6. Lovastatin (see picture), is a potent competitive inhibitor of HMG-COA reductase (B-hydroxy- B-methylglutaryl-COA reductase). In addition, the synthetic compound, Terbinafine (see picture), is a potent inhibitor of squalene monooxygenase. Both compounds could be used to treat hypercholesterolemia, a genetic disorder where the patient synthesizes too much cholesterol regardless of dietary intake of cholesterol. a. Predict and explain the effect of these drug on serum cholesterol levels in humans. b. Based on squalene monooxygenase's role in synthesizing sterols, explain why terbinafine is marketed as an anti-fungal agent, and not for hypercholesterolemia. но COO Lovastatin OH на R, CH „CH3 Terbinafine R2 н,с

6. Lovastatin (see picture), is a potent competitive inhibitor of HMG-COA reductase (B-hydroxy- B-methylglutaryl-COA reductase). In addition, the synthetic compound, Terbinafine (see picture), is a potent inhibitor of squalene monooxygenase. Both compounds could be used to treat hypercholesterolemia, a genetic disorder where the patient synthesizes too much cholesterol regardless of dietary intake of cholesterol. a. Predict and explain the effect of these drug on serum cholesterol levels in humans. b. Based on squalene monooxygenase's role in synthesizing sterols, explain why terbinafine is marketed as an anti-fungal agent, and not for hypercholesterolemia. но COO Lovastatin OH на R, CH „CH3 Terbinafine R2 н,с

Biology 2e

2nd Edition

ISBN:9781947172517

Author:Matthew Douglas, Jung Choi, Mary Ann Clark

Publisher:Matthew Douglas, Jung Choi, Mary Ann Clark

Chapter7: Cellular Respiration

Section: Chapter Questions

Problem 9RQ: GTP or ATP is produced during the conversion of isocitrate into ketoglutarate succinyl CoA into...

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1. Select the INCORRECT statement about Glutamate dehydrogenase : a. Catalyzes the removal of NH4+ into glutamate b.Catalyzes the incorporation of NH*4 into a-ketoglutarate c. Catalyzes the removal of NH*4 from glutamate C d. Catalyzes the incorporation of NH'4 into a-keto acid
Consider the docosanoic acid, C21H43CO2H a. Label the a and B carbons b. Draw the acyl CoA derived from this fatty acid c. How many acetyl CoA molecules are formed by complete B-oxidation? d. How many cycles of B-oxidation are needed for complete oxidation? e. How many molecules of ATP are formed from the complete catabolism of this fatty acid?
Consider the complete oxidation of one mole of arachidic acid (20:0). ___________ a. How many rounds of the β-oxidation pathway will be involved? ___________ b. How many acetyl CoA will be produced? ___________ c. How many NADH will be produced from all the rounds of the β-oxidation pathway? ___________ d. How many ATP will eventually be produced from the complete oxidation of one mole of arachidoyl CoA?
Five coenzymes are required by a-ketoglutarate dehydrogenase, the enzyme in the citric acid cycle that converts a-ketoglutarate to succinyl-CoA.a. Identify the coenzymes.b. Propose a mechanism for the reaction. A-ketoglutarate dehydrogenase A-ketoglutarate succinyl-CoAOO OO O−O O− −O SCoA + CO2
10a) Outline the mechanism for the conversion of alpha-ketoglutarate to succinyl-CoA which is catalyzed by alpha-ketoglutarate dehydrogenase. b) Of the five steps involved with this process, which would most likely be metabolically irreversible under physiological conditions?
1) Which of the following is NOT TRUE following β-oxidation in the liver? a) The formation of propionyl CoA could lead to the production of glucose from B-oxidation b) The formation of acetyl CoA could lead to ketone bodies synthesis c) Acetyl CoA could be converted to pyruvate allowing for the production of glucose d) Acetyl CoA could be used for the synthesis of HMG CoA e) Acetyl CoA might be oxidized by the TCA cycle 2) When undergoing strenuous exercise the Cahill cycle is functioning. Which of the following substrates is being delivered to the liver tissue as part of this cycle? A. Glucose B. Lactate C. Galactose D. Pyruvate E. Alanine
1.Enumerate the enzymes of the alpha ketoglutarate dehydrogenase complex and write its mechanism of action
1. Consider the oxidation of the fatty acid with the common name arachidic acid. a. Draw the structure of arachidic acid. b. How many turns of the fatty acid oxidation cycle is required for the complete oxidation of arachidic acid? c. How many moles of ATP are formed from one mole of arachidic acid if the acetyl CoA produced go to the citric acid cycle and oxidative phosphorylation? Assume 1 mole of NADH is equivalent to 3 moles ATP and 1 mole FADH2 is equivalent to 2 moles of ATP. Show how you arrived at your answer
The synthesis of the activated form of acetate (acetyl-CoA) is carried out in an ATP-dependent process: Acetate + CoA + ATP → acetyl-CoA + AMP + PPi (a) The ∆G’o for the hydrolysis of acetyl-CoA to acetate and CoA is - 32.2 kJ/mol and that for hydrolysis of ATP to AMP and PPi is - 30.5 kJ/mol. Calculate ∆G’o for the ATP-dependent synthesis of acetyl-CoA. (b) Almost all cells contain the enzyme inorganic pyrophosphatase, which catalyzes the hydrolysis of PPi to Pi. What effect does the presence of this enzyme have on the synthesis of acetyl-CoA? Explain.
Malonyl-CoA synthesized by the action of acetyl-CoA carboxylase II is primarily used:a. To synthesize fatty acidsb. To inhibit fatty acid oxidationc. Both a and bd. Neither a nor b
1) Humans do not undergo net synthesis of carbohydrate from acetyl- CoA, yet carbons of acetyl -CoA can be incorporated into glucose and amino acids. Show pathways as to how this can happen. 2) A molecule -X inhibits oxidation of stearoyl-CoA by isolated mitochondria but has no effect on palmitoyl-carnitine oxidation, explain.
In the presence of saturating amounts of oxaloacetate, the activity of citrate synthase from pig heart tissue shows a sigmoid dependence on the concentration of acetyl‑CoA. When succinyl‑CoA is added, the curve shifts to the right and the sigmoid dependence is more pronounced.