1
Q

Synthesizes the parental purine from scratch on a ribophosphate backbone

A

Purine de novo pathway

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2
Q

Synthesizes the parental pyrimidine from scratch and THEN attaches it to the ribophosphate backbone

A

Pyrimidine de novo pathway

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3
Q

Recycles an existing ring structure and attaches it to a ribophosphate backbone

A

The salvage cycle for purines and pyrimidines

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4
Q

All nucleotides are comprised of which three entities?

A

Sugar, phosphate, and a base

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5
Q

Comprise the backbone structure of the nucleotide

A

The sugar and phosphate

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6
Q

Composed of a two ring structure

A

Purines (adenine and guanine)

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7
Q

Composed of a single ring structure

A

Pyrimidines (cytosine, thymine, and uracil)

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8
Q

When we have just a base and ribose, but no phosphate, we have a

A

Nucleoside (adenosine, guanosine, cytidine, uridine, and thymidine)

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9
Q

Step 1 of de novo purine synthesis is creating the

A

Ribose phosphate backbone (PRPP)

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10
Q

The source of the ribose phosphate moiety in all pathways of nucleotide synthesis for both purines and pyrimidines

A

PRPP

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11
Q

Ribose-5-phosphate is converted to PRPP by the enzyme

A

PRPP synthetase

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12
Q

How much ATP is required for the conversion of R-5-P to PRPP?

A

1 ATP

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13
Q

Activated by inorganic phosphate, signifying a need for nucleotides

A

PRPP synthetase

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14
Q

PRPP synthetase is inhbited by the

A

Purine ribonucleotides (ADP, ATP, GDP, GTP)

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15
Q

What is the committed step of purine synthesis?

A

Conversion of PRPP tp PRA

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16
Q

Which enzyme catalyzes the committed step of purine synthesis?

A

PRPP-amido-transferase

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17
Q

In the conversion of PRPP to PRA, PRPP receives an amie group from

-releases a high energy pyrophosphate

A

Glutamine

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18
Q

Effectively activated by its substrate, PRPP, because PRPP concentrations are held well below the enzyme’s saturation capacity

A

PRPP-amido-transferase

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19
Q

PRPP-amido-transferase is inhibited by

A

AMP, GMP, and IMP

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20
Q

Irreversible inhibitors of PRPP-amido-transferase

-structurally similar to glutamine

A

Azaserine and DON

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21
Q

Azaserine and DON are potent inhibitors of

A

Purine nucleotide metabolism

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22
Q

Nine more steps, all of which are unregulated, convert PRA to

A

IMP

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23
Q

A parental purine because it serves as the precursor to the purines AMP and GMP

A

IMP

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24
Q

How many molecules of ATP are consumed in the conversion of PRA to IMP

A

4 ATP

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25
Q

What are the 5 contributors toward making the purine ring of IMP?

A

CO2, Aspartate, Glycine, Glutamine, and THF

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26
Q

Essential for the synthesis of purines

A

THF

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27
Q

Humans create THF by modifying

A

Dietary folic acid

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28
Q

Dietary Folic acid is converted to dihydrofolate (DHF) and then to THF by the enzyme

A

DHF Reductase (DHFR)

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29
Q

Inhibit DHFR, thereby stifling nucleotide synthesis and killing rapidly growing tumores

A

Chemotherapeutic agents such as aminopterin and methotrexate

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30
Q

Another DHFR inhibitor. Binds much more strongly to bacterial DHFR, making it an effective antibiotic

A

Trimethoprim

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31
Q

Unlike humans, who rely on dietary folic acid, bacteria synthesize their own folate from a molecule called

A

PABA

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32
Q

Antibiotics structurally similar to PABA, which competitively inhibit folic acid synthesis in bacteria

