Bchem EV Super Set

(class 36 Self) Which enzyme is responsible for the conversion of glycerol to glycerol-3-phosphate for entry into the glycolytic pathway? A. Glycerol kinase B. Glycerol-3-phosphate dehydrogenase C. Glycerol dehydrogenase D. Glycerol-3-phosphate kinase

(A) Glycerol is phosphorylated to glycerol-3-phosphate (G3P) by glycerol kinase. (slide 5) Glycerol enters glycolysis through a series of three reactions that convert it to glyceraldehyde-3-phosphate, an intermediate in the glycolytic pathway. The first step is the conversion of glycerol to glycerol-3-phosphate by glycerol kinase, which requires ATP as a phosphate donor. The second step is the oxidation of glycerol-3-phosphate to dihydroxyacetone phosphate by glycerol-3-phosphate dehydrogenase, which generates NADH as a reducing equivalent. Finally, dihydroxyacetone phosphate is converted to glyceraldehyde-3-phosphate by triose phosphate isomerase, which is an enzyme in the glycolytic pathway. Once glycerol is converted to glyceraldehyde-3-phosphate, it can enter the glycolytic pathway and be metabolized for energy production. The rest are wrong because: B. catalyzes the conversion of DHAP to glycerol-3-phosphate in glycolysis. C. catalyzes the conversion of glycerol to DHAP, which can then enter the glycolytic pathway through the triose phosphate isomerase reaction. D. catalyzes the conversion of glycerol-3-phosphate to 1,3-bisphosphoglycerate in the glycolytic pathway

(group) Why are triglycerides able to provide more energy than carbohydrates "gram for gram"? A. Carbohydrates are already in a more oxidized state than triglycerides. B. Triglycerides have an extremely high group transfer potential. C. Triglycerides are less soluble in water than carbohydrates. E. Triglycerides have more thioester groups.

(A) Imagine that every single hydrogen on a saturated hydrocarbon is +1 point of energy (more available electrons to donate during cellular respiration.) Carbohydrates like glucose is nearly 50% -OH groups and therefore have fewer points of energy to offer during breakdown. C. True, but doesn't explain why there is more energy in them. E. Triglycerides have ester bonds, not thioester groups which contain sulfur. This is also not why they have more energy. B. Triglycerides do not have a high group transfer potential. In fact, they have a lower group transfer potential compared to carbohydrates. Group transfer potential refers to the amount of free energy released upon hydrolysis of a compound. Carbohydrates have a higher group transfer potential because they have more highly polarized bonds that are more susceptible to hydrolysis. In contrast, triglycerides have more nonpolar bonds, such as C-H and C-C bonds, which are less polarized and have lower group transfer potential.

(Class 33 clicker) The electron-transfer chain generates ATP by _________? a. Creating a proton-motive force b. Substrate-level phosphorylation c. Activating uncoupling protein 1 (UCP1) d. Pumping phosphate ions into the intermembrane space. e. Adding electrons to ADP from ATP

(A) force that promotes movement of protons across membranes downhill the electrochemical potential, protons are forced through ATP synthase The rest are wrong because: b. Phosphate group transferred to ATP from ADP (glycolysis and TCA) c. UCP allows protein to freely cross membrane, no gradient d. ETC pumps H+ ions into intermembrane space, not phosphate e. ADP is phosphorylated to ATP by the transfer of electrons from NADH/FADH2 to oxygen through a series of electron carriers in the electron transport chain, which generates a proton gradient that drives ATP synthesis by ATP synthase.

(Hannah) Which complex does not contribute to the proton-motive force? A. Complex I B. Complex II C. Complex III D. Complex IV

(B) Complex II, also known as succinate dehydrogenase, does not pump protons. Instead, it contributes to the electron transport chain by transferring electrons from FADH2 to ubiquinone, which is then carried to Complex III.

(Class 33 clicker) The addition of oligomycin, an inhibitor of ATP synthase, to mitochondria suspended in a buffered medium blocks both ATP synthesis and respiration (protons build up in the intermembrane space to the point where reduction of compounds in the ETC does not provide enough energy to over come 𝚫p, and electron transport halts). What would happen if the uncoupler 2,4-dinotrophenol (DNP) were also added to the suspension? a. Respiration and ATP synthesis would both resume. b. Respiration would resume without ATP synthesis c. ATP synthesis would resume without respiration. d. Neither respiration nor ATP synthesis would resume

(B) Nothing is halting the rest of the ETC processes from occurring, however the lack of proton-motive force created by sequestering hydrogen ions on one side of the membrane, would not allow ATP synthase to work. The rest are wrong because: a. Uncoupler would ruin proton-motive force, ATP synthesis would NOT resume. Uncoupling agent: allows protons to diffuse freely across the membrane. c. The opposite would occur, see response for A and B d. Again, see answer for B. Nothing is halting the rest of the ETC processes from occurring.

(Class 32 clicker) Why are reactive oxygen species (ROS) generated? a. Molecular oxygen recombines with hydrogen to produce dihydrogen oxide b. Stray electrons bind to oxygen, creating a free radical species. c. There are high ADP levels. d. there is a high NAD⁺/NADH ratio e. Transfer of a H⁺ across the inner mitochondrial membrane is uncoupled from ATP synthase.

(B) Stray electrons can bind to oxygen to create free radical species, such as superoxide, which can lead to ROS generation through a series of reactions. ROS are highly reactive and can form from oxidative metabolism/oxidoreductase reactions/metal oxidation reactions. The rest are wrong because: a. This is fancy name for water (H₂O) c. high ADP levels actually stimulate oxidative phosphorylation, leading to increased ATP production and lower ROS generation d. High NAD⁺/NADH ratio is associated with a more oxidized state, which actually leads to lower ROS generation. e. This describes a state where complexes I-IV continue to function, but ATP synthase has ceased to function. Since it is complex IV that reduces 1/2 O2 with hydrogen and electrons to make water, this would still occur, reducing ROS generation, not increasing it.

