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Assessment 1.3

Nucleotide Metabolism: Purine Metabolism

THe stock of nucleotides is maintained at essentially a constant level by many metabolic pathways Salvage bases from other cellular processes (from scratch)
Synthesize nucleotides directly from amino acids and other precursors
The cell can interconvert between specific nucleotides
The basis for this "fixed" concentration of nucleotides is that de novo synthesis and salvage pathways are very rigidly controlled under normal conditions.
De Novo Purine Sythesis synthesis of the purine nucleotides from other unrelated compounds (scratch)
In practice purines, are synthesized using three components: amino acids (carbon & nitrogen donors), tetrahydrofolate (carbon donor), & carbon dioxide (carbon donor)
occurs entirely in the cytosol
not all cells are capable of de novo purine synthesis (white and red blood cells)
IMP: AMP & GMP are synthesized thru a common intermediate inosine monophosphate- IMP; requires a lot of energy
PRPP Synthesis: de novo synthesis and all savage pathways use a common reactant called phosphoribosylpyrophosphate (PRPP), Highly Regulated- inhibited by other nucleotides
PRA Synthesis: Once PRPP is available, de novo purine synthesis can occur, which begins with the synthesis of 5-phosphoribosylamine (PRA)
Regulation of PRA Synthesis: COMMITTED STEP, IMP must be formed after this step, this enzyme is the rate limiting step for de novo synthesis (can only occur as fast as you make PRA); Highly Regulated, PRPP is an activator; IMP,GMP, & AMP are inhibitos.
There is no regulation of IMP synthesis after this step
IMP Utilization: Conversion of IMP to AMP and GMP is regulated_ each product regulates its own synthesis, AMP inhibits AMP synthesis & GMP inhibits GMP synthesis
Synthesis of AMP from IMP requires GTP as an energy source, Synthesis of GMP from IMP requires ATP as an energy source. This reciprocal arrangement ensure that when there is a sufficient ATP in the cell GMP will be synthesized from IMP and vice versa
GMP Synthesis- nitrogen comes from Glutamine, AMP Synthesis- nitrogen comes from Aspartate
Formation of Purine NTP- are formed from either AMP or GMP by the action of two enzymes, which this stage of synthesis is unregulated
Purine Salvage Biosynthesis Stray purine nucleobases can be reused to give nucleotides , much more energetically favorable than de novo purine sythesis, de novo and salvage parthways are interconnected to provide a near constant amount of nucleotides
Two nucleotides are responsible for purine nucleobase salvage: hypoxanthine-guanine phosphoribosyl transferase (HGPRT) & adenine phosphoribosyl (APRT). Both catalyze the reaction of their respective nucleobases with PRPP to give the nucleotide
HGPRT reacts hypoxanthine or guanine with PRPP, APRT reacts adenine with PRPP
Purine Salvage Regulation Regulated, the products inhibit the pathways, HGPRT is inhibited by IMP & GMP, APR is inhibited by AMP
Use of this pathway inhibits the de novo synthesis pathwa by lowering the level of PRPP, raising the level of purine NTP
Nucleoside Salvage- only the sugar and base no phosphate group specific enzymes, stray purine nucleosides can also be salvaged
Purine Nucleotide Interconversion advantageous for the cell to be able to interconvert between AMP & GMP which occurs indirectly thru IMP
IMP can then be converted thru the de novo pathway to either AMP OR GMP as needed
Interconversion Regulation Interconversion of nucleotides is regulated to maintain a suppply of both
AMP conversion to IMP is inhibited by GTP & GDP but enhanced by ATP
GMP conversion is IMP is strongly inhibited by XMP but increase by GTP
XMP tell that the cell is actively making GMP
Purine Nucleotide Catabolism Catabolism of Purines- the breakdown of purines follows a common path to uric acid; unregulated, nucleases breakdown either DNA or RNA
Guanine Catabolism- guanosine, guanine and xanthine
Adenine Catabolism- look at page 22 of notes
Purine Catabolism- Xanthine is oxidized by xanthine oxidase to give uric acid which is then secreted
Defects in Metabolism Gout- defect in purine metabolism; hyperuricemia- uric acid overproduction & blood and urine concentration are elevated. uric acid is very poorly soluble which causes sodium urate crystals are deposited in joints and in the kidneys
Caused by: increased de novo synthesis and purine catabolism and decrease in purine salvage. Allopurinol is the usual treatment(is a xanthine oxidase and prevents the formation of uric acid)
Lesch Nyhan Syndrome- defect of purine nucleotide salvage, the cause of this disease is a severe or complete deficiency of HGPRT. HGPRT is located on the x chromosome so this disease is exclusively limited to males.
Hyperuricemia can be treated with allopurinol , there is no known treatment for the neurological symptoms
Created by: lisagoette