Unformatted text preview: NAME (print, no nicknames): Key WRITE YOUR NAME LEGIBLY ON EVERY PAGE CHECK TO BE SURE YOU HAVE 5 PAGES INCLUDING COVER PAGE. I swear/affirm that I have neither given nor received any assistance with this exam. Signature: Date: BIOCHEMISTRY 460 EXAM 3A April 28, 2010 Read each question carefully Budget your time wisely BE SURE TO STATE UNITS OF ANY NUMERICAL ANSWERS. USEFUL CONSTANTS: F (Faraday's constant) 96,500 JV1mol1= 96.5 kJV1mol1 Page 1 of 5 NAME (print, no nicknames): Key 1. (5 pts) What class of molecules are the dietary precursors to coenzymes (one word answer to this)? What purpose do coenzymes serve in the catalysis of chemical reactions? Vitamins Cofactors supply additional functional groups that allow enzymes to catalyze more types of reactions (carboxylations, decarboxylations, oxidation-reduction) 2. (4 pts) What is the advantage to using a multisubunit complex (i.e. pyruvate dehydrogenase) to catalyze the conversion of pyruvate to acetyl CoA? Substrate channeling: products of one reaction immediately become substrates for the next without diffusion ("passing off") 3. (4 pts) The citrate cycle requires a supply of inorganic phosphate to remain active. Why is inorganic phosphate a critical substrate for the citrate cycle? Pi is necessary for the in the substrate level phosphorylation step: succinyl CoA +GDP + Pi -> succinate + GTP + CoA 4. (4 pts) Studies suggest that Mycobacterium tuberculosis, the infectious agent that causes tuberculosis in humans, use the glyoxylate cycle to convert fatty acids to carbohydrates during their latency period. Given this information, would a drug that specifically inhibits enzymes in the glyoxylate cycle be a reasonable target for a therapy against this bacteria? Would you expect significant side effects in humans? Why or why not? You could argue either way if this is reasonable, points awarded for logic of response. Given the information provided you would not expect side effects because humans don't have the glyoxylate pathway 5. In the electron transport system found in the mitochondria, electrons are passed through several one- electron carrier proteins. One of these is the small soluble protein cytochrome c, and another is cytochrome a3 which is part of complex IV. Given the following information, cytochrome c(Fe3+) + cytochrome a3(Fe2+) cytochrome c(Fe2+) + cytochrome a3(Fe3+) E' = 0.096 V A. (4 pts) Calculate the change in free energy under standard conditions for the transfer of an electron in the reaction as written above. Show your work and state units. DG= -nfDE DG= -1(96500 J/molV)(-.096) = 9.3 kJ/mol B. (2 pts) Is this reaction as written favorable or unfavorable under standard conditions? unfavorable p.2_______ p.3________ Page 2 of 5 p.4 ________ p. 5_______ Total______ NAME (print, no nicknames): Key 6. (4 points) 2.5 molecules of ATP are generated for every molecule of NADH oxidized through the mitochondrial electron transport system but only 1.5 molecules of ATP are generated for every molecule of FADH2. Use your knowledge of the electron transport chain to explain why these numbers are different. Complex II does not pump protons, complex 1 does -> more protons more gradient more ATP 7. (14 points) Compare and contrast mitochondrial electron transport system and oxidative phosphorylation to photosynthetic electron transport system and photophosphorylation Mitochondrial Electron Transport Photosynthetic Electron System and Oxidative Transport System and Phosphorylation Photophosphorylation H2O NADP+ plastocyanin Original electron donor for NADH or FADH2 ETS Terminal electron acceptor for ETS Mobile protein electron carrier between protein complexes Mobile lipid electron carrier between protein complexes Where is ATP made? O2 Cytochrome c Ubiquinone (CoQ OK) plastiquinone Matrix Stroma Proton gradient (or pmf) or light Chlorophyll or pigments in light harvesting antennae Source of energy to power Proton gradient (or pmf) or ATP synthesis glucose/fatty acid Capture light energy None 8. (6 points) We discussed several reasons why carbon dioxide fixation (the Calvin Cycle) does not occur in the dark. Please explain two of the reasons. Any two: rubisco activated by light, pH change, substrate availability, oxidizing conditions If there is no photosynthesis in the dark, what pathways are actively synthesizing ATP? Cellular respiration (glycolysis and/or oxidative phosphorylation) Page 3 of 5 /24 NAME (print, no nicknames): Key 9. (5 pts) What are the two products of the oxidative phase of the pentose phosphate pathway? Which one is needed in red blood cells? Why? NADPH and ribulose 5 phosphate. Red blood