(Class 32 clicker) Which complex does NOT transport H⁺ from the mitochondrial matrix to the intermembrane space? a. Complex I b. Complex II c. Complex III d. Complex IV e. Complex V

(B) Takes electrons off FADH₂ and passes them to ubiquinone. Complex II is not a source of proton motive force as no hydrogens pass through it. (FADH₂ has equivalent redox potential as ubiquinone) The rest are wrong because: a. NADH loses protons making NAD. In this process it donates its electrons to Complex I producing energy for Complex I to pump protons into the intermembrane space. c. -Receives electrons donated from complexes I and II and put on ubiquinone to produce energy for Complex III to pump protons into the intermembrane space. d. -Receives electrons donated from CytoC to produce energy for Complex IV to pump protons into the intermembrane space. e. ATP synthase (Complex V) pumps protons back into the mitochondrial matrix from the intermembrane space creating ATP.

(group) The chemiosmotic theory states that synthesis and release of ATP and the mitochondrion from the F1-ATPase is directly driven by _________ A.The direct formation of high energy compound in electron transport B. the discharge of a proton gradient between the inner membrane space and the matrix of the mitochondria C. the discharge of a proton gradient between the ETC and the inner membrane space D. the discharge of sodium gradient between the inner membrane space and the mitochondrial matrix E. the reduction of oxygen at the end of the electron transport chain

(B) the chemiosmotic theory proposes that the synthesis and release of ATP by the F1-ATPase is directly coupled to the proton gradient across the inner mitochondrial membrane. This proton gradient is formed by the electron transport chain, which pumps protons from the mitochondrial matrix to the intermembrane space. The potential energy stored in this gradient is then used by ATP synthase to generate ATP from ADP and inorganic phosphate. Answers A, C, D, and E do not accurately describe the chemiosmotic theory and are therefore incorrect.

(group) the rotation of____________subunit of ATP synthase causes conformational changes in the catalytic sites that produce ATP A. 𝛂 (alpha) B. 𝛃 (beta) C. Ɣ (gamma) D. F0 E. omega

(C) Gamma structure spins so it can push the back of beta subunits to change conformation D is tempting but it spins the gamma and it's really the gamma that causes the conformational changes.

Achieve) Researchers add O2 to an anaerobic suspension of cells...... How does the onset of O2 consumption slow down the rate of glucose consumption? a. Aldolase inhibition slows the rate of fructose 1,6‑bisphosphate cleavage in glycolysis. b. Hexokinase inhibition slows the rate of glucose phosphorylation in the first step of glycolysis. c. Phosphofructokinase‑1 inhibition slows the rate of glucose entry into glycolysis. d. Triose phosphate isomerase inhibition slows the rate of triose phosphate interconversion in glycolysis.

(C) PFK is the rate limiting step of glycolysis. Increased O2 increases oxidative phosphorylation which makes lots of ATP. PFK is inhibited by ATP because high ATP levels signal sufficient energy. With PFK inhibited, the rate of glycolysis is decreased. The rest are wrong because: None of them are directly affected by O2 concentration.

(Class 32 clicker) Which electron-carrier complex in the respiratory chain oxidizes ubiquinone? a. Complex I b. Complex II c. Complex III d. Complex IV e. Complex V

(C) Uses electrons on ubiquinone from both complexes I and II that then travel to complex III where they are taken off (oxidized) and then put onto cytochrome C, which travels to complex IV. The rest are wrong because: a. Takes electrons off NADH and puts them on ubiquinone. b. Uses succinate dehydrogenase to take electrons off succinate and put them on FAD and then onto ubiquinone. d. Passes electrons to the final electron acceptor, Oxygen. Not involved with ubiquinone electron transfers. e. Some people like to call this another name for ATP Synthase, but since complex I-IV is actually the electron transport chain and can function outside of ATP synthase, it is a very poor nickname. It's better to think of ATP synthase as just ATP synthase and that there are only 4 complexes.

(Hannah) Which of the following best characterizes the process of fatty acid synthesis? A. Two reductions followed by a dehydration and bond formation. After several repeats, it's cleaved. B. Reduction followed by activation, bond formation, dehydration, and reduction. After several repeats, it's cleaved. C. Activation followed by bond formation, reduction, dehydration, and reduction. After several repeats, it's cleaved. D. Activation followed by bond formation, oxidation, dehydration, and reduction. After several repeats, it's cleaved.

(C.) Activation->reduction->dehydration->reduction->Repeat and cleavage - 1) release of CO2 is condensation occurs after malonyl-CoA attacks acetyl-ACP, keto group formed - 2) keto group reduced (NADPH oxidized to NADP+) - 3) removal of H2O (hydroxyl and a H), unsaturated Pi bond reduced (NADPH oxidized to NADP+)

(Class 37) Which molecule can be produced rapidly from glycerol in only three steps, allowing an interaction between carbohydrate and lipid metabolism? A. acetyl-CoA B. glucose C. pyruvate D. glyceraldehyde 3-phosphate E. phosphoenolpyruvate

(D) The process has three steps. - Step 1: Glycerol is phosphorylated to glycerol-3-phosphate by the enzyme glycerol kinase, which uses ATP as a phosphate donor. - Step 2: Glycerol-3-phosphate is oxidized to dihydroxyacetone phosphate by the enzyme glycerol-3-phosphate dehydrogenase, which also generates NADH in the process. - Step 3: Dihydroxyacetone phosphate is converted to glyceraldehyde 3-phosphate by the enzyme triose phosphate isomerase. Rest are incorrect because: A. Acetyl-CoA is produced from the breakdown of fatty acids and cannot be synthesized from glycerol directly. Glucose (B), pyruvate(C), and phosphoenolpyruvate (E) are produced from the breakdown of carbohydrates and cannot be synthesized from glycerol.

