ch 21 Practice Q's ATP Synthase

BIOCHEM unit 3

the proton-motif force consists of which two components?

A. Chemical gradient and concentration gradient

B. Electrical gradient and membrane potential

C. Chemical gradient and electrical gradient

D. ATP gradient and ADP gradient

C. chemical gradient and electrical gradient

the proton-motive force (pmf) is indeed composed of both a chemical gradient (ΔpH) and an electrical gradient (ΔΨ), which together drive ATP synthesis. This combination makes the pmf a powerful electrochemical force that can be quantified in millivolts.

true/false: the F0 portion of ATP synthase is located in the mitochondrial matrix.

false

the F0 portion is embedded in the inner mitochondrial membrane, not located in the matrix. the F1 portion extends into the matrix where ATP synthesis actually occurs. this membrane-spanning arrangement is essential for coupling proton flow to ATP production.

in the binding change mechanism, ATP synthesis occurs in which conformational state of the β subunit?

A. Open (O)

B. Loose (L)

C. Tight (T)

D. All three states equally

C. tight (T)

ATP is synthesized when ADP and Pi are compressed together in the tight (T) conformation. the rotation of the γ subunit forces conformational changes that cycle each β subunit through O, L, and T states, but actual bond formation occurs in the T state.

which component of ATP synthase contains the rotating c-ring?

A. F₁ subunit

B. F₀ subunit

C. γ subunit

D. α3β3 hexomer

B. F0 subunit

the c-ring is part of the F0 subunit and rotates within the membrane as protons pass through. this rotation is mechanically coupled to the γ subunit, which then drives conformational changes in the F1 catalytic subunits.

true/false: in mammals, each c subunit in the c-ring contains a glutamate residue that can bind and release protons.

true

each c subunit contains a conserved glutamate reside that is essential for proton binding and release. this residue undergoes protonation and deprotonation as the c-ring rotates, which is the molecular basis for converting proton flow into mechanical rotation.

the malate-aspartate shuttle is primarily found in

A. Kidney and lung tissue

B. Muscle and brain tissue

C. Heart and liver tissue

D. All tissues equally

C. heart and liver tissue

the malate-aspartate shuttle predominates in heart and liver tissue, where maximum ATP yield from glucose is crucial. these tissues have high energy demands and benefit from the shuttle’s ability to deliver electrons to complex I for maximal ATP production.

match each shuttle system with its ATP yield per cytoplasmic NADH

1. glycerol-3-phosphate shuttle

2. malate-aspartate shuttle

1. 1.5 ATP

2. 2.5 ATP

the malate-aspartate shuttle delivers electrons to complex I (yielding 2.5 ATP), while the glycerol-3-phosphate shuttle bypasses complex I and feeds electrons to complex II via FADH2 (yielding 1.5 ATP). this one-ATP difference per cytoplasmic NADH significantly impacts total glucose ATP yield

true/false: the glycerol-3-phpsphate shuttle delivers electrons directly to complex I of the electron transport chain

false

the glycerol-3-phosphate shuttle delivers electrons to complex II (via FAD-GPDH in the inner membrane), not complex I. this bypass of complex I is why this shuttle yields only 1.5 ATP per cytoplasmic NADH instead of 2.5 ATP.

if a c-ring contains 12 subunits and F1 produces 1 ATP per 120° rotation, how many protons are required to synthesize 1 ATP?

A. 3 protons

B. 4 protons

C. 12 protons

D. 36 protons

B. 4 protons

With 12 c subunits and 1 ATP produced per 120° rotation (one-third of a full turn), you need 12 ÷ 3 = 4 protons per ATP. This H⁺/ATP ratio varies among organisms (typically 3-4 in mammals) depending on c-ring size.

a patient’s mitochondria show normal electron transport chain activity but no ATP synthesis. the most likely explanation is

A. Complex I is inhibited

B. There is no oxygen present

C. The c-ring is damaged

D. NADH levels are too low

C. the c-ring is damaged

if the ETC is functioning normally (maintaining the proton gradient) but not ATP is synthesized, the defect must be in ATP synthase itself. damage to the c-ring would prevent mechanical coupling of proton flow to rotation, blocking ATP production despite a normal pmf

during intense exercise, muscle cells would be expected to have:

A. High ATP/ADP ratio and low oxygen consumption

B. Low ATP/ADP ratio and high oxygen consumption

C. High ATP/ADP ratio and high oxygen consumption

D. Low ATP/ADP ratio and low oxygen consumption

B. low ATP/ADP ratio and high oxygen consumption

during intense exercise, ATP is rapidly consumed (lowering the ATP?ADP ratio), which stimulates oxidative phosphorylation through acceptor control. this increases oxygen consumption as the ETC works harder to regenerate ATP. this is a classic example of demand-driven metabolism

true/false: if the inner mitochondrial membrane became freely permeable to protons, ATP synthesis would increase dramatically

false

if the membrane became freely permeable to protons, the proton-motive force would collapse as protons leak back across the membrane without passing through ATP synthase. this would halt ATP synthesis.

a cell using primarily the glycerol-3-phosphate shuttle instead of the malate-aspartate shuttle would produce

A. More ATP per glucose

B. The same amount of ATP per glucose

C. Less ATP per glucose

D. No ATP from glucose

C. less ATP per glucose

the glycerol-3-phosphate shuttle produces 1.5 ATP per cytoplasmic NADH versus 2.5 ATP for the malate-aspartate shuttle. with 2 cytoplasmic NADH per glucose, this represents a loss of 2 ATP per glucose (30 ATP vs. 32 ATP total).

UCP-1 (thermogenin) in brown adipose tissue functions to

A. Increase ATP synthesis efficiency

B. Block electron transport

C. Prevent oxidative damage

D. Generate heat by bypassing ATP synthase

D. generate heat by bypassing ATP synthase

UCP-1 creates a proton leak that allows protons to return to the matrix without passing through ATP synthesis, dissipating the pmf as hear instead of capturing it in ATP. this is crucial for non-shivering thermogenesis in newborn and cold-adapted mammals

Rand the following scenarios from highest to lowest rate of oxidative phosphorylation:

I. High ADP, functioning ATP synthase

II. Low ADP, functioning ATP synthase

III. High ADP