Fluoroacetate is used as a poison for rat control. After entering a cell, fluoroacetate isconverted to fluoroacetyl-CoA in a reaction catalyzed by the enzyme acetate thiokinase:acetate thiokinaseFCH₂COO-+ COASH + ATPFCH₂CO-SCOA+ AMPPP₁The toxic effect of fiuoroacetate was studied in an experiment using intact isolated rat heart. After theheart was perfused with 0.22 mM fluoroacetate, the measured rate of glucose uptake and glycolysisdecreased, and glucose 6-phosphate and fructose 6-phosphate accumulated. Examination of citricacid cycle intermediates revealed that their concentration were below normal, except for citrate, witha concentration 10-fold higher than normal.(i) Where does the block in the citric acid cycle occur? What causes citrate to accumulate andthe other cycle intermediates to be depleted? How might the inhibition be overcome?(ii). Fluoroacetyl-CoA is enzymatically transformed in the citric acid cycle. What is the structureof the end product of fluoroacetate metabolism? Why does it block the citric acid cycle?

The first step in the citric acid cycle is the formation of citric acid, by the condensation of…

Answered: Fluoroacetate is used as a poison for…

Biochemistry

9th Edition

ISBN:9781319114671

Author:Lubert Stryer, Jeremy M. Berg, John L. Tymoczko, Gregory J. Gatto Jr.

Publisher:Lubert Stryer, Jeremy M. Berg, John L. Tymoczko, Gregory J. Gatto Jr.

Chapter1: Biochemistry: An Evolving Science

Section: Chapter Questions

Problem 1P

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The enzyme mutase which is important for the synthetic of tyrosine and phenylalanine in saccharomyces cerevisiae has been studied as an example of an allosteric enzyme. Tyrosine acts as a negative effector for this enzyme. What effects would you see on the action of the enzyme were you to increase the concentration of tyrosine? The chorismate mutase would shift to its R conformation The curve showing the kinetics or chorismate mutase would shift to the right The curve showing the kinetics of chorismate mutase would shift to the left The chorismate mutase would become saturated more rapidly
Human xanthine oxidase catalyzes the oxidation of hypoxanthine to xanthine and can further catalyze the oxidation of xanthine to uric acid. For the treatment of hyperuricemia and gout, several medications are used to inhibit the activity of xanthine oxidase and reduce the production of uric acid. You are a biochemist and just discovered a chemical that can inhibit the activity of the human xanthine oxidase. When analyzing its mode of inhibition, you found that the enzyme inhibitor complex requires 450kJ.mol-1 to dissociate and that it displayskinetics somehow similar to noncompetitive inhibition. You sent your inhibitor to the ministry of health for approval as a medication for gout. Based on the data provided, are they going to authorize it as a medication or not? Explain?
The following Michaelis-Menten plot shows the response of phosphofructokinase-1 (PFK-1), an enzyme in the glycolytic pathway, to the presence of ATP and AMP. Based on the data below, which of the following statements apply? Select all that apply. No inhibitors (low (ATP)) 1 mM ATP + 0.1 mM AMP 1 mM ATP 1.0 2.0 (Fructose-6-phosphate) mM Fig. : Regulation of PFK activity AMP is an allosteric modifier that enhances the binding of the substrate fructose 6-phosphate а. O b. AMP is an allosteric modifier that reduces the binding of the substrate fructose 6-phosphate ATP is an allosteric modifier that reduces the binding of the substrate fructose 6-phosphate O c. O d. ATP is an allosteric modifier that enhances the binding of the substrate fructose 6-phosphate Phosphofructokinase activity
Answer the following questions about the inhibition of acetylcholine esterase by neostigmine. 5a. Does neostigmine have a structure that enables it to bind reversibly to the ACbE active site? 5b. Is neostigmine catalytically processed by ACHE? 5c. How does the stability of the carbamolyl-enzyme intermediate produced by treatment of ACbE with neostigmine compare to the stability of the acetyl- enzyme intermediate produce when ACb, is hydrolyzed?
Corticosteroids (a type of hormone), and Nonsteroidal Anti-inflammatory Drugs (NSAIDs) are non-narcotic pain relievers. Both medications are prescribed to reduce inflammation in the body. NSAIDs such as aspirin, acetaminophen, and ibuprofen are able to reduce pain, fever, and inflammation by blocking the action of the cyclooxygenase enzyme (COX) that catalyzes the conversion of arachidonic acid into prostaglandins. Common corticosteroids include prednisone, cortisone, and methylprednisolone. Choose one of these three corticosteroids. Do some internet research on the corticosteroid that you choose and then explain how the drug works to reduce inflammation.
How is cigarette smoking related to elastase function? Methionine sulfoxide is formed by cigarette smoke in the antitrypsin protein, which leads to the full manifestation of the disease in individuals heterozygous for emphysema. Oxidation of methionine 358 by cigarette smoke of the elastase inhibitor active site leads to an increased inhibition of elastase and subsequent overaccumulation of mucus in the lungs. The inhibitor of elastase is axidized by cigarette smoke so elastase doesn't function properly in healthy individuals. Cigarette smoke modifies the elastase methionine residues such that the enzyme activity is blocked.

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