(class 34) What directly or indirectly determines the transition temperature? A. The ability of lipid molecules to be packed together. B. Whether the fatty acid chains of the lipids are saturated or unsaturated. C. The extent to which the fatty acid chains of the lipids contain double bonds. D. The length of the fatty acid chains. E. All of these are correct.

(E) all true things that determine transition temperature.

(hannah) Why is it preferable to cleave thioester links rather than typical ester links in aerobic Metabolism? A. Oxygen must be conserved for the electron transport chain. B. Thioester hydrolysis has a higher energy yield C. Typical ester hydrolysis cannot occur in vivo D. Thioester cleavage requires more energy

B. Thioester hydrolysis has a higher energy yield Explanation: -CoASH hydrolysis is the most efficient way to get energy due to high energy yield. Ester links do not provide that amount of energy

(class34) Organisms that are not warm-blooded, such as plants, need to make their membranes more fluid when the temperature drops. What is one way plants might do this? A. Insertion of cholesterol into the membrane. B. Increasing the number of covalent bonds among membrane lipids. C. Reducing the number of lipid molecules from the membrane to create more space for movement. D. Increasing the number of saturated bonds in membrane lipids. E. Increasing the number of unsaturated bonds in membrane lipids

E. A is wrong because cholesterol is not found in plant cell membranes. B, C, and D are incorrect because they would make the membrane less fluid not MORE fluid.

(class 36) Where is the carboxyl group added to acetyl-CoA to make malonyl-CoA incorporated into the palmitic acid by FAS? A. at the end attached to FAS B. carbons 3, 6, 9, 12 and 15 from the free end C. carbons 1, 4, 7, 10 and 13 from the free end D. at the free end E. It is not incorporated into the growing fatty acid.

Option E is correct because malonyl-CoA is not incorporated into the growing fatty acid; rather, it serves as a substrate for FAS to extend the fatty acid chain A, B, and C are incorrect because the carboxyl group is not added to the end attached to FAS, nor is it added to specific carbons from the free end. Option D is incorrect because the carboxyl group is added to the acetyl-CoA unit, not at the free end of the growing fatty acid.

(Class 37) Which sequence of electron carriers transfers electrons from a fatty acyl- CoA to the mitochondrial respiratory chain? ETF stands for Electron-Transferring Flavoprotein. A. ETF→ubiquinone→ETF:ubiquinone oxidoreductase→FADH2 B. FADH2→ETF → ETF:ubiquinone oxidoreductase →ubiquinone C. ETF→FADH2 →ETF:ubiquinone oxidoreductase→ubiquinone D. FADH2 → ETF:ubiquinone oxidoreductase → ubiquinone → ETF

(B) - Fatty acyl-CoA is oxidized and produces FADH2. - FADH2 is oxidized by ETF (electron transfer flavoprotein) to produce FAD. These hydrogens reduce ETF (ETFH2). - The e- from ETFH2 are transferred to ubiquinone via the ETF:ubiquinone oxidoreductase enzyme. Ultimately, the e- from ubiquinone are passed on to complex III (cytochrome bc1 complex) in the mitochondrial respiratory chain. Bonus: An electron transfer flavoprotein (ETF) is a protein that contains FAD as a prosthetic group. It acts as an electron carrier between several enzymes in the mitochondrial electron transport chain, shuttling electrons from fatty acid oxidation and other metabolic pathways to the ubiquinone pool.

Achieve) researchers add O2 to an anaerobic suspension of cells......Why does the presence of O2 decrease the rate of glucose consumption? a. In the presence of oxygen, the cell is unable to reoxidize NADH to NAD+. b. The ATP yield from oxidizing glucose aerobically is much larger than from glycolysis under anaerobic conditions. c. Under aerobic conditions, there is no terminal electron acceptor to accept electrons from NADH. d. During glycolysis, the cell requires less glucose to generate the same amount of pyruvate when oxygen is present.

(B) Aerobic respiration produces far more ATP per glucose molecule than fermentation. Enough ATP means you don't need to keep breaking down glucose, so the rate of glycolysis slows down. A hack to remembering relationships like this is that products of a pathway generally inhibit the same pathway as they build up. The rest are wrong because: a. Sometimes there is a leak of (e-) from the ETC and the presence of O provides an alternative electron acceptor to allow NADH to be reoxidized. Therefore, oxygen increases, doesn't decrease, glucose consumption. C. oxygen serves as the terminal electron acceptor in the electron transport chain. Process would increased, not decrease. D. Glycolysis is anerobic, it doesn't matter if there is oxygen or not.

Achieve) Different individuals with a disease caused by the same specific defect in the mitochondrial genome may have symptoms ranging from mild to severe. What could account for the variable severity of a mitochondrial disease? a. Some individuals may inherit nonmutated versions of the mitochondrial gene from their father. b. Some individuals may have fewer mutant mitochondria in cells and tissues because of heteroplasmy. c. Some individuals may have a functional version of a mutant mitochondrial gene in their nuclear genome. d. Some individuals may depend less on mitochondrial function and more on glycolysis for ATP production.

