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- One of the regulators of the TCA cycle is succinyl CoA. Discuss the rationale for this molecule to be used to regulate the TCA cycle. For what TCA enzymes does succinyl CoA act as an inhibitor?One of the regulators of the TCA cycle is succinyl CoA. Discuss the rationale for this molecule to be used to regulate the TCA cycle [include chemical structures and chemical equations where appropriate]. What is an allosteric inhibitor? How does it operate? For what TCA enzymes does succinyl CoA act as an inhibitor? What is the metabolic role of succinyl CoA? So then why is this molecule a reasonable choice as an inhibitor of the TCA?Which of the following statements is/are TRUE for the Krebs' cycle? Reaction 1: condensation of acetyl-CoA and oxaloacetate; produces H20. Reaction 3: oxidation of isocitrate to a-ketoglutarate; produces NADH and CO2. Reaction 6: oxidation of succinate to fumarate; produces FADH2 and CO2 Reaction 5: hydrolysis of succinyl-CoA to succinate; produces ATP.
- (c) (1 ) Fluoroacetate, prepared commercially for rodent control, is also produced by a South Afri- can plant. After entering a cell, fluoroacetate is converted to fluoroacetyl-CoA in a reaction catalyzed by the enzyme acetate thiokinase: F-CH2COO¯ + COA-SH + ATP F-CH2CO-SCOA + AMP + PPj The toxic effect of fluoroacetate 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 the cit- ric acid cycle intermediates revealed that their concentrations were below normal, except for citrate, with a concentration 10-fold higher than normal. Where did the block in the citric acid cycle occur? What caused citrate to accumulate and the other cycle intermediates to be depleted? Explain. Why does it block the citric acid cycle? Fluoroacetyl-CoA is enzymatically transformed in the citric acid cycle.…10 ATP/Acetyl-CoA * 2 acetyl-CoA = 20 ATP 1 GTP/ Acetyl-CoA * 2 acetyl-CoA = 2 GTP 1,5 ATP/ FADH2 * 1 FADH2= 1,5 ATP 2,5 ATP/ NADH * 3 NADH = 7,5 ATP 7,5 + 1,5 + 20 = 29 ATP och 2 GTP All of this is round off, how to calculate without rounding off? 2-Acetyl-CoA and 15 subunitsWhich of the following most accurately describes the impact acetyl-CoA has in the cytosol of the liver cell? Acetyl CoA serves as an allosteric inhibitor of PFK Acetyl CoA serves as an allosteric inhibitor of pyruvate kinase Acetyl CoA serves as an allosteric activator of PFK Acetyl CoA serves as an allosteric activator of pyruvate kinase Acetyl CoA serves as an allosteric activator of fructose-2,6-bisphosphatase Acetyl CoA serves as an allosteric activator of PFK-2
- The degradation of CH3 (CH₂ )10 - COOH via the beta-oxidation pathway requires: 6FAD + 6NAD+ + 5C0A-SH + 6H₂O 5FAD + 5NAD+ + 6C0A-SH+ 5H₂O 5FAD + 5NAD + 5C0A-SH + 5H₂0 6FAD + 6NAD+ + 6C0A-SH + 6H₂OThe glutamate dehydrogenase (GDH) catalyses the following reaction: +H₂N- H - - CH₂ - CH₂ COO acide glutamique COO™® + NAD+ + H₂O GDH COO C: CH₂ CH₂ COO™ O + NH4+ NADH + H* The activity of GDH is monitored in the sense of the formation of glutamate using the following conditions: -0.2 mL of 5 M ammonium sulphate 2.4 mL of buffer at pH 8 0.1 mL of NADH at 6.15 mg.mL-¹ (M = 709 g.mol-¹) 0.2 mL of 1 M a-ketoglutarate solution Warm mixture at 25 °C for 5 min - Add 0.1 mL of GDH solution containing 1.6 mg.mL-¹protein to start the reaction. acide a-cétoglutarique The change in absorbance at 340 nm is monitored, in a 1-cm cuvette, every minute for 10 min. Results are given in the table below: Data: ENADH at 340 nm = 6220 M¹.cm¹ Time (min) 1 2 3 4 5 6 7 8 9 1.760 1.718 1.675 1.635 1.595 1.550 1.510 1.489 1.476 A340 10 1.451 - Draw the graph A = f(t). Calculate A340 at t = 0 and place this point on the curve. - Comment the shape of the curve, particularly the portion that corresponds to a…(b) Fluoroacetate, prepared commercially for rodent control, is also produced by a South African plant. After entering a cell, fluoroacetate is converted to fluoroacetyl-CoA in a reaction catalyzed by the en- zyme acetate thiokinase: F-CH2COO + CoA-SH + ATP F-CH2CO-SCOA + AMP + PP The toxic effect of fluoroacetate 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 the citric acid cycle intermediates revealed that their concentrations were below normal, except for citrate, with a concentration 10-fold higher than normal. (b1) the other cycle intermediates to be depleted? Explain. Why does it block the citric acid cycle? Where did the block in the citric acid cycle occur? What caused citrate to accumulate and (b2) structure of the end product of fluoroacetate metabolism?…
- Some bacteria use the citric acid cycle intermediate, a-ketoglutarate, plus acetyl-CoA, as the starting point for lysine biosynthesis. The first part of this biosynthetic pathway uses the same chemical strategy found in the citric acid cycle. Propose a four-step pathway for the conversion of a-ketoglutarate to 2-oxoadipate. Draw the three missing intermediates, and indicate the chemistry involved in each reaction. Include any cofactors that you think might be required for specific steps.If the carbonyl carbon of acetyl-CoA were marked with 14C, where would that carbon be located within oxaloacetate after one turn of the TCA cycle?How many acetyl CoA molecules are produced in one cycle of beta oxidation? How many cycles would it take to catabolize a stearic acid molecule (a fatty acid, [18:0]) into acetyl Co A units? a)How many acetyl CoA molecules would be produced? b) How many reduced nucleotides would be produced? c) If a molecule of glucose produces a net 32 ATP when completely catabolized, which do you think will produce more energy, one molecule of glucose or one molecule of stearic acid? Justify your answer.