Questions:

1. The enzyme of glycolysis that converts dihydroxyacetone phosphate to glyceraldehyde-3-phosphate can be categorized into one of six types of enzymes. This enzyme is most appropriately called a(n):
  1. Oxidoreductase
  2. Transferase
  3. Hydrolase
  4. Lyase
  5. Isomerase
2. Diisopropylphosphofluroridate and sarin are mechanism based inhibitors. They form:
  1. Weak bonds with enzymes like xanthine oxidase
  2. Hydrogen bonds with enzymes like acetylcholinesterase
  3. Van Der Waals bonds with cyclooxygenase
  4. Covalent bonds with enzymes like xanthine oxidase
  5. Covalent bonds with enzymes like acetylcholinesterase
3. On the following plot, N represents the curve for an allosteric enzyme with no allosteric activators or inhibitors added. If an allosteric activator was added, which curve would one obtain?
  1. Curve A
  2. Curve B
  3. Curve C
  4. Curve D
Five possible curves for an allosteric activator added to an allosteric enzyme.

4. This small protein can have dramatic effects on the activities of enzymes in response to changes in intracellular calcium ion concentration:
  1. Calcitonin
  2. Calsequesterin
  3. Calmodulin
  4. Calcitriol
  5. Calciferol
5. Pennicillin inhibits a vital enzyme step in bacterial growth. It is highly specific for the enzyme and binds the active site very tightly because:
  1. is a Machaelis-Menten substrate
  2. it resembles the transition state
  3. it is a pure carbohydrate
  4. it is an positive allosteric modifier of the enzyme
  5. it contains two fatty acids where the enzyme has two charged aspartate residues
6. In the liver, most ingested ethanol is initially converted to which compound and by which enzyme, respectively?

  1. acetone, alcohol dismutase
  2. methanol, alcohol kinase
  3. acetaldehyde, alcohol dehydrogenase
  4. ketone bodies, NADH
  5. thiamine, thiamin pyrophosphate
7. Dennis "the menace" Veere ingested the insecticide malathion. His symptoms of salivating, tearing, sweating, and defecating were caused specifically by the organophosphate toxin binding to which of the following?
  1. Prostaglandins
  2. Smooth muscle cell membranes
  3. Neurotransmitters
  4. Hexokinases
  5. Acetylcholinesterases
8. Allopurinol is a drug used to treat gout. It acts as a suicide inhibitor of which of the following?
  1. Hypoxanthine
  2. Glycopeptidyl transpeptidase
  3. Uric acid
  4. Xanthine oxidase
  5. Guanine
9. Which of the following statements about allosteric enzymes is CORRECT?
  1. The binding of substrate to any active site affects the other active sites
  2. The plot of initial velocity vs. substrate concentration is a straight line
  3. The Keq of the reaction is increased when allosteric activator is bound
  4. The enzymes contains only one polypeptide chain
  5. Allosteric activators bind to all active sites equally

10. The most likely effect of a non-competitive inhibitor on an Michaelis-Menten enzyme is to
  1. Increase the Vmax
  2. Decrease the Vmax
  3. Increase both the Vmax and the Km
  4. Decrease both the Vmax and the Km
  5. Shift the curve to the left
11. Enzymes catalyze reactions by
  1. Increasing the free energy of the system so that the change in free energy is positive
  2. Increasing the free energy of the substrate so that it is greater than the free energy of the product
  3. Changing the equilibrium constant for the reaction
  4. Decreasing the free energy of activation
  5. Decreasing the free energy of the product so that it is less than the free energy of the substrate
12. The enzyme hexokinase is
  1. Usually found in liver
  2. Uses fructose as a substrate
  3. Requires sulfate as a substrate
  4. Is found everywhere glucokinase is found
  5. Is inhibited by glucose-6-phosphate
13. cAMP
  1. is created by the enzyme phosphodiesterase
  2. is destroyed by the enzyme protein kinase A
  3. is destroyed by the enzyme adenylate cyclase
  4. will bind to the regulatory subunit of protein kinase A
  5. increases in concentration whenever insulin is present.
14. Epinephrine binds to α1-receptors in the liver membrane. This binding
  1. increases the concentration of phosphatidyl inositol trisphosphate in the membrane
  2. activates phospholipase C
  3. decreases the concentration of diacylglycerol
  4. increases calcium stored in the endoplasmic reticulum
  5. inhibits protein kinase C
15.Assume the patient is fasting and then begins to eat a high carbohydrate meal. Following an increase in blood glucose, the message of glucagon is, in part, terminated by
  1. decreasing proteolysis in the liver
  2. increasing glucagon release from alpha-cells of the pancreas
  3. decreasing the GTPase activity of Gαs-stimulatory subunit
  4. decreasing the cAMP phosphodiesterase activity
  5. increasing protein phosphatase activity in the cell