A

The Sulfonamides

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33
Q

IMP is committed to becoming either

A

AMP or GMP

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34
Q

The conversion process of IMP to either AMP or GMP requires

A

2 steps

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35
Q

Required for the conversion of IMP to adenylosuccinate

A

GTP and aspartate

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36
Q

The enzyme which converts IMP to adenylosuccinate is inhibited by

A

AMP

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37
Q

In a second reaction, adenylosuccinate is converted to AMP, a process which results in the release of

A

Fumarate

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38
Q

IMP is converted to the intermediate XMP by the enzyme IMP dehydrogenase. This requires

A

NAD+

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39
Q

IMP dehydrogenase is inhibited by

A

GMP

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40
Q

Required for the conversion of XMP to GMP

A

ATP and glutamine

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41
Q

An antiviral used to treat hepatitis C that also inhibits IMP dehydrogenase

A

Ribavirin

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42
Q

Depletes intracellular pools of guanine nucleotides

A

Ribavirin

43
Q

The synthesis of AMP and GMP are regulated by

A

Feedback inhibition

44
Q

AMP and GMP synthesis is also regulated so as to coordinate the relative amounts of AMP and GMP to one another. This process is called

A

Reciprocity

45
Q

Required to convert IMP to AMP

A

GTP

46
Q

Required to convert IMP to GMP

A

ATP

47
Q

In step 5 of purine synthesis, AMP and GMP are phosphorylated by

A

Nucleoside monophosphate kinases

48
Q

This phosphorylation produces

A

ADP and GDP

49
Q

ADP and GDP are further phosphorylated by nucleoside diphosphate kinase to create

A

ATP and GTP

50
Q

Has a broad specificity for all nucleotide diphosphates

A

Nucleoside diphosphate kinase

51
Q

Takes advantage of the fact that free-floating bases including adenine, guanine, and hypoxanthine are present in the cell from other metabolic pathways

A

Purine salvage pathway

52
Q

The nitrogenous base of IMP

A

Hypoxanthine

53
Q

Simply attaches a preformed purine base to the PRPP backbone

A

Purine salvage pathway

54
Q

Converts adenine to AMP in the purine salvage pathway

A

Aenine Phosphoribosyl Transferase (APRT)

55
Q

Recognizes both guanine and hypoxanthine as substrates to catalyze the formation of GMP and IMP respectively

A

Hypoxanthine-Guanine Phosphoribosyl Transferase (HGPRT)

56
Q

A disease caused by the deficiency of HGPRT

A

Lesch-Nyhan Syndrome

57
Q

An X-linked congenital defect that results in neurological deficits including spasticity, mental retardation, aggression, and self-mutilation

A

Lesch-Nyhan Syndrome

58
Q

The biochemical basis for the neurological symptoms is thought to be due to insufficient cell supplies of

A

GTP

59
Q

Relies much more heavily on the salvage pathway for the synthesis of nucleotides

A

Brain tissue

60
Q

Consequently, Lesch-Nyhan Syndrome patients have a neuronal deficiency of

A

GMP

61
Q

Thought to be involved in a number of cell signaling pathways that may be involved in the developmental process of dopaminergic neurons

A

GTP

62
Q

This may explain why patients with Lesch-Nyhan have fewer

A

Dopaminergic nerves

63
Q

GTP is also a precursor for tetrahydropterin, which is a cofactor in the biosynthesis of

A

Dopamine

64
Q

The HGPRT deficiency results in increased levels of

A

PRPP

65
Q

The increased levels of PRPP increases

A

De novo purine biosynthesis

66
Q

This is because PRPP is an activator of

A

PRPP-amido-transferase

67
Q

One additional problem of patients with Lesch-Nyhan syndrome is that they have excess buildup of

A

Uric acid (results in gout)

68
Q

A deficiency of HGPRT leads to increased levels of the enzymes substrates

A

Hypoxanthine and Guanine

69
Q

Without salvage, these purine bases are destined to become

A

Uric acid

70
Q

What is step 1 of the degradation of purines to uric acid?

