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Biochemistry > Nucleotides > Flashcards

Nucleotides Flashcards

1
Q

Purine salvage pathway is mediated by how many enzymes , name them

A

2 ,
APRTase HGPRTase

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2
Q

Committed step of de novo purine synthesis in

A

Reaction catalyzed by amidotransferase

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3
Q

What is xanthine oxidase

A

A metalloflavoprotein containing FAD , molybdenum,iron

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4
Q

Allopurinol inhibits what

A

Xantine oxidase

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5
Q

Allopurinol inhibiting xanthine oxidase is example of

A

Suicide inhibitoion

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6
Q

End product of purine catabolism is , and it’s normal level in the serum

A

Uric acid , 3-7mg/dL

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7
Q

A condition when serum level of uri acid is not normal

A

Gout (increased)

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8
Q

What causes tophi

A

Uric acid acid crystals accumulated in the cooler parts of the body

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9
Q

What’s tophi

A

A deposit if crystalline uric acid or substances , at the surface of skin , joint ,cartilage

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10
Q

Lesh -Nyhan syndrome is

A

x linked inherited
disorder Of purine metabolism
Due to deficiency of HGPRTase
Characterized by self-mutilation tendency

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11
Q

Adenosine deaminase deficiency has been treated by

A

gene replacement therapy

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12
Q

Why’s can we consider that Salvage and de novo are closely related

A

Substrate /starting material is the same , PRPP

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13
Q

Free purines are salvaged by how many enzymes , name then

A
  1. : APRTase
    HGPRTase
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14
Q

Tissues where only salvage and no denovo takes place

A

Brain , RBCs

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15
Q

The salvage pathway economize

A

Intercellular energy expenditure

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16
Q

The step one in de novo synthesis is catalyzed by what and inhibited by what

A

Catalyzed by amino-transferase
Inhibited by AMP , GMP

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17
Q

In the regulation on purine synthesis what acts as allosteric modifiers and how

A

AMP , GMP
binds to the enzyme converts monomeric active form to dimeric inactive form
AMP , GMP bind to same molecule at different sites ,act synergistically

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18
Q

Which molecules inhibit their own formation and how

A

AMP & GMP
By feedback inhibition of adenylsuccinate synthetase and IMP dehydrogenase

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19
Q

How is AMP formed

A

From IMP requiring GTP
GTP formation requires ATP

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20
Q

How are GTP& ATP , Made available in sufficient quantities

A

AMP formation requires GTP
GMP requires ATP

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21
Q

Another regulatory factor in purine synthesis

A

Availability of PRPP
Activity of PRPP synthetase is regulated by negative modifiers , purine and pyrimidine nucleotides

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22
Q

Conversion of IMP to GMP enzymes involved

A

IMP dehydrogenase
Amino transferase

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23
Q

Specific clinical syndromes are produced in salvage pathway when

A

Absence of enzymes

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24
Q

What is step 0 or preparatory step in de novo synthesis

A

PRPP synthesis

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25
Q

What is the function of PRPP in de novo

A

Ribose-5-phosphate donor

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26
Q

Ribose -5-phosphate +ATP ——->

A

prpp +ADP

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27
Q

Other functions of prpp, other than de novo

A

Salvage , synthesis of pyrimidines nucleotides , nucleotide coenzymes

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28
Q

Why is prpp synthesis no considered a step in de novo synthesis

A

Common for synthesis of pyrimidine nucleotides , nucleotide coenzymes and salvage pathway

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29
Q

The number of ATP required for the synthesis of one molecule of purine nucleotide

A

6 ATP

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30
Q

Rate limiting step in de novo synthesis

A

First step

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31
Q

What inhibits step 4 of de novo

A

Azaserine , a anti cancer drug

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32
Q

What is inhibited by 6- mercaptopurine , an anti cancer drug

A

IMP to AMP

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33
Q

How is AMP produced .?

A

Amination of IMP

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34
Q

Number of steps to convert IMP to GMP

A

Two

35
Q

Explain the steps to convert IMP - GMP

A

1.oxidation of IMP to XMP (Xanthosine monophosphate / xanthylic acid ).
By NAD+ dependent dehydrogenase
2. An amino transferase transfers NH2 group from glutamine to XMP to form GMP
ATP is hydrolysed to AMP in this level

