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Nucleotide Metabolism I Flashcards

(103 cards)

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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
What are the 5 contributors toward making the purine ring of IMP?
CO2, Aspartate, Glycine, Glutamine, and THF
26
Essential for the synthesis of purines
THF
27
Humans create THF by modifying
Dietary folic acid
28
Dietary Folic acid is converted to dihydrofolate (DHF) and then to THF by the enzyme
DHF Reductase (DHFR)
29
Inhibit DHFR, thereby stifling nucleotide synthesis and killing rapidly growing tumores
Chemotherapeutic agents such as aminopterin and methotrexate
30
Another DHFR inhibitor. Binds much more strongly to bacterial DHFR, making it an effective antibiotic
Trimethoprim
31
Unlike humans, who rely on dietary folic acid, bacteria synthesize their own folate from a molecule called
PABA
32
Antibiotics structurally similar to PABA, which competitively inhibit folic acid synthesis in bacteria
The Sulfonamides
33
IMP is committed to becoming either
AMP or GMP
34
The conversion process of IMP to either AMP or GMP requires
2 steps
35
Required for the conversion of IMP to adenylosuccinate
GTP and aspartate
36
The enzyme which converts IMP to adenylosuccinate is inhibited by
AMP
37
In a second reaction, adenylosuccinate is converted to AMP, a process which results in the release of
Fumarate
38
IMP is converted to the intermediate XMP by the enzyme IMP dehydrogenase. This requires
NAD+
39
IMP dehydrogenase is inhibited by
GMP
40
Required for the conversion of XMP to GMP
ATP and glutamine
41
An antiviral used to treat hepatitis C that also inhibits IMP dehydrogenase
Ribavirin
42
Depletes intracellular pools of guanine nucleotides
Ribavirin
43
The synthesis of AMP and GMP are regulated by
Feedback inhibition
44
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
Reciprocity
45
Required to convert IMP to AMP
GTP
46
Required to convert IMP to GMP
ATP
47
In step 5 of purine synthesis, AMP and GMP are phosphorylated by
Nucleoside monophosphate kinases
48
This phosphorylation produces
ADP and GDP
49
ADP and GDP are further phosphorylated by nucleoside diphosphate kinase to create
ATP and GTP
50
Has a broad specificity for all nucleotide diphosphates
Nucleoside diphosphate kinase
51
Takes advantage of the fact that free-floating bases including adenine, guanine, and hypoxanthine are present in the cell from other metabolic pathways
Purine salvage pathway
52
The nitrogenous base of IMP
Hypoxanthine
53
Simply attaches a preformed purine base to the PRPP backbone
Purine salvage pathway
54
Converts adenine to AMP in the purine salvage pathway
Aenine Phosphoribosyl Transferase (APRT)
55
Recognizes both guanine and hypoxanthine as substrates to catalyze the formation of GMP and IMP respectively
Hypoxanthine-Guanine Phosphoribosyl Transferase (HGPRT)
56
A disease caused by the deficiency of HGPRT
Lesch-Nyhan Syndrome
57
An X-linked congenital defect that results in neurological deficits including spasticity, mental retardation, aggression, and self-mutilation
Lesch-Nyhan Syndrome
58
The biochemical basis for the neurological symptoms is thought to be due to insufficient cell supplies of
GTP
59
Relies much more heavily on the salvage pathway for the synthesis of nucleotides
Brain tissue
60
Consequently, Lesch-Nyhan Syndrome patients have a neuronal deficiency of
GMP
61
Thought to be involved in a number of cell signaling pathways that may be involved in the developmental process of dopaminergic neurons
GTP
62
This may explain why patients with Lesch-Nyhan have fewer
Dopaminergic nerves
63
GTP is also a precursor for tetrahydropterin, which is a cofactor in the biosynthesis of
Dopamine
64
The HGPRT deficiency results in increased levels of
PRPP
65
The increased levels of PRPP increases
