CHEM 210 MODULE 8 EXAM 2026/2027 | Urea Cycle, ETC &
ATP Synthesis | Geneva College / Portage Learning | Verified
Q&A | Pass Guaranteed - A+ Graded
Q1: Which enzyme catalyzes the rate-limiting step of de novo purine synthesis and
represents a major regulatory point for this pathway?
A. Adenylosuccinate lyase
B. IMP dehydrogenase
C. Glutamine-PRPP amidotransferase [CORRECT]
D. Hypoxanthine-guanine phosphoribosyltransferase (HGPRT)
Correct Answer: C
Rationale: Glutamine-PRPP amidotransferase catalyzes the committed step of purine
synthesis: conversion of PRPP (5-phosphoribosyl-1-pyrophosphate) to
5-phosphoribosylamine. This is the first and rate-limiting step, making it the primary
regulatory site. It is inhibited by AMP and GMP (end-product feedback inhibition) and
activated by PRPP.
● A is incorrect: Adenylosuccinate lyase catalyzes a later step (conversion of
adenylosuccinate to AMP); not rate-limiting.
● B is incorrect: IMP dehydrogenase catalyzes IMP → XMP (branch point toward
GMP synthesis); regulated but not the committed step of the entire pathway.
● D is incorrect: HGPRT is part of the purine salvage pathway, not de novo
synthesis. Mutations cause Lesch-Nyhan syndrome, but this enzyme does not
catalyze the committed step of de novo synthesis.
Clinical correlation: Understanding this regulatory point is crucial for cancer
chemotherapy—inhibitors of this pathway (e.g., 6-mercaptopurine) target rapidly
dividing cells.
,Q2: A patient presents with severe gout and is found to have elevated PRPP levels and
increased de novo purine synthesis. Which enzyme deficiency is most likely
responsible?
A. Xanthine oxidase
B. Hypoxanthine-guanine phosphoribosyltransferase (HGPRT) [CORRECT]
C. Adenosine deaminase
D. Purine nucleoside phosphorylase
Correct Answer: B
Rationale: Partial HGPRT deficiency causes increased PRPP accumulation because less
PRPP is consumed by the salvage pathway. This excess PRPP stimulates
glutamine-PRPP amidotransferase (substrate activation), leading to accelerated de novo
purine synthesis and overproduction of uric acid → gout. Complete HGPRT deficiency
causes Lesch-Nyhan syndrome (gout + neurological symptoms + self-mutilation).
● A is incorrect: Xanthine oxidase deficiency causes xanthinuria (xanthine stones,
not gout) and reduced uric acid production.
● C is incorrect: Adenosine deaminase deficiency causes severe combined
immunodeficiency (SCID); purine metabolism is disrupted but not through this
mechanism.
● D is incorrect: Purine nucleoside phosphorylase deficiency causes T-cell
immunodeficiency with uric acid levels that are low or normal, not elevated.
Clinical correlation: This explains why allopurinol (xanthine oxidase inhibitor)
helps in gout but does not address the root cause in HGPRT deficiency—PRPP
levels remain high.
Q3: Which of the following is a key difference between purine and pyrimidine de novo
synthesis?
, A. Purines are assembled on the ribose sugar; pyrimidines are synthesized as a base
first, then attached to ribose [CORRECT]
B. Both pathways require folate derivatives for C1 transfer
C. Both pathways use PRPP as the initial substrate
D. Both pathways produce UMP as the first nucleotide product
Correct Answer: A
Rationale: This is the fundamental architectural difference between the pathways:
Purines: assembled atom-by-atom on PRPP (ribose first, then base built on it).
Pyrimidines: base (orotate) synthesized first, then attached to PRPP by orotate
phosphoribosyltransferase to form OMP. This difference has therapeutic
implications—pyrimidine synthesis inhibitors target different enzymatic steps.
● B is incorrect: Only purine synthesis requires folate derivatives (10-formyl-THF)
for C1 incorporation at two steps; pyrimidine synthesis does not use folate.
● C is incorrect: While both use PRPP, purines use it as the foundation for
assembly; pyrimidines attach it after base synthesis. The timing and mechanism
differ fundamentally.
● D is incorrect: UMP is the first pyrimidine nucleotide; IMP (inosine
monophosphate) is the first purine nucleotide.
Study tip: Remember: "Purines = Build on Ribose; Pyrimidines = Base First, Then
Ribose"
Q4: The enzyme ribonucleotide reductase is critical for DNA synthesis because it:
A. Converts dUMP to dTMP
B. Synthesizes PRPP from ribose-5-phosphate
C. Converts ribonucleotides to deoxyribonucleotides [CORRECT]
ATP Synthesis | Geneva College / Portage Learning | Verified
Q&A | Pass Guaranteed - A+ Graded
Q1: Which enzyme catalyzes the rate-limiting step of de novo purine synthesis and
represents a major regulatory point for this pathway?