16. Concerning Mya Sthenia who has myasthenia gravis, she has
  1. hypreactive nerves releasing too much epinephrine
  2. too many epinephrine receptors
  3. too little active acetylcholineesterase
  4. too little acetylcholine
  5. too few acetylcholine receptors
17. During the fasting state, the release of fatty acids from adipose tissue is increased. At least part of the signal for this release is carried by
  1. insulin from beta-cells of the pancreas
  2. epinephrine from alpha-cells of the pancreas
  3. epinephrine from the adrenal medula
  4. glucagon from the adrenal medula
  5. cortisol from the alpha-cells of the pancreas
18. Which of the following hormones binds to a receptor in the nucleus or cytosol of target cells?
  1. adrenalin
  2. cortisol
  3. epinephrine
  4. insulin
  5. glucagon
19. In the Ras and MAP kinase pathway, the last step in the pathway is catalyzed by MAP-kinase. MAP-kinase
  1. phosphorylates a transcription factor
  2. binds to Grb-2
  3. activates adenylate cyclase
  4. activates phospholipase C
  5. binds to a glucocorticoid response element
20. In the insulin signal transduction pathway that leads to increases in the diacylglycerol and inositoltrisphosphate second messengers, What is the first signal transduction protein that binds to the IRS?
  1. Phosphatidylinositol-3-kinase
  2. GRB2
  3. Phospholipase C
  4. MAP Kinase
  5. Adenylate cyclase (adenylyl cyclase)
21. The following enzyme reaction is catalyzed by Acetyl CoA Carboxylase during fatty acid synthesis:

Acetyl CoA + CO2 + ATP = Malonyl CoA + AMP + Pi

This enzyme is most appropriately called a(n):

  1. Oxidoreductase
  2. Transferase
  3. Hydrolase
  4. Lyase
  5. Ligase

22. How does the aspirin (acetylsalicylic acid) inhibit prostaglandin endoperoxide synthase (cyclooxygenase)?
  1. It acetylates the active site serine
  2. It acts as a feed back inhibitor
  3. It acts as a product inhibitor
  4. It causes glycosylation of the N-terminus
  5. It forms a disulfide bond with glycine at the active site
23. Phosphorylase kinase activates muscle glycogen phosphorylase by
  1. Converting glycogen phosphorylase a to glycogen phosphorylase b
  2. Phosphorylating a seryl residue on glycogen phosphorylase
  3. Activating protein phosphatase
  4. Binding to the AMP allosteric binding site
  5. Acting as a negative allosteric effector
24. Concerning Al Martini who is an alcoholic, assume that the Vmax of cytosolic alcohol dehydrogenase enzyme and the MEOS system are equal in Al's liver and that the KM's are 0.04 mM and 11 mM, respectively. If Al consumes one ounce of alcohol so that his blood level is 6.4 mM,
  1. The MEOS will oxidize more alcohol than the alcohol dehydrogenase enzyme
  2. The alcohol dehydrogenase enzyme will oxidize more alcohol than the MEOS system
  3. The MEOS will reduce more alcohol than the alcohol dehydrogenase enzyme
  4. The alcohol dehydrogenase enzyme will reduce more alcohol than the MEOS system
  5. Since the Vmax's are the same the amount of alcohol converted by the two systems will be equal

Answers:

As a reference point, previous classes scored a combined mean of 75% for questions 1 through 24.
1. Answer: E, 46%. Chapter 8, Objective 20; ""Be able to name the 6 major classes of enzymes. Given one of the following reactions, be able to match it with one of the 6 major classes of enzyme reactions catalyzed: alcohol dehydrogenase, glucokinase, chymotrypsin, aldolases, triosephosphate isomerase, and pyruvate carboxylase."
2. Answer: E, 46%. Chapter 8, Objective 15; ""What is the normal function of acetylcholinesterase? Explain how diisopropylphosphofluoridate causes the symptoms associated with it. Is this an irreversible inhibitor? Why?"
3. Answer: B, 91%. Chapter 9, Objective 10; "Understand the effect that allosteric activators and inhibitors have on the conformation of an allosteric enzyme and on the plot of velocity versus substrate concentration. What about the S0.5?"
4. Answer: C, 88%. Chapter 9, Objective 16; "Explain how an increase in calcium in muscle cells simultaneously activates muscle contraction and glycogenolysis. Which system uses ATP and which helps to produce ATP?"
5. Answer: B, 80%. Chapter 8, Objective 17; "Concerning penicillin, why does it bind so readily to the active site of the enzyme? Is penicillin an irreversible inhibitor? Is penicillin a suicide inhibitor? Why?"
6. Answer: C, 96% Chapter 8, Objectives 12, 21, and 24; "Concerning NAD+, what vitamin is it synthesized from? When lactate dehydrogenase or alcohol dehydrogenase oxidize their substrates, what is transferred to NAD+?" "Besides pyruvate and acetaldehyde, what is the other reaction product? What is the function of the ADP portion of NAD+?" 20. Be able to name the 6 major classes of enzymes. Given one of the following reactions, be able to match it with one of the 6 major classes of enzyme reactions catalyzed: alcohol dehydrogenase, glucokinase, chymotrypsin, aldolases, triosephosphate isomerase, and pyruvate carboxylase." "Concerning Al Martini, be able to write the equation for the first step in alcohol metabolism in humans. What vitamin is the coenzyme of this reaction synthesized from? What is the common vitamin deficiency seen in alcoholics? Why does it occur?"
7. Answer: E, 72% Chapter 8, Objective 22; "Concerning Dennis "the menace" Veere, Explain how Malathion causes the symptoms associated with it. Is the inhibition irreversible? Why? Is this an example of a suicide inhibitor? Why?"
8. Answer: D, Chapter 8, Objectives 18 and 23; "What is the normal function of xanthine oxidase. Explain why allopurinol is used to treat gout. Is allopurinol an irreversible inhibitor? Is allopurinol a suicide inhibitor? Why?" "Concerning Lotta Topaigne, Explain why allopurinol is used to treat gout. What is the normal reaction inhibited by this drug? Is allopurinol an irreversible inhibitor? Is allopurinol a suicide inhibitor? Why?"
9. Answer: A, 63% Chapter 9, Objectives 8 and 10; "The substrates of allosteric enzymes exhibit positive cooperativity. Explain positive cooperativity in terms of subunits, conformation, and activity of the active site." " Understand the effect that allosteric activators and inhibitors have on the conformation of an allosteric enzyme and on the plot of velocity versus substrate concentration. What about the S0.5?"
10. Answer: B, 75% Chapter 9, Objectives 4 and 5; "What is the effect of a competitive inhibitor on the KM and Vmax?" "What is the effect of a noncompetitive inhibitor on the KM and Vmax?"
11. Answer: D, 94% Chapter 9, Objectives 1 and 4; "Define catalytic power.""Explain catalytic power in terms of the transition state and activation energy."
12. Answer: E, 70% Chapter 9, Objective 25; "25. Concerning Ann O'Rexia, in which of her tissues do you find hexokinase and glucokinase and what is the reaction these enzymes catalyze? When glucose-6-phosphate inhibits hexokinase, is this product inhibition?"
13. Answer: D, 80% Chapter 11, Objective 24; "Name the enzyme that synthesizes cAMP, the enzyme that hydrolyses cAMP and the enzyme that is activated allosterically by cAMP. Which of these three enzyme reactions is affected by insulin?"