(B) Heteroplasmy is defined as the presence of both normal and mutant mitochondrial DNA in a cell or individual. After many divisions of embryonic development, the resulting somatic cells differ in their proportion of defective mitochondria. This heteroplasmy results in mutant phenotypes of varying degrees of severity. In some individuals, a mitochondrial mutation may affect only a small proportion of cells and tissues, because most mitochondria in these cells and tissues have normal genomes and the few mutant mitochondria do not significantly compromise the ability to produce ATP. Conversely, other individuals may have many cells in which the majority of mitochondria are defective, resulting in more severe symptoms. The rest are wrong because: a. You can't inherit mitochondria from your father at all, only your mother. c. Animals also do not have copies of mitochondrial genes in their nuclear genomes. d. All animals require functioning mitochondria or they die.

(hannah) Which of the following directly provides the energy needed to form ATP in the mitochondria? A. Electron transfer in the electron transport chain B. An electrochemical proton gradient C. Oxidation of acetyl-CoA D. Beta oxidation of fatty acids

(B) Protons from electrochemical proton gradient is what is turning ATP synthase in the mitochondria making ATP DIRECTLY. The rest are wrong because: A. Electron transport does provide energy but not directly (partial ATP here and there). C. Oxidation of acetyl-Coa gives intermediates from the TCA cycle. D. Beta oxidation of fatty acids produces reducing agents (NADH and FADH2) that are used by the ETC to generate a proton gradient and drive ATP synthesis. However, beta oxidation itself does not directly produce ATP

(achieve) In electron transfer, only the quinone portion of ubiquinone undergoes oxidation‑reduction; the isoprenoid side chain remains unchanged. What is the function of the isoprenoid side chain? a. It carries Pi and ADP to the inner mitochondrial membrane for ATP synthesis. b. It makes ubiquinone lipid soluble, anchoring it and allowing it to diffuse within the inner mitochondrial membrane. c. It creates a highly specific proton channel through the inner mitochondrial membrane. d. It makes the ubiquinone lipid soluble, anchoring it and allowing it to diffuse within the outer mitochondrial membrane.

(B) Ubiquinone is lipid soluble which allows it to diffuse within inner mitochondrial membrane. Lipid solubility is crucial as ubiquinone carries protons and electrons from Complexes I and II to Complex III and it needs to move free. The rest are wrong because: a. The isoprenoid side chain of ubiquinone does not carry Pi or ATP. Carries protons/electrons. c. The isoprenoid side chain does not create a highly specific proton channel. Only Complexes I, III, and IV act as proton channels. d. Ubiquinone does not have a critical function in the outer mitochondrial membrane

(Class 37) The simultaneous activation of β oxidation and fatty acid synthesis in the same cells is a futile cycle. No biological work is accomplished. Which molecule prevents this futile cycle by preventing fatty acid transport through a membrane? A. acetyl-CoA B. malonyl-CoA C. palmitoyl-CoA D. ADP E. methylmalonyl-CoA

(B) malonyl-CoA is a key intermediate in fatty acid synthesis and also inhibits the transport of fatty acids into the mitochondria for β-oxidation, thus preventing the futile cycle. The rest are wrong because: (A)Acetyl-CoA is the product of β-oxidation (C) palmitoyl-CoA is the initial substrate for β-oxidation, D) ADP is involved in cellular energy metabolism (E) Methylmalonyl-CoA is a molecule involved in the metabolism of branched chain amino acids and is not related to fatty acid metabolism.

(group) Before free fatty acids can be incorporated into triglycerides or phospholipids they must be activated to _____________ A. NADPH B. CMP-phosphesters C. Thioesters of coenzyme A D. Thioesters of Acyl carrier proteins E. Dihydroxyacetone phosphoesters

(C) Explanation: The last step of fatty acid biosynthesis is that thioester bond is cleaved between the acyl carrier protein and the hydrocarbon chain. The ACP is swapped out for CoA. The rest are incorrect because: A. NADPH is a reducing agent not directly involved in activating fatty acids. Fatty acid activation involves the formation of thioesters between the fatty acid and coenzyme A. B. CMP-phosphesters are involved in the synthesis of complex polysaccharides which are carbs, not FA D. Thioesters of Acyl carrier proteins cannot activate free FA. They are intermediates in the FA synthesis pathway. E. Dihydroxyacetone phosphoesters are intermediates in glycerolipid biosynthesis - do not activate FA

(Hannah) Fatty acids enter the catabolic pathway in the form of: A. Glycerol B. Adipose tissue C. Acetyl-CoA D. Ketone bodies

(C) Fatty acids are first broken down into acetyl-CoA before entering the citric acid cycle for ATP production in the mitochondria. The rest are wrong because: A. Glycerol is a component of triglycerides, not the fatty acids themselves. B. Adipose tissue is a storage site for triglycerides, not a form in which fatty acids enter the pathway. C. Ketone bodies are a product of the pathway, not a form in which fatty acids enter it.

Achieve) When researchers add O2 to an anaerobic suspension of cells consuming glucose at a high rate, the rate of glucose consumption declines greatly. The cells consume the O2, and accumulation of lactate ceases. This effect is characteristic of most cells capable of aerobic and anaerobic glucose catabolism. Why does the accumulation of lactate cease after the addition of O2? a. The large, positive Δ𝐺′° for the conversion of pyruvate to lactate favors the reverse reaction. b. The cell ceases glycolytic production of pyruvate and NADH in the presence of oxygen. c. The cell regenerates NAD+ by respiratory electron transfer and oxidative phosphorylation. d. The cell ferments glucose to ethanol and CO2, rather than fermenting glucose to lactate.

(C) In an anaerobic suspension, cells synthesize ATP through glycolysis. They reoxidize NADH by reducing pyruvate to lactate via lactic acid fermentation. Upon the addition of O2, the cells shift from lactic acid fermentation to oxidative phosphorylation. Therefore, accumulation of lactate ceases. The rest are wrong because: A. Although true, it has nothing to do with why the cell switched from anaerobic fermentation to aerobic oxidative phosphorylation. B. This literally doesn't happen. Glycolysis is anerobic process. It's what is does with pyruvate that depends on the presence of oxygen. with no oxygen, it has to use pyruvate converting to lactate to replenish the NAD+ . With oxygen, TCA cycle is a better option and it chooses that. D. We're talking about lactate and glucose and O2, not ethanol. This answer was here to distract you.

