Neucloetides Metaboilism- week 4 Flashcards

1
Q

Nucloetide vs side

Nucleic acid?

A

Side- sugar and base
Tide- sugar base and phosphate

Nucleic acid- chain of nucloetides

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2
Q

Purines vs Pyridines

A

Purines- A and G

Pyridines- C, U , T

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3
Q

What bases and sugar does DNA use? RNA?

A

DNA- deoxyribose- A, T, C, G

RNA- ribose A, U, C and G

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4
Q

Functions of Nucleotides

A
  1. Building block for DNA and RNA
  2. Energy supply from high energy P-P (ATP and GTP)- quick through hydrolyzation
  3. Coenzymes that have nucleotide portion- NAD, NADP, FAD, CoA
  4. Ingredients for active metabolic precursors
  5. Physiological Mediators- Signal transduction (GTP), cAMP, Adenosine (regulates blood flow),
  6. Allosteric effectos of metabolic enzymes
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5
Q

Source of nucleotide

A
  1. Diet (5%)- plants/animals- anything with cells
  2. De novo synthesis
  3. Salvage from existing bases (majority)- because synthesis purines and pyridines is expensive
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6
Q

Exmaple the digestion of DNA/Nucleic Acids

A

Nucleotides- denatured in the stomach but mostly digested by pancreatic enzymes

Nucleases make oligonucleotides
Phosphodiesterases- mononucleotides
Nucleotidases make nucleosides
Nucelsidases make- base

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7
Q

Absorption of Nucleic Acids

A

Sugars (most absorbed and reused to PPP or channeled to glycolysis) taken up by intestinal mucosal cells and enter circulation

Bases- only 5% enter circulation because mucosal cells degrade them so they are converted to uric acid and excreted. This is why we need salvage and de novo synthesis because we excrete what comes in from diet

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8
Q

Disorders in Nucleotides Metabolism

A

Gout- purine synthesis or degradation

Lesch-nyhan- defecnt in purine salvage

Orotic aciduria- defect in de novo pyriminidine synthesis

CMB agents- drugs that block de novo pathways are successfully used as chemo agents

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9
Q

Rate limiting step of purine de novo snthesis

A

PRPP—glutamine phosphoribosyl amidotransferase–> IMP

Down regulated by IMP, AMP, GMP (downstream products)

upregulated by PEPP

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10
Q

Methotroxeate

A

Acts on steps where formyl THF is needed- this is a component of purine synthesis so this drug stops purine synthesis

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11
Q

What does myochenolic acid do

A

It inhibts IMP DH so does not allo T and B cells to form

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12
Q

What enzyme is regulated in purine degradation? What drug treats it?

A

Xanthine Oxidase- this enzyme can take electrons nad protons to the electron transport chain and is the one means of energy from purine degradation

Can be inhibited by allopurinol and this drug is given to ppl who have accumulation of uric acid because hypoxanthine and xanthine are easier to excrete

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13
Q

Consequences of gout

Treatments

A

Acute inflmmation and kidney stones

Colchicine- acts on leukocytes and tappers down inflmmatio doesn’t solve the main problem

Urisouric acid- help promote excretion of uric acid

Alloputurinol- inhibit xanthineoxidase which decrease the amount of uric acid produce and allow purines to be secreted as hypoxanthine and xanthine

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14
Q

What two enzymes are important in the salvage pathway

A

HGRTase and APRTase

Hypoxanthine– HGRTase—> IMP

Gaunine— HRGTase–> GMP

Adenine— APRTase–> AMP

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