cells need NADPH to reduce reactive oxygen species 10. (4 pts) List three metabolic fates of glucose 6- phosphate (i.e. what metabolic pathways is it a part of). any three- glycolysis, gluconeogenesis, glycogen synthesis, pentose phosphate pathway 11. (4 points) What are the likely consequences of a genetic disorder that renders fructose 1,6 bisphosphatase (FBPase-1) less sensitive to regulation by fructose 2,6 bisphosphate? Cannot inhibit gluconeogenesis. (Substrate cycling occurs.) Net result: more glucose, less pyruvate, lower ATP yield from the oxidation of glucose 12. (5 points) McArdle's Disease is a glycogen metabolism disorder resulting from defects in the enzyme muscle glycogen phosphorylase. Explain why a defect in this enzyme makes it very difficult for these individuals to run up a flight of stairs. Cannot mobilize muscle glycogen 13. (6 points) Consider the graph at the right: What does it say about the regulation of glycogen synthase and glycogen phosphorylase? Reciprocally regulated Assume that upon adding glucose insulin levels rise. Explain what happens on a molecular level that changes the activities of the two enzymes. Phosphorylation/Dephosphorylation or conformational change Would the regulation by insulin be allosteric or covalent? covalent 14. (5 points) Explain why continued lipolysis in the adipocyte (due to insulin resistance) leads to ketone body synthesis in the liver? (Hint: What intermediate is building up in the liver?) What condition could result if this remains uncontrolled? When acetyl-CoA levels rise, the citrate cycle becomes "overwhelmed" favoring ketone body synthesis. If these ketone bodies are not taken up by the other tissues ketoacidosis can occur /29 Page 4 of 5 NAME (print, no nicknames): Key 15. Stearate is a saturated C18 fatty acid that is converted to stearoyl-CoA and then degraded in the mitochondrial matrix through a series of reactions that yield acetyl-CoA, NADH, and FADH2. These metabolites can be further oxidized by energy conversion processes in the mitochondrial matrix to yield CO2, H2O, and ATP. Fill in the bookkeeping values below that quantify these products. A. (3 pts) One mole of C18 stearoyl-CoA is converted to _9___ moles of acetyl-CoA, _8___ moles of NADH, and ____8__ moles of FADH2. B. (5 pts) Each mole of acetyl-CoA that is fully oxidized by the citrate cycle produces 3 moles of NADH, 1 mole of FADH2, and 1 mole of ATP (from GTP). Considering that 5 ATP are generated for every 2 NADH (2.5 ATP/NADH), and 3 ATP for every 2 FADH2, (1.5 ATP/FADH2), that are oxidized by the electron transport system, calculate the overall ATP yield from the complete oxidation of stearate. ____67.5_ ATP generated from the NADH produced by oxidation of the acetyl-CoA molecules __13.5___ ATP generated from the FADH2 produced by oxidation of the acetyl-CoA molecules __20__ ATP generated from the NADH produced by stearoyl-CoA oxidation __12__ATP generated from FADH2 produced by stearoyl-CoA oxidation Then subtract __2__ ATP invested to make stearoyl-CoA And add ___9_ ATP (from GTP) generated during the oxidation of acetyl-CoA molecules For a total yield of __120____ ATP for the complete oxidation of stearate. 16. (4 points) Acetyl CoA carboxylase, the enzyme that catalyzes the synthesis of malonyl CoA from acetyl CoA and CO2 during fatty acid synthesis, polymerizes into filaments that are large enough to be viewed under electron microscopy. Does filament formation activate or inhibit the activity of this enzyme? How is filament formation affected by the addition of an allosteric effector such as citrate? Filament formation activates acetyl CoA carboxylase. Citrate promotes filament formation. 17. (4 points) Explain why cholesterol synthesis is drastically reduced when one eats a diet high in cholesterol. HMG CoA reductase is inhibited by cholesterol (whether it comes from the diet or from de novo synthesis pathways). 18. (4 points) We discussed three molecules that are precursors to urea- name two of them. NH4+, CO2 (bicarbonate ion), and aspartate 19. (4 points) Glyphosate, also known as Round-Up, is an herbicide that kills plants by inhibiting an enzyme in the amino acid biosynthetic pathway responsible for phenylalanine synthesis. Would it be safe to use glyphosate in areas where farm animals may accidentally eat plants that have been sprayed? Explain. Yes- animals don't have the shikimate pathway and obtain phenylalanine from their diets. Page 5 of 5 /24 ...
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This note was uploaded on 05/06/2010 for the course BIOC 460 taught by Professor Ziegler during the Spring '07 term at Arizona.
- Spring '07