1. Which enzyme is the rate-limiting step of ketogenesis?
Mitochondrial HMG-CoA synthase
Explanation
Mitochondrial HMG-CoA synthase is the rate-limiting enzyme of ketogenesis. Thiophorase is instead required for ketolysis in extrahepatic tissues.
Mitochondrial HMG-CoA synthase
Explanation
Mitochondrial HMG-CoA synthase is the rate-limiting enzyme of ketogenesis. Thiophorase is instead required for ketolysis in extrahepatic tissues.
DNA polymerase can extend DNA only in the 5′→3′ direction on an antiparallel template
Explanation
Because the template strands are antiparallel and synthesis proceeds 5′→3′, the lagging strand must be made discontinuously as Okazaki fragments.
Pyruvate to acetyl-CoA, CO₂, and NADH
Explanation
The pyruvate dehydrogenase complex irreversibly converts pyruvate into acetyl-CoA, CO₂, and NADH in the mitochondrial matrix. Its irreversibility distinguishes it from many reversible downstream metabolic reactions.
They lack mitochondria needed for oxidative metabolism
Explanation
Red blood cells lack mitochondria, so they depend on anaerobic glycolysis and convert pyruvate to lactate.
At the enzyme’s active site
Explanation
The substrate is the substance acted on by an enzyme and binds specifically at its active site. An allosteric regulator binds at a different site.
PDH kinase is activated, phosphorylating and inhibiting PDH
Explanation
High ATP, NADH, and acetyl-CoA activate PDH kinase, which phosphorylates and inhibits the pyruvate dehydrogenase complex when energy is abundant. Dephosphorylation, not phosphorylation, activates PDH.
G6P to G1P, G1P to UDP-glucose, and UDP-glucose to glycogen
Explanation
Glycogenesis proceeds from G6P to G1P, then to UDP-glucose, which is incorporated into glycogen. The enzymes involved are phosphoglucomutase, UDP-glucose pyrophosphorylase, and glycogen synthase.
The cycle includes citrate, isocitrate, α-ketoglutarate, succinyl-CoA, succinate, fumarate, malate, and regenerated oxaloacetate
Explanation
The eight TCA intermediates are citrate, isocitrate, α-ketoglutarate, succinyl-CoA, succinate, fumarate, malate, and oxaloacetate, with oxaloacetate regenerated at the end.
α(1→4) bonds in linear chains and α(1→6) bonds at branch points
Explanation
Glycogen is a highly branched glucose-storage polymer with α(1→4) linkages in its linear chains and α(1→6) linkages at branch points.
One acetyl-CoA, one NADH, and one FADH₂
Explanation
Every β-oxidation cycle produces one acetyl-CoA, one NADH, and one FADH₂. These products subsequently contribute to the citric acid cycle and oxidative phosphorylation.
Converting toxic ammonia into urea for renal excretion
Explanation
The urea cycle detoxifies ammonia by converting it into urea, mainly in the liver; urea then travels in blood to the kidneys and urine.
Pyruvate carboxylase uses ATP and biotin in mitochondria, whereas PEP carboxykinase uses GTP
Explanation
Pyruvate carboxylase is a mitochondrial, biotin-dependent enzyme that uses ATP and is activated by acetyl-CoA. PEP carboxykinase uses GTP.
RNA polymerase II
Explanation
In eukaryotes, RNA polymerase II produces the precursor to mRNA. Polymerase I produces major rRNAs, while polymerase III produces tRNA and 5S rRNA.
Muscle lacks glucose-6-phosphatase, so its glycogen-derived glucose is used within muscle
Explanation
The liver can release glucose into the blood, but muscle lacks glucose-6-phosphatase. Therefore, muscle glycogen primarily supplies energy for muscle itself.
DNA polymerase III performs main synthesis and proofreading, while DNA polymerase I removes RNA primers
Explanation
In bacteria, DNA polymerase III carries out most DNA synthesis and proofreading, whereas DNA polymerase I removes RNA primers and fills the resulting gaps.
Vitamin A deficiency
Explanation
Night blindness is the early deficiency sign associated with vitamin A. Vitamin D deficiency is associated with rickets or osteomalacia.
