BIBC 102 – METABOLC BIOCHEM - FINAL RANDY HAMPTONFALL QUARTER 2003 12/09/20031Good morning! You are at the end of thisbeginning on the road to metabolism.You have learned over three hundredterms, hundreds of reactions, and come tosee that life is an astonishing, self-regulating blizzard of moleculartransactions. Every time I teach this classI learn something (for example: it ispossible to get tired of eating steak…).Really, it is a pleasure and an honor toteach you these things, so thanks for yourattention and interest.You should have one seat between you and your neighbors on each side.Not 2, not 3. One. That way all can have a seat with a writing surface.For all questions, choose the BEST answer from those offered, and enter itonto the appropriate space of the scantron sheet.Use a number 2 pencil only.You can keep this question sheet after the exam. I advise you to write thecorrect answer beside each question, and only then to enter the number onthe scantron sheet. That way, you will be more careful in making yourentries, also you will have a reference for the answers you chose for post-testlearning. Good luck!BIBC 102 – METABOLC BIOCHEM - FINAL RANDY HAMPTONFALL QUARTER 2003 12/09/200321. Fully reduced ubiquinolA) Is a substrate for complex IIB) Is a substrate for complex IVC) is a substrate for complex IIID) is a product of complex IV2. Fatty acids derived from the foods we eat most oftenA) Are hydrolyzed from the foods we eat and then used to synthesizetriglyceridesB) Are hydrolyzed from the ingested molecules and then enter the bloodstreamdirectlyC) Are transferred directly from the gut to the bloodstreamD) Are absorbed directly and then packaged as free fatty acids into lipoprotein3. Lesch-Nyhan diseaseA) Is a genetic defect in pyrmidine salvageB) Is a genetic defect in de novo purine synthesisC) Is a genetic defect in amino acid catabolismD) Demonstrates the importance of salvage pathways4. What type of molecule does not bind to the active site of an enzymeA) A homotropic allosteric regulatorB) A product that causes inhibition by slow dissociationC) A heterotropic allosteric regulatorD) A competitive inhibitor5. The fatty acid synthase (FAS) complex in mammalsA) Uses NADPH in both reduction stepsB) Uses a free ACP as part of the complexC) Has more proteins than the bacterial complexD) Has the same number of proteins as the bacterial complex6. A spontaneous chemical reactionA) Must have a negative DH and a positive DSB) Must have a positive DHC) Must have a negative DSD) Can have a negative DH or a positive DS7. Glucose monomers are added to a growing glycogen chain by the action ofglycogen synthase on:A) glucose-1-PB) CDP-glucoseC) AMP-glucoseD) UDP-glucoseBIBC 102 – METABOLC BIOCHEM - FINAL RANDY HAMPTONFALL QUARTER 2003 12/09/200338. What feature of chloroplast glyceraldehyde-3-phosphate dehydrogenase(GAPDH) is different from cytosolic GAPDH?A) The choloroplast version catalyzes production of G3P whereas the cytosolic onecatalyses the consumption of G3PB) The chloroplast version uses PiPi (pyrophosphate) whereas the cytsolic one usesPiC) The cytosolic one uses NAD+ /NADH, whereas the chlorplast one usesNADP+/NADPHD) The chloroplast version is a rate-limiting enzyme9-12 Is it nada, or ENADA?.. You be the judge… Here’sone of those metabolites you can buy in Whole Foods. It is ourold friend, NADH, and the package claims that it “improvescellular energy”, and “elevates mental clarity” along with“improving alertness and concentration”. Hmmm. Lets thinkabout ENADA9. What is the main function of NADH in the cellA) It serves as the main source of electrons for respirationB) It is the main anabolic reducing agent in cellsC) It is consumed by the Krebs cycle as a substrateD) It is a substrate of a glycolytic reaction10. What would the effects of “ENADA” (NADH) be on the Krebs cycle?A) It would slow the Krebs cycleB) It would stimulate the Krebs cycleC) It would hasten the Krebs cycle by increasing respiratory electron flowD) It would have no effect on Krebs because that cycle uses NADP+ as a substate11. What are the effects of consumption of large amounts of ethanol on the levelsof NADH, our natural “ENADA” (from the problem set)A) A large increase in glycolytic rateB) A large increase in Krebs cycle activityC) A large decrease in the NADH/ NAD+ ratioD) A large increase in the NADH/ NAD+ ratio12. Could “ENADA” affect the biochemistry of the mitochondrial matrix,assuming it can get into the cytosol?A) No! It is impermeable to the mitochondrial inner membraneB) Yes! It will directly react with complex IC) No! It is not a substate for any of the matrix-localized reactionsD) Yes! It will send its electrons in by the malate-aspartate shuttleEnd of: Is it nada, or ENADA?.. You be the judgeBIBC 102 – METABOLC BIOCHEM - FINAL RANDY HAMPTONFALL QUARTER 2003 12/09/2003413. When describing the involvement of the chemiosmotic gradient in chloroplastATP synthesisA) The electrical potential across the membrane is more importantB) The H+ concentration gradient is more importantC) The two components are of equal importanceD) The concentration of H+ ions is higher in the stroma than in the lumen14. How many adenine nucleotide binding sites are there in the assembled F1 ATPsynthase?A) oneB) twoC) threeD) none15. Ketone body synthesisA) Shares the first two steps of cholesterol synthesisB) Occurs in the mitochondrial matrixC) Is caused by excessive glycolysis when Krebs cycle activity is lowD) Involves malonyl-CoA as an intermediate16. Insulin regulates the glycogen processing enzymes by:A) increasing phosphorylation of both glycogen synthase and glycogenphosphorylaseB) increasing phosphorylation of glycogen synthase but decreasing phosphorylationof glycogen phosphorylaseC) decreasing phosphorylation of glycogen synthase but increasing phosphorylationof glycogen phosphorylaseD) decreasing phosphorylation of both glycogen synthase and glycogenphosphorylase17. Type 2 diabetesA) is less prevalent than type 1 diabetesB) occurs at a fairly constant frequency in people over timeC) has strong but complex genetic determinants in peopleD) is usually observed early in a person’s life18. An inhibitor of mitochondrial ATP synthase wouldA) increase electron flow through the respiratory chainB) stop electron flow through the respiratory chainC) activate the Krebs cycleD) have no effect on the respiratory chain19. The
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