Both AMP &GMP can be converted to di-, triphisphates

36
Q

No.of steps in de novo synthesis pathway

A

10

37
Q

How are the enzymes in denovo arranged

A

Multi enzyme complex in eukaryotic cells
Arrangement increases efficiency

38
Q

Different sources involved in the formation of Purine ring

A

Glycine
Methenyl THFA
Formyl THFA
Amide N of glutamine
Amino group of aspartate

39
Q

Why are humans called prototrophs

A

Synthesize purine and pyrimidine bases de novo

40
Q

Which tissues does purine synthesis occur in and which organelle

A

Most tissues , major site is liver .
In cytoplasm

41
Q

Steps in de novo synthesis that require atp

A

Steps 1 ,3 ,5 ,6, 7, 8

42
Q

Endproduct of purine nucleotide metabolism .
This degrading takes place mainly in the

A

Uric acid (urate)
In liver

43
Q

Most common abnormality of elevation of Utica acid level in blood

A

Hyperuricemia

44
Q

The relation between gout and alcohol

A

Alcohol contains purine and it also increase the metabolism of purine to uric acid .
Alcohol lead to accumulation of alcohol

45
Q

The main metabolic abnormality in patients with gout

A

An increased cellular pool of PRPP, substrate for rate limiting step

46
Q

Gout is due to a defect in

A

PRPP synthetase
HGPRT
glucose 6 phosphatase

47
Q

Most common abnormality caused by a disorder of purine metabolism

A

Hyperuricemia
Elevation of Uric acid level in blood . Serum Uric acid concentration exceeding 7mg/dL in male , 6 in female .
May or not be associated with uricosuria

48
Q

Reason for manifestation of Hyperuricemia

A

Low solubility of Uric acid in water . At 30°C solubility is lowered to 4.5 mg/d
L
Therefore Uric acid is deposited in cooler areas of the body to cause tophi .
Tophi is seen in distal joints of foot .

49
Q

The main metabolic abnormality in patients with gout

A

is an increased cellular pool of PRPP. The resultant activity of amino transferase lead to excess production of nucleotides resulting in Hyperuricemia

50
Q

What is gout due to

A

Accumulation of urate crystals in the synovial fluid resulting in the inflammation leading to acute arthritis .

51
Q

Causes of primary gout

A

5-phosphoribosyl amido transferase
Abnormal PRPP synthetase - higher Vmax which leads to increased production of PRPP
Deficiency of enzymes of salvage pathway
G6Pase deficiency

52
Q

von Gierke’s disease

A

Glycogen storage disease due to G6Pase enzyme deficiency .
G6P cannot be converted to glucose .
More glucose is channeled into pentose phosphate shunt pathway ,
increased availability of ribose 5 phosphate .
Increased formation of PRPP
It causes primary gout

53
Q

How does deficiency of enzymes in salvage pathway cause primary gout

A

Reactions which consume PRPP and produce more nucleotides which inhibit the enzyme (salvage pathway )

54
Q

Causes of secondary Hyperuricemia

A

*Increased production of Uric acid
*reduced excretion rate

55
Q

When can increased production of Uric acid be seen (leading to 2°) Hyperuricemia ?

A

i. Rapidly growing malignant tissues (leukaemia , lymphomas , polycythemia )
ii.also in cancer patients on radiotherapy or chemotherapy (tumour lysis syndrome )due to increased cell turnover .
Patients are given allopurinol to decrease Uric acid levels . Rasburicase (urate oxidase ) is also found effective .
iii.increased tissue damage due to trauma and raised rate of catabolism as in starvation

56
Q

Reduced excretion rate leading to 2° Hyperuricemia

A
  1. Renal failure
    2.Treatment with thiazide diuretics which inhibit tubular secretion of Uric acid
  2. Lactic acidosis and keto acidosis due to inference with tubular secretion
57
Q

Gouty attacks maybe precipitated by

A

A high purine diet and increased intake of alcohol
Alcohol lead to accumulation of lactic acid .

58
Q

A typical gouty arthritis affects the

A

first metatarsophalangeal joint (big toe) , may affect other joints . Joints in general painful .
Synovial fluid show birefringent urate crystals .

59
Q

The total urate pool in normal , gout with tophi and without is

A

Normal - 1200 mg
Without tophi - 3000 mg
With tophi - 30000 mg

60
Q

Chronic cases of gout , the swellings are composed of what ?

A

Sodium urate
UA get deposited around joints causing swelling composed of

61
Q

Where else do urate crystals deposit in chronic gout

A

In renal medulla , progresses to urolithiasis and renal damage .
May cause deposition in UT leading to calculi or stone formation with renal damage

62
Q

Treatment of gout / reduce urate

A

1.reduce purine intake , alcohol
2. Increase renal excretion by URICOSURIC DRUGS,
3. Reduce production by allopurinol hypoxanthine analog .
4. Colchicine , an anti inflammatory agent very useful to arrest arthritis in gout
5. Use of PEG (Polyethylene glycol ) uricase and conversion of Uric acid to allatonin ( more water soluble ) easily excreted .
Also tried as therapeutic measure to reduce body uric acid pool .