Vitamin K—carboxylation of clotting factors; vitamin B1—TPP
Explanation
Vitamin K is required for carboxylation of clotting factors, while the active form of vitamin B1 is thiamine pyrophosphate (TPP).
Reduced NADPH limits glutathione regeneration, increasing oxidative damage to red blood cells
Explanation
G6PD deficiency lowers NADPH production, which reduces regeneration of reduced glutathione and weakens antioxidant protection. Oxidant drugs can therefore trigger oxidative damage and hemolysis, especially in red blood cells.
A cytosolic pathway of 10 reactions that converts glucose into two pyruvate molecules
Explanation
Glycolysis occurs in the cytosol and consists of 10 reactions that convert one six-carbon glucose molecule into two three-carbon pyruvate molecules.
Acetoacetate, β-hydroxybutyrate, and acetone
Explanation
The three ketone bodies are acetoacetate, β-hydroxybutyrate, and acetone.
DNA glycosylase removes the abnormal base, AP endonuclease cuts the AP site, and DNA polymerase and ligase complete repair
Explanation
Base excision repair begins with DNA glycosylase removing the abnormal base, followed by AP endonuclease cleavage and gap filling and sealing by DNA polymerase and ligase.
Nucleotide excision repair
Explanation
Xeroderma pigmentosum results from defective nucleotide-excision repair, impairing removal of UV-induced lesions and increasing UV sensitivity and skin-cancer risk.
5′→3′
Explanation
DNA polymerases synthesize DNA in the 5′→3′ direction while reading the antiparallel template strand.
Increasing the concentration of substrate
Explanation
A competitive inhibitor occupies the active site, so increasing substrate concentration can help the substrate outcompete the inhibitor. Noncompetitive inhibition occurs at another site and reduces catalytic activity.
Fat-soluble vitamins include A, D, E, and K and are stored more readily, increasing toxicity risk
Explanation
Vitamins A, D, E, and K are fat-soluble, stored in liver or adipose tissue, and carry greater toxicity risk. The B-complex vitamins and vitamin C are water-soluble.
Ammonia, aspartate, and CO₂ or HCO₃⁻
Explanation
One nitrogen comes from ammonia, the second from aspartate, and the carbon enters from CO₂ or HCO₃⁻.
Phosphofructokinase-1
Explanation
PFK-1 is the major regulatory and rate-limiting enzyme of glycolysis, and ATP inhibits it. Hexokinase catalyzes the first step but is not the principal regulatory enzyme described here.
Frameshift mutation
Explanation
An insertion or deletion not in a multiple of three shifts the reading frame, making it a frameshift mutation. Silent, missense, and nonsense mutations describe different effects on codons or amino acids.
CPS-I, OTC, argininosuccinate synthetase, argininosuccinate lyase, arginase
Explanation
The urea-cycle enzymes are CPS-I, ornithine transcarbamoylase, argininosuccinate synthetase, argininosuccinate lyase, and arginase, in that order.
The enzyme increases reaction rate without being consumed, while the substrate is converted into product
Explanation
An enzyme acts as a biological catalyst and is not consumed, whereas the substrate is acted upon and converted into product.
It stimulates glycolysis and opposes gluconeogenesis
Explanation
Increased fructose-2,6-bisphosphate stimulates glycolysis, whereas decreased levels stimulate gluconeogenesis.
They use the carnitine shuttle, and malonyl-CoA inhibits CPT-I
Explanation
Long-chain fatty acids require the carnitine shuttle to cross into the mitochondrial matrix. Malonyl-CoA inhibits CPT-I, limiting fatty-acid entry during fatty-acid synthesis.
The oxidative phase is irreversible and produces two NADPH per glucose-6-phosphate
Explanation
The oxidative phase is irreversible and generates two NADPH molecules per glucose-6-phosphate. The non-oxidative phase is the reversible portion of the pathway.
TPP, lipoic acid, CoA, FAD, and NAD⁺
Explanation
The five PDH cofactors are thiamine pyrophosphate, lipoic acid, CoA, FAD, and NAD⁺. The other choices substitute cofactors used by different enzymes or pathways.