(Class 33 clicker) Which statement regarding the proton-motive force is FALSE? a. It is a result of electron flow through the respiratory chain. b. It is used by ATP synthase to synthesize ATP c. It results from an [H+] gradient across the outer mitochondrial membrane d. It is both chemical and electrical potential energy e. It can be used to power transport.

(C) Inner not outer: outer mitochondrial membrane would not create proton motive force, protons would float around the cytoplasm. The rest are TRUE a. Transport of electrons with release of H+ b. ATP synthase uses H+ gradient with proton motive force to 'churn' out ATP d. pH gradient is used with [H+], electrical potential (charge separation across the membrane) is utilized as well. E is tempting but! The proton motive force generates a proton gradient across the inner mitochondrial membrane, and this gradient powers the rotation of the rotor ring in ATP synthase. As the rotor ring rotates, it causes conformational changes in the catalytic subunits, which leads to the synthesis of ATP from ADP and Pi. *In this way, the proton motive force is directly coupled to the transport of protons*

(Class 33 clicker) The 𝛽 subunits of ATP synthase: a. Have three distinct isozymes b. Are each associated with a 𝜕 (omega )subunit c. Have three distinct conformations d. Will act as an ATPase if protons flow through the Fo domain in the mitochondrion.

(C) The 𝛽 subunit of ATP synthase has three distinct conformations: but the binding change mechanism of ATP synthase involves four steps. - Open (ADP+ PI enter) - Loose (ADP + Pi) these pieces are getting closer together - Tight (catalyzes ATP synthesis) - Open (ATP released) A is incorrect because the 𝛽 subunits of ATP synthase do not have distinct isozymes. B is incorrect because each 𝛽 subunit is associated with an alpha subunit, not a 𝜕 subunit. D in the presence of ADP and inorganic phosphate (Pi), the 𝛽 subunits will only act as an ATP synthase, not as an ATPase which is an enzyme that hydrolyzes ATP to ADP and inorganic phosphate, releasing energy.

(class 36) What enzymatic step is considered to be the rate-limiting step of fatty acid biosynthesis? A. fatty acid synthase B. thiolase C. malonyl-CoA decarboxylase D. acetyl-CoA carboxylase E. fatty acid elongase

(D) Acetyl-CoA carboxylase catalyzes the formation of malonyl-CoA by adding CO2 from bicarbonate. It is irreversible and is the rate-limiting step. The rest are wrong because: A. FAS is the entire enzyme complex, not an enzymatic step. B. Thiolase: cleaves the 16-carbon fatty acid from FAS and releases it C. Malonyl-CoA decarboxylase: converts malonyl-CoA to acetyl-CoA to exit the pathway E. Fatty acid elongase: adds two-carbon units to the growing fatty acid chain.

(Class 36 CGPT) Which of the following is NOT a factor that contributes to the ability of small (< 12 carbons) fatty acids to diffuse freely across mitochondrial membranes? A. Their small size B. Their lower degree of hydrophobicity compared to larger fatty acids C. Their lower degree of polarity compared to larger fatty acids D. The presence of transporters or carriers for small fatty acids in the mitochondrial membrane

(D) the statement implies that transporters for small fatty acids exist in the mitochondrial membrane and that they would actually facilitate the movement of small fatty acids across the membrane, rather than hinder it. However, the fact is that small fatty acids can diffuse freely across the membrane without the help of transporters or carriers. It's FA larger than 12 carbons that need facilitated transport i.e Carnitine shuttle The rest are wrong because: A. Their small size helps it diffuse B and C are a subtle fact about larger fatty acids. As large as they are, it is more possible they could become temporarily polarized and mildly hydrophobic. In this way, a smaller fatty acid has lower change of becoming polar and hydrophobic and this fact contributes to it's ability to diffuse.

(group) the first step in fatty acid synthesis is the formation of __________ from acetyl-CoA and carbon dioxide? A. Acetoacetyl-ACP B. Glycerol 3-phosphate C. Acetoacetyl-CoA D. Acetyl-ACP E. Malonyl-CoA

(E) first step of fatty acid synthesis is malonyl-CoA formation that will next turn to malonyl acyl protein (ACP) Incorrect answers: A. Acetoacetyl-ACP is an intermediate in fatty acid synthesis. B. Glycerol 3-phosphate is involved in the synthesis of triacylglycerols. D. Acetyl-ACP is also an intermediate in fatty acid synthesis.

(Achieve) Isocitrate dehydrogenase is found only in the mitochondria, but malate dehydrogenase is found in both the cytosol and mitochondria. What is the role of cytosolic malate dehydrogenase? *(multiple answers)* a. It plays a key role in the transport of reducing equivalents across the inner mitochondrial membrane via the malate‑aspartate shuttle. b. It plays a key role in the conversion of mitochondrial pyruvate to cytosolic oxaloacetate to fuel gluconeogenesis. c. It is a point of electron entry into the mitochondrial respiratory chain. d.It delivers the reducing equivalents from NADH through FAD to ubiquinone and thus into Complex III. e. It catalyzes the oxidation of malate to oxaloacetate, coupled to the reduction of NAD+ to NADH, in the last reaction of the citric acid cycle.