De novo purine biosynthesis
66
This is because PRPP is an activator of
PRPP-amido-transferase
67
One additional problem of patients with Lesch-Nyhan syndrome is that they have excess buildup of
Uric acid (results in gout)
68
A deficiency of HGPRT leads to increased levels of the enzymes substrates
Hypoxanthine and Guanine
69
Without salvage, these purine bases are destined to become
Uric acid
70
What is step 1 of the degradation of purines to uric acid?
The phosphate is removed
71
Removes the phosphate group from AMP, GMP, and IMP resulting in the formation of adenosine, guanosine, and inosine respectively
A 5' nucleosidase
72
There is also a pathway for the direct conversion of AMP to IMP via the enzyme
AMP deaminase
73
In step two of the degradation of AMP to uric acid, adenosine is converted to
Inosine
74
Converts adenosine to inosine
Adenosine Deaminase (ADA)
75
This reaction serves as a point of convergence in the degredation of both AMP and IMP
Conversion of adenosine to inosine
76
A deficiency of the enzyme ADA results in a subtype of
Severe Combined Immunodeficiency
77
ADA deficiency is characterized by a severe lack of
B and T lymphocytes
78
Is often fatal, but can be treated with a bone marrow transplant
ADA deficiency
79
Removes the ribose group from inosine and guanosine, converting them to their respective nitrogenous bases hypoxanthine and guanosine
Purine Nucleoside Phosphorylase (PNP)
80
Interestingly, mutations in PNP result in another subtype of SCID known as PNP deficiency, which is characterized by a
T-cell deficiency
81
Predisposes patients to bacterial, viral, and opportunistic infections and commonly presents in childhood
PNP deficiency
82
Hypoxanthine and guanine are then degraded to
Xanthine
83
Hypoxanthine is converted to Xanthine by the enzyme
Xanthine oxidase
84
Guanine is converted to xanthine by the enzyme
Guanase
85
These two enzymes serve as the convergence in the degradation of all three purine nucleotides, AMP, GMP, and IMP
Xanthine oxidase and guanase
86
Then, Xanthene is converted to -also catalyzed by xanthene oxidase
Uric Acid
87
Deposit throughout the body's tissues when uric acid levels rise beyond their solubility limit
Insoluble crystal of sodium urate
88
This results in a condition known as
Gout
89
Characterized by monoarticular, excruciating joint pain, swelling, warmth, redness, and tenderness
Gout
90
Gout is directly caused by
Hyperuricemi
91
Most commonly affects the first metatarsophalangeal joint, knees, ankles, and wrists
Gout
92
Caused from an inborn error in uric acid metabolism, resulting in overproduction of uric acid
Primary hyperuricemia
93
Overactive PRPP synthetase, deregulation of PRPP-amido-transferase, and Lesch-Nyahn syndrome all cause
Hyperuricemia
94
Prevents salvage, which allows hypoxanthine and guanine to be diverted towards the degrative pathway, increasing uric acid
HGPRT deficiency
95
Caused from an accumulation of uric acid due to another disease state such as malignancies, chronic renal insufficiency, G6P deficiency, and use of HCTZ
Secondary hyperuricemia
96
Gout is treated with an analog of hypoxanthine that inhibits xanthine oxidase. This medicine is called
Allopurinol
97
Serves as a competitive inhibitor of xanthine oxidase
Allopurinol
98
Xanthine oxidase converts allopurinol into -a potent inhibitor of xanthine oxidase
Alloxanthine
99
More soluble than uric acid and can be excreted
Xanthine and hypoxanthine
100
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
Urate
101
Another mechanism by which allopurinol exerts its effects is by leading to the buildup of
Hypoxanthine
102
This hypoxanthine can then be salvaged to produce
IMP
103
Serves as an inhibitor of PRPP-amido-transferase, the key enzyme in purine synthesis
IMP

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