63
Q

Function of uricosuric drugs

A

Decrease the reabsorption of Uric acid from kidney tubules . Eg: probenecid

64
Q

Allopurinol and it’s use I’m reducing urate production

A

*An analog of hypoxanthine.
*Competitive inhibitor of xanthine oxidase , decrease formation of Uric acid .
*xanthine and hypoxanthine are more soluble - excreted more easily
* xanthine oxidase converts allopurinol to alloxanthine(more effective inhibitor of xaox
Suicide inhibition

65
Q

Allopurinol was synthesised by

A

Ellion and hitchings

66
Q

Lesch nyhan syndrome

A
  • X linked inherited disorder of purine metabolism
  • different mutations in HGPRTase gene identified
    *Incidence 1 in 10k
  • deficiency of HGPRTase
  • rate of salvage decreased resulting in accumulation of PRPP , decreased level of inhibitory purine nucleotides .
    Allopurinol is used in treatment , since salvage in deficient , effective only to inhibit xanthine oxidase
67
Q

Lesch x nyhan syndrome is characterised by

A

Self mutilation
Mental retardation
Excessive Uric acid
Nephrolithiasis ( kidney stone )

68
Q

What does the neurological manifestations of lesch-nyhan suggest

A

Brain depends on salvage pathway for the requirements of IMP , GMP

69
Q

Name a hypouricemic condition

A

ADA adenosine deaminase deficiency

70
Q

ADA Deficiency

A

*Severe immunodeficiency,both T and B cells deficient
*inherited autosomal recessive
* ADA deficiency leads to accumulation of
Adenosine and dATP - - inhibit further production of precursors of precursor for DNA synthesis especially dCTP
* lymphocytes usually contain high levels of ADA
Reduced lymphocytes-common manifestation
*this leads to impaired C i and hum oral immunity

71
Q

Xanthine oxidase deficiency

A

Genetic defect
Characterised by hypouricemia, increased excretion of hypoxanthine , xanthine and liver damage .

72
Q

Treatment ADA

A

Antibiotics and periodic injections of immunoglobulin - live saving
Weekly intra muscular injections of bovine ADA = beneficial
Bone marrow stem cells will increase both B and T cells
First successful gene replacement therapy tried in this

73
Q

Purine nucleotide phosphorylase deficiency produces

A

immune deficiency but only B cell function in affected

74
Q

Other functions of ADA

A
  • rapid diagnosis of tuberculosis
    *ADA estimation csf is used for diagnosis of TB meningitis
  • ADA levels estimated in various body fluids like blood , CSF , pleural fluid , pericardial fluid , ascitic fluid
    Cut off value for CSF is 10.0 U/L , other fluids 60 U/L
    *EXTRA pulmonary TB diagnose by pleural or as it’s fluid
75
Q

Normal blood level of Uric acid ranges

A

2-5 mg/dL in females
3-7 mg/dL in males
UA is sparingly soluble in water , an antioxidant .
Nucleic acid content is more in non-veg diet

76
Q

Normal daily excretion of Uric acid

A

500- 700 mg

77
Q

First enzyme in purine synthesis by de novo

A

Phospho ribosyl amido transferase

78
Q

What would affect the reactions involving one carbon group transfers

A

Folate antagonists (methotrexate)

79
Q

Other synthetic nucleotide analogs used as anti cancer agents

A

6-thio guanine and 8- aza guanine

80
Q

A glutamine antagonist that inhibits reactions involving glutamine ( step 1 and 4)

A

Azaserine ( diazoacetyl-L- serine )

81
Q

Useful anti cancer drugs that are analogs as purine synthesis inhibitors

A

Competitive inhibitors of naturally occurring nucleotides ,
Utilized to synthesise DNA , such DNA functionally inactive , cell division arrested
*mercaptopurine
*folate antagonists (methotrexate)
*azserine (diazoacetyl-L- serine)
* 6-thio guanine, 8- aza guanine

82
Q

Caffeine

A

*trimethyl derivative of xanthine
* inhibits phosphodiesterase causes prolonged action of cyclic AMP and increases the activity of hormone sensitive lipase
* enhances the effect of epinephrine on glycogenolysis

83
Q

Degradation of purine nucleotides take solace mainly in

A

Liver

Biochemistry (10 decks)

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