A & B. there are two distinct malate dehydrogenase (MDH) enzymes, one found in the mitochondrial matrix and the other found in the cytosol. They catalyze the same reaction of converting malate to oxaloacetate, but they are located in different compartments of the cell and use different cofactors. The mitochondrial MDH uses NAD+ and cytosolic MDH uses NADP+. The explanation of A applies here because the hydrogens attached to malate carry electrons, so in this way, it helps transport reducing equivalents. B applies because oxaloacetate has no transporter, malate does. So Oxa (which came from the pyruvate that entered the TCA cycle) is reversed to malate via the mitochondrial MDH, transported via malate-aspartate shuttle, and then the cytosolic MDH converts the malate back to oxaloacetate. Then into glycolysis to either contribute to making more pyruvate or gluconeogenesis. The others are wrong because: C. Cytosolic MDH is not a point of electron entry into the respiratory chain. Succinate dehydrogenase (Complex II) is. D. This choice describes the glycerol 3‑phosphate shuttle used in skeletal muscle and brain tissue, not Cytosolic MDH. E. When referring to the the conversion of malate to oxaloacetate in the TCA--that happens in the mitochondria, not the cytosol and we're discussing Cytosolic MDH

(Class 33) If you wanted to test the importance of a particular membrane-spanning helix to the function of an enzyme, one way to do that would be to do site-directed mutagenesis in which you change the sequence of the gene encoding protein. In particular you would cause a substitution in which one of the amino acids making up the helices was replaced with another. Which of the following amino acids would you most likely substitute into the helix if you wanted to disrupt the interaction with the membrane? a. Lysine b. Phenylalanine c. Methionine d. Alanine e. Leucine

A) Hydrophobic, pos charged, polar. Not getting past that nonpolar membrane. The rest are wrong because they are all Hydrophobic and uncharged. This is an expected arrangement for the membrane, so would not interrupt it.

(Class 33 clicker) A fat is called _______ if all carbons of the hydrocarbon chain are single bonded to 2 other carbons and 2 hydrogens. a. Saturated b. Polyunsaturated c. Unsaturated d. Monounsaturated e. None of the above is correct

A) No missing hydrogen atoms, no double bonds The rest are wrong because: B. Contain several unsaturated bonds C. Presence of many double bonds D. Presence of single unsaturated bond

Achieve) How might defective mitochondria lead to cancer? a. Mitochondrial defects can lead to increased production of reactive oxygen species. These species can react with nuclear DNA and convert proto‑oncogenes to oncogenes. b. Mitochondrial defects can force cells to rely on anaerobic glycolysis, which can result in a buildup of carcinogenic compounds. c. Mitochondrial defects can accelerate ATP production. The resulting increase in the [ATP]/[ADP] ratio drives cells to replicate uncontrollably. d. Mitochondrial defects can lead to increased oxygen consumption in affected tissues. The resulting hypoxia causes tumor formation.

A. Defects can make ETC accept more e- than it can transport = more ROS. More ROS damages DNA. DNA damages can be all sorts, but can convert proto‑oncogenes to oncogenes, which stimulate unregulated cell division and tumor formation. OR mutate genes encoding enzymes that protect against ROS damage, such as superoxide dismutase and glutathione peroxidase. The rest are wrong because. b. glycolysis has always been anaerobic. in the case of fermentation, lactic acid isn't a carcinogen c. no way a defect causes better ATP production and cancer cells are inefficient and use up lots of glucose. d. hypoxia does not cause tumor formation; defective mitochondria typically consume less oxygen than normal mitochondria.

(achieve) Although both pyruvate dehydrogenase and glyceraldehyde 3‑phosphate dehydrogenase use NAD+ as their electron acceptor, the two enzymes do not compete for the same cellular NAD pool. Why? a. The mitochondria and cytosol contain separate pools of NAD. b. Pyruvate dehydrogenase and glyceraldehyde 3‑phosphate dehydrogenase never catalyze reactions simultaneously. c. NAD+ freely diffuses across the inner mitochondrial membrane to act as an electron acceptor for either enzyme. d. The cell converts the NAD+ used as an electron acceptor for pyruvate dehydrogenase to NADP+.

A. Pyruvate dehydrogenase is located in the mitochondrion, whereas glyceraldehyde 3‑phosphate dehydrogenase is located in the cytosol. The rest are wrong because b. These two different processes do occur simultaneously. An example of two processes that wouldn't occur simultaneously would be glycolysis and gluconeogenesis (futile cycling) c. NADH cannot diffuse freely, only way it can travel is through the membrane is through a shuttle. d. pyruvate dehydrogenase and glyceraldehyde 3‑phosphate dehydrogenase use NAD+. that NAD can be converted to NADP is irrelevant to the question.

Achieve) Scientists attach a magnetic nanobead to the 𝛾𝜖 subunit of isolated F1. They affix the F1 to the bottom of a microscopic glass chamber such that the bead-F1𝛾𝜖 portion can freely rotate. ---In the first solution containing 500 nM ATP, they observe that the bead-F1𝛾𝜖 complex spontaneously rotates counterclockwise. These spontaneous rotations stop once the ATP is depleted-----2nd, in a solution containing 200 nM ATP, 100 μM ADP, and 10 mM Pi, the scientists apply a magnetic field that rotates the bead clockwise. When the magnetic field is switched off, the bead-F1𝛾𝜖 complex reverts to spontaneous counterclockwise rotations. These spontaneous rotations last longer than those observed in the first experiment starting with 500 nM ATP. WHY *choose 1 or more* a. Condensation of ADP and Pi drives rotation of the F1‑ATPase 𝛾𝜖 subunit. b. Reversing the direction of the F1 complex's spontaneous rotation results in condensation of ADP and Pi. c. The F1 complex can hydrolyze ATP independently of the Fo complex. d. The Fo complex is required to drive ATP synthesis by FoF1 transporter in vivo.