Fatty-acid oxidation raises acetyl-CoA while oxaloacetate is diverted to gluconeogenesis
Explanation
During fasting, fatty-acid oxidation produces abundant acetyl-CoA, while oxaloacetate is used for gluconeogenesis, favoring ketone-body formation in the liver.
2 ATP, 2 NADH, and 2 pyruvate
Explanation
The net products of glycolysis per glucose are 2 ATP, 2 NADH, and 2 pyruvate.
It synthesizes RNA from DNA in the 5′→3′ direction without requiring a primer
Explanation
Transcription produces an RNA molecule from a DNA template in the 5′→3′ direction, and RNA polymerase initiates synthesis without a primer.
CPS-I uses two ATP and is activated by N-acetylglutamate; OTC deficiency is X-linked and most common
Explanation
CPS-I uses 2 ATP and requires activation by N-acetylglutamate. OTC deficiency is the most common inherited urea-cycle disorder and is X-linked.
Nucleotide excision repair
Explanation
Nucleotide excision repair removes bulky DNA lesions, including UV-induced thymine dimers. Base excision repair instead removes individual abnormal bases.
It forms glucose from non-carbohydrate precursors
Explanation
Gluconeogenesis is the formation of glucose from non-carbohydrate precursors, occurring mainly in the liver and to a lesser extent in the kidney. Glycolysis, in contrast, breaks glucose down.
Pyruvate to PEP, fructose-1,6-bisphosphate to fructose-6-phosphate, and glucose-6-phosphate to glucose
Explanation
Gluconeogenesis bypasses three irreversible glycolytic steps: pyruvate to PEP, fructose-1,6-bisphosphate to fructose-6-phosphate, and glucose-6-phosphate to glucose.
A 7-methylguanosine cap is added to the 5′ end, a poly-A tail to the 3′ end, and introns are removed by splicing
Explanation
The 5′ cap contains 7-methylguanosine, the poly-A tail is added at the 3′ end after the AAUAAA signal, and splicing removes introns while retaining exons.
The liver lacks thiophorase, and red blood cells lack mitochondria
Explanation
The liver cannot perform ketolysis because it lacks thiophorase, while red blood cells cannot use ketone bodies because they have no mitochondria.
Skin D3 to liver 25-hydroxy-D to kidney 1,25-dihydroxy-D
Explanation
Vitamin D is activated sequentially in the skin, liver, and kidney, producing calcitriol, or 1,25-dihydroxy-D, in the kidney.
An active enzyme consisting of an apoenzyme and its required cofactor or coenzyme
Explanation
A holoenzyme is the active form made of an apoenzyme together with its necessary cofactor or coenzyme. The apoenzyme alone is inactive.
Succinate dehydrogenase
Explanation
Succinate dehydrogenase is the only TCA-cycle enzyme that produces FADH₂. Malate dehydrogenase and several other dehydrogenases produce NADH instead.
In the mitochondrial matrix, where it supports oxidation of carbohydrates, fats, and amino acids
Explanation
The TCA cycle occurs in the mitochondrial matrix and serves as a central pathway for the oxidation of carbohydrate, fat, and amino-acid carbon skeletons.
Dehydrogenation producing FADH₂, hydration, oxidation producing NADH, and thiolysis producing acetyl-CoA
Explanation
Each β-oxidation cycle proceeds through dehydrogenation with FADH₂ production, hydration, a second oxidation with NADH production, and thiolysis yielding acetyl-CoA.
Helicase unwinds the DNA double helix
Explanation
Helicase separates the DNA strands. Primase makes the RNA primer, topoisomerase relieves supercoiling, and SSB proteins prevent strand reannealing.
NADPH and ribose-5-phosphate
Explanation
The cytosolic pentose phosphate pathway produces NADPH and ribose-5-phosphate. Unlike glycolysis, its defining products are not a net ATP yield and NADH.
Memorize the answers with 86 flashcards on Biochemistry Master Exam Review.
What is an enzyme?
A biological catalyst that increases reaction rate without being consumed.
What is the substrate in enzyme catalysis?
The substance acted on by an enzyme.
Where does the substrate bind on an enzyme?
At the enzyme’s active site.
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