A

The phosphate is removed

71
Q

Removes the phosphate group from AMP, GMP, and IMP resulting in the formation of adenosine, guanosine, and inosine respectively

A

A 5’ nucleosidase

72
Q

There is also a pathway for the direct conversion of AMP to IMP via the enzyme

A

AMP deaminase

73
Q

In step two of the degradation of AMP to uric acid, adenosine is converted to

A

Inosine

74
Q

Converts adenosine to inosine

A

Adenosine Deaminase (ADA)

75
Q

This reaction serves as a point of convergence in the degredation of both AMP and IMP

A

Conversion of adenosine to inosine

76
Q

A deficiency of the enzyme ADA results in a subtype of

A

Severe Combined Immunodeficiency

77
Q

ADA deficiency is characterized by a severe lack of

A

B and T lymphocytes

78
Q

Is often fatal, but can be treated with a bone marrow transplant

A

ADA deficiency

79
Q

Removes the ribose group from inosine and guanosine, converting them to their respective nitrogenous bases hypoxanthine and guanosine

A

Purine Nucleoside Phosphorylase (PNP)

80
Q

Interestingly, mutations in PNP result in another subtype of SCID known as PNP deficiency, which is characterized by a

A

T-cell deficiency

81
Q

Predisposes patients to bacterial, viral, and opportunistic infections and commonly presents in childhood

A

PNP deficiency

82
Q

Hypoxanthine and guanine are then degraded to

A

Xanthine

83
Q

Hypoxanthine is converted to Xanthine by the enzyme

A

Xanthine oxidase

84
Q

Guanine is converted to xanthine by the enzyme

A

Guanase

85
Q

These two enzymes serve as the convergence in the degradation of all three purine nucleotides, AMP, GMP, and IMP

A

Xanthine oxidase and guanase

86
Q

Then, Xanthene is converted to

-also catalyzed by xanthene oxidase

A

Uric Acid

87
Q

Deposit throughout the body’s tissues when uric acid levels rise beyond their solubility limit

A

Insoluble crystal of sodium urate

88
Q

This results in a condition known as

A

Gout

89
Q

Characterized by monoarticular, excruciating joint pain, swelling, warmth, redness, and tenderness

A

Gout

90
Q

Gout is directly caused by

A

Hyperuricemi

91
Q

Most commonly affects the first metatarsophalangeal joint, knees, ankles, and wrists

A

Gout

92
Q

Caused from an inborn error in uric acid metabolism, resulting in overproduction of uric acid

A

Primary hyperuricemia

93
Q

Overactive PRPP synthetase, deregulation of PRPP-amido-transferase, and Lesch-Nyahn syndrome all cause

A

Hyperuricemia

94
Q

Prevents salvage, which allows hypoxanthine and guanine to be diverted towards the degrative pathway, increasing uric acid

A

HGPRT deficiency

95
Q

Caused from an accumulation of uric acid due to another disease state such as malignancies, chronic renal insufficiency, G6P deficiency, and use of HCTZ

A

Secondary hyperuricemia

96
Q

Gout is treated with an analog of hypoxanthine that inhibits xanthine oxidase. This medicine is called

A

Allopurinol

97
Q

Serves as a competitive inhibitor of xanthine oxidase

A

Allopurinol

98
Q

Xanthine oxidase converts allopurinol into

-a potent inhibitor of xanthine oxidase

A

Alloxanthine

99
Q

More soluble than uric acid and can be excreted

A

Xanthine and hypoxanthine

100
Q

Plays an important role in the serum s an antioxidant, scavenging highly reactive and harmful oxygen species

-the reason we evolved to excrete uric acid

A

Urate

101
Q

Another mechanism by which allopurinol exerts its effects is by leading to the buildup of

A

Hypoxanthine

102
Q

This hypoxanthine can then be salvaged to produce

A

IMP

103
Q

Serves as an inhibitor of PRPP-amido-transferase, the key enzyme in purine synthesis

A

IMP

GI (59 decks)

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