B & D) B. is correct because ADP+Pi condensation is another way of saying ATP synthesis. In the description, it was rotating counterclockwise to hydrolyze- so if we reverse it, we're synthesizing. D is correct because in vivo (in our body) the Fo complex is required for F1 to rotate. In the experiment, they got around that with the magnetic bead. Other two are incorrect because: a. condensation of ADP and Pi doesn't drive rotation, it drives ATP synthesis. Rotation is caused by the proton motive force. c. F1 complex can't hydrolysis ATP without the Fo Complex. Longer explanation: ATP synthase can rotate in either a clockwise or counterclockwise direction depending on the direction of the proton gradient across the mitochondrial inner membrane. Counterclockwise hydrolyzes ATP and clockwise makes ATP. *it rotates clockwise unless certain conditions or met, so assume clockwise as the default.* In the first solution, in the presence of only ATP and zero ADP+Pi components, F1 spontaneously rotates counterclockwise until there isn't anymore ATP and there is only ADP+Pi and stops. In the 2nd solution, the bead is forced to rotate clockwise in the presence of a LOT of ADP and Pi. This makes more ATP than the first solution. Upon release, ATP synthase proceeds to rotate counter clockwise for longer than solution 1, because it began with a larger amount of ATP to hydrolyze.

Achieve) Predict the effect of a relatively low concentration of uncoupling agent on the rate of electron transfer and the P/O ratio. (phosphorous to oxygen ratio) a. The electron transfer rate increases, and the P/O ratio increases. b. The electron transfer rate increases, and the P/O ratio decreases. c. The electron transfer rate decreases, and the P/O ratio increases. d. The electron transfer rate decreases, and the P/O ratio decreases.

B) Electron transfer, which has high -DeltaG, is tightly coupled to the demand for ATP synthesis, which has high +deltaG . with too many uncoupling agents, protons continue getting pumped, but there aren't enough protons to create a gradient for ATP synthesis. In the presence of *relatively low* levels of an uncoupling agent, the cell compensates for the decreased rate of ATP synthesis by *increasing* the rate of electron flow. Oxygen consumption increases, causing the P/O ratio to decrease as the cell maintains relatively normal ATP levels. The rest are wrong because: Option a is incorrect because uncoupling agents cause electron transfer to become independent of ATP synthesis. Option c is incorrect because uncoupling agents increase proton leak across the inner mitochondrial membrane, reducing the proton gradient required for ATP synthesis. Option d is incorrect because the electron transfer rate is typically unchanged or only slightly decreased by low concentrations of uncoupling agents.

(Class 35) The equation for palmitate synthesis by fatty acid synthase is: Acetyl-CoA + 7 malonyl-CoA + 14NADPH + 14H+ → palmitate + 7CO2 + 8CoA + 14NADP+ + 6H2O Why are only six waters produced by palmitate synthesis, not seven? A. One water is used to form the initial acetyl-CoA. B. One water is used to liberate palmitate from the synthase. C. One water is permanently bound to the active synthase. D. One water is used for "charging" the synthase. E. The final translocation requires an extra water.

B. During the final step of palmitate synthesis, the newly synthesized palmitate molecule is attached to a thioester bond with the enzyme, and one water molecule is required to hydrolyze this bond and release the palmitate from the synthase. The six remaining water molecules are produced as byproducts of the various chemical reactions that occur during the synthesis of palmitate. The rest are wrong because" A. False. C. Water is never permanently bound anywhere. D. Charging an enzyme typically refers to the addition of a cofactor or substrate necessary for the enzyme to function, or modifying the enzyme to improve its activity or stability. E. attachment of the fatty acid to carnitine occurs through a high-energy thioester bond between the carboxyl group of the fatty acid and the hydroxyl group of carnitine. It does not involve water.

(Hannah) A patient has been exposed to a toxic compound that increases the permeability of mitochondrial membranes to protons. Which of the following metabolic changes would be expected in this patient? A. Increased ATP levels B. Increased oxygen utilization C. Increased ATP synthase activity D. Decreased pyruvate dehydrogenase activity

B. The increased permeability of mitochondrial membranes to protons is a bad thing! it would allow protons to leak out of the mitochondrial intermembrane space, decreasing the proton motive force that drives ATP synthesis. This would lead to decreased ATP levels, not increase them (A) and increased oxygen utilization to compensate for the decreased ATP production (B). There would be no reason to expect an increase in ATP synthase activity (C) or a decrease in pyruvate dehydrogenase activity (D) the PDH complex is at the step that pyruvate enters the matrix and has little to do with the Oxidative phosphorylation system.

(Class 37) Which pathway would obviously be MOST affected by increased β oxidation of fatty acids? A. glycolysis B. the citric acid cycle C. the glyoxylate pathway D. the pentose phosphate pathway E. gluconeogenesis

B. increased β-oxidation leads to an increase in acetyl-CoA production, which can inhibit pyruvate dehydrogenase complex and the citric acid cycle. Although this inhibition can shift metabolism towards gluconeogenesis, it has more of a direct affect on the TCA cycle. The rest are incorrect because: A. The regulatory enzyme for glycolysis is PFK (phosphofructokinase). That is inhibited by high levels of ATP and citrate, and low levels of AMP. None of that is Acetyl CoA, which is what beta ox makes. C. The glyoxylate pathway is only present in plants and bacteria D. The pentose phosphate pathway is primarily involved in the production of NADPH and pentoses for nucleotide synthesis and not related to Beta Oxidation. E. As above

(Class 37) How do fatty acids get into the mitochondrial matrix? A. spontaneously B. via the malate shuttle C. via carnitine palmitoyltransferase D. via palmitoyl-CoA transferase E. via the citrate shuttle

C) Carnitine palmitoyltransferase transfers the acyl group of fatty acids from CoA to carnitine, allowing it to cross the mitochondrial membrane and enter the mitochondrial matrix for β-oxidation. The rest are wrong because: A. They are too polar to cross the membrane without special transport. B. Refers to the malate-aspartate antiport shuttle. It transports reducing equivalents, malate, and aspartate, not FA D palmitoyl-CoA transferase is a fake enzyme name that kind of reads like Palmitoyl-CoA. That is an acyl-CoA thioester, are themselves needing transport, and cannot transport an FA. (E) the citrate shuttle is responsible for transporting citrate, not fatty acids.