A. Adenylosuccinate lyase
B. IMP dehydrogenase
C. Glutamine-PRPP amidotransferase [CORRECT]
D. Hypoxanthine-guanine phosphoribosyltransferase (HGPRT)
Correct Answer: C
Rationale: Glutamine-PRPP amidotransferase catalyzes the committed step of purine
synthesis: conversion of PRPP (5-phosphoribosyl-1-pyrophosphate) to
5-phosphoribosylamine. This is the first and rate-limiting step, making it the primary
regulatory site. It is inhibited by AMP and GMP (end-product feedback inhibition) and
activated by PRPP.
● A is incorrect: Adenylosuccinate lyase catalyzes a later step (conversion of
adenylosuccinate to AMP); not rate-limiting.
● B is incorrect: IMP dehydrogenase catalyzes IMP → XMP (branch point toward
GMP synthesis); regulated but not the committed step of the entire pathway.
● D is incorrect: HGPRT is part of the purine salvage pathway, not de novo
synthesis. Mutations cause Lesch-Nyhan syndrome, but this enzyme does not
catalyze the committed step of de novo synthesis.
Clinical correlation: Understanding this regulatory point is crucial for cancer
chemotherapy—inhibitors of this pathway (e.g., 6-mercaptopurine) target rapidly
dividing cells.
,Q2: A patient presents with severe gout and is found to have elevated PRPP levels and
increased de novo purine synthesis. Which enzyme deficiency is most likely
responsible?
A. Xanthine oxidase
B. Hypoxanthine-guanine phosphoribosyltransferase (HGPRT) [CORRECT]
C. Adenosine deaminase
D. Purine nucleoside phosphorylase
Correct Answer: B
Rationale: Partial HGPRT deficiency causes increased PRPP accumulation because less
PRPP is consumed by the salvage pathway. This excess PRPP stimulates
glutamine-PRPP amidotransferase (substrate activation), leading to accelerated de novo
purine synthesis and overproduction of uric acid → gout. Complete HGPRT deficiency
causes Lesch-Nyhan syndrome (gout + neurological symptoms + self-mutilation).
● A is incorrect: Xanthine oxidase deficiency causes xanthinuria (xanthine stones,
not gout) and reduced uric acid production.
● C is incorrect: Adenosine deaminase deficiency causes severe combined
immunodeficiency (SCID); purine metabolism is disrupted but not through this
mechanism.
● D is incorrect: Purine nucleoside phosphorylase deficiency causes T-cell
immunodeficiency with uric acid levels that are low or normal, not elevated.
Clinical correlation: This explains why allopurinol (xanthine oxidase inhibitor)
helps in gout but does not address the root cause in HGPRT deficiency—PRPP
levels remain high.
Q3: Which of the following is a key difference between purine and pyrimidine de novo
synthesis?
, A. Purines are assembled on the ribose sugar; pyrimidines are synthesized as a base
first, then attached to ribose [CORRECT]
B. Both pathways require folate derivatives for C1 transfer
C. Both pathways use PRPP as the initial substrate
D. Both pathways produce UMP as the first nucleotide product
Correct Answer: A
Rationale: This is the fundamental architectural difference between the pathways:
Purines: assembled atom-by-atom on PRPP (ribose first, then base built on it).
Pyrimidines: base (orotate) synthesized first, then attached to PRPP by orotate
phosphoribosyltransferase to form OMP. This difference has therapeutic
implications—pyrimidine synthesis inhibitors target different enzymatic steps.
● B is incorrect: Only purine synthesis requires folate derivatives (10-formyl-THF)
for C1 incorporation at two steps; pyrimidine synthesis does not use folate.
● C is incorrect: While both use PRPP, purines use it as the foundation for
assembly; pyrimidines attach it after base synthesis. The timing and mechanism
differ fundamentally.
● D is incorrect: UMP is the first pyrimidine nucleotide; IMP (inosine
monophosphate) is the first purine nucleotide.
Study tip: Remember: "Purines = Build on Ribose; Pyrimidines = Base First, Then
Ribose"
Q4: The enzyme ribonucleotide reductase is critical for DNA synthesis because it:
A. Converts dUMP to dTMP
B. Synthesizes PRPP from ribose-5-phosphate
C. Converts ribonucleotides to deoxyribonucleotides [CORRECT]