14. Answer: B, 80%. Chapter 11, Objective 23; " What is the response when epinephrine binds to an a1-adrenergic receptor? What is the response when epinephrine binds to a b-receptor? That is, what kind of G-protein is activated and what are the initial second messengers produced?"
15. Answer: E, 60% Chapter 11, Objective 26; "Glucagon is released when blood sugar is low. How is its signal terminated (or lowered) following a high carbohydrate meal that increases the blood sugar?"
16. Answer: E, 80% Chapter 11, Objective 27; "Concerning Mya Sthenia who has myasthenia gravis, explain how her chemical messenger system differs from a normal person. How did this happen? Why do the anticholinesterase drugs do to temporarily alleviate the problem?"
17. Answer: C. 93% Chapter 11, Objective 28; "Concerning Ann O'Rexia who has been fasting and is jogging, what was the stimulus for the release of glucagon, epinephrine, norepinephrine, and cortisol? From what cells and what tissue did glucagon originate? From what tissues did epinephrine, norepinephrine, and cortisol originate? What is the effect of all these hormones upon the release of glucose from liver and free fatty acids from adipose tissue?"
18. Answer: B. 90% Chapter 11, Objective 5; "What is a major difference between chemical messengers that are specific for intracellular receptors and those that are specific for plasma membrane receptors??"
19. Answer: A, 60% Chapter 11, Objective 10; "In the Ras and MAP kinase pathway, how does the occupied receptor activate Grb2? What is the last step in the pathway that is catalyzed by MAP-kinase and what is the effect?"
20. Answer: C, 50% Chapter 11, Objective 20; "In the insulin signal transduction pathway that leads to increases in the diacylglycerol and inositoltrisphosphate second messengers, What is the first signal transducer protein that binds to the IRS? Why does it bind to the IRS"
21. Answer: E, 70% Chapter 8, Objective 20; "Be able to name the 6 major classes of enzymes. Given one of the following reactions, be able to match it with one of the 6 major classes of enzyme reactions catalyzed: alcohol dehydrogenase, glucokinase, chymotrypsin, aldolases, triosephosphate isomerase, and pyruvate carboxylase."
22. Answer: A, 63% Chapter 8, Objective 16; "How does aspirin inhibit cyclooxygenase?"
23. Answer: B, 70% Chapter 9, Objective 13; "Using the terms seryl residue, phosphorylation, positive allosteric effector allosteric site, phosphorylase b, phosphorylase a, conformation, and enzyme activity, explain how either AMP or phosphorylase kinase activates muscle glycogen phosphorylase. What is the effect of protein phosphatase upon phosphorylase a?"
24. Answer: B, 70% Chapter 9, Objective 23; "Concerning Al Martini, assume that the Vmax of cytosolic alcohol dehydrogenase enzyme and the MEOS system are equal in Al's liver and that the KM's are 0.04 mM and 11 mM, respcctively. Which will oxidize most of the alcohol consumed when the blood alcohol content is low. For example, after consuming 1 oz of alcohol and a blood alcohol of 6.4 mM. Why?"