Achieve) What role does superoxide dismutase play in ameliorating the effects of reactive oxygen species? a. It directly transforms superoxide into water. b. It synthesizes superoxide by transferring a free electron onto O2. c. It catalyzes the conversion of superoxide to hydrogen peroxide and O2. d. It generates superoxide by reacting ubisemiquinone with O2.

C) There are multiple points in the ETC process where ROS can be created. Which is why we have superoxide dismutase. It catalyzes the conversion of superoxide to hydrogen peroxide & O2. 2 O2 + 2H+ ⟶ H2O2 + O2 +2⁢H+ ⟶ H2⁢O2 + O2 The enzyme glutathione peroxidase then eliminates hydrogen peroxide by converting it into water in a reaction coupled to the oxidation of reduced glutathione. a. Not directly. There are 2-3 steps. b. This enzyme doesn't make superoxide, it converts it. d. Although superoxide radicals do form from the reaction of ubisemiquinone with O2, these transformations occur spontaneously, not through the activity of superoxide dismutase.

(class 36) What is the reducing equivalent necessary for fatty acid synthesis? A. NADH B. FADH2 C. NADPH D. FAD E. None of the answers is correct.

C. From the pentose phosphate pathway. Also NADPH tends to be involved in *anabolic* reactions Rest are incorrect because: A. mainly involved in *catabolic* reactions. B & D are both mainly involved in the electron transport chain.

Achieve) Although ATP synthesis requires both ADP and Pi, the rate of synthesis depends mainly on the concentration of ADP, not Pi. Why? A. Pi freely diffuses across the mitochondrial membrane in a concentration dependent manner. B. GDP and other molecules use Pi, making it an unspecific regulator. C. Because Pi is not an organic compound, [Pi] does not contribute to the mass‑action ratio. D. The steady‑state concentration of Pi in the cell is much higher than that of ADP.

D. Cellular activities require an abundance of Pi, which contributes to many biochemical reactions. As a result, the cellular steady‑state concentration of Pi is much higher than that of ADP. The other are incorrect because A. Pi does not freely diffuse across the mitochondrial membrane. Phosphate translocase promotes the symport of one H2PO−4H2⁢PO−4 and one H+H+ into the mitochondrial matrix. B. As [ADP] rises as a result of ATP consumption, there is little change in [Pi], so Pi cannot serve as a regulator. C. [Pi] does contribute to the mass‑action ratio, [ATP][ADP][Pi].

(class 34) Which factor is NOT associated with acetyl-CoA carboxylase? A. production of malonyl-CoA B. biotin cofactor C. catalysis of an irreversible reaction D. production of oxaloacetate

D. Oxaloacetate is only made in TCA (or via conversion from malate in the cytosol.)

(class 34) What is the primary metabolic source of the reducing power required for fatty acid synthesis and desaturation? A. the glycerol 3-phosphate shuttle B. glycolysis C. the citric acid cycle D. the pentose phosphate pathway E. the acetate shuttle system

D. PPP A is incorrect because it's involved in the transfer of electrons between cytosolic and mitochondrial NADH. B & C generate NADH or NADH and FADH2 respectively. E is incorrect because there's no such thing as the acetate shuttle system.

(Achieve) Single nucleotide changes in the gene for succinate dehydrogenase (Complex II) are associated with midgut carcinoid tumors. What mechanism could explain this observation? a. Defects in succinate dehydrogenase completely block the citric acid cycle, causing carcinogenic intermediates to accumulate. b. Defects in succinate dehydrogenase completely block oxidative phosphorylation, and the lack of intracellular ATP triggers apoptosis. c. Defects in succinate dehydrogenase lead to a buildup of NADH, which stimulates cells to divide more rapidly than usual, leading to tumor growth. d. Defects in succinate dehydrogenase result in increased production of ROS, damage to DNA, and mutations that lead to unregulated cell division.

D. Succinate dehydrogenase defects cause reactive oxygen species (ROS). ROS damage DNA, causing mutations Why the rest are bad choices:: A. Intermediates of the TCA cycle are not known carcinogens. B. A defect here wouldn't block oxidative phosphorylation. functional NADH dehydrogenase would still allow electrons to enter the respiratory chain. Apoptosis is the body's solution to improper cells, so this would fix the problem, not cause cancer. C. a defect in succinate dehydrogenase does not buildup of NADH, nor would such a build stimulate rapid cell division.

(Class 37) Why does β oxidation occur in the mitochondrial matrix? A. to allow coordinated regulation with fatty acid synthesis B. to coordinate production of acetyl-CoA with the introduction into the citric acid cycle C. to compartmentalize D. because necessary oxidative enzymes are present E. All of the answers are correct.

E, these are all true.

(Class 35)Identify the four-step sequence that facilitates fatty acid synthesis. A. carboxylation, oxidation, hydration, oxidation B. condensation, oxidation, dehydration, oxidation C. condensation, reduction, dehydration, reduction D. carboxylation, reduction, hydration, reduction

Pre Step: Carboxylation of Acetyl-CoA to Malonyl-CoA 1. condensation of two-carbon units 2. reduction of the carbonyl group 3. dehydration of the alcohol 4. reduction of the double bond Post step: Cleavage of the 16C FA from FAS for release