Fluoroacetate is used as a poison for rat control. After entering a cell, fluoroacetate is converted to fluoroacetyl-CoA in a reaction catalyzed by the enzyme acetate thiokinase: acetate thiokinase FCH₂COO- + COASH + ATP FCH₂CO-SCOA + AMP + PPi The toxic effect of fiuoroacetate was studied in an experiment using intact isolated rat heart. After the heart was perfused with 0.22 mM fluoroacetate, the measured rate of glucose uptake and glycolysis decreased, and glucose 6-phosphate and fructose 6-phosphate accumulated. Examination of citric acid cycle intermediates revealed that their concentration were below normal, except for citrate, with a concentration 10-fold higher than normal. (i) Where does the block in the citric acid cycle occur? What causes citrate to accumulate and the 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 structure of the end product of fluoroacetate metabolism? Why does it block the citric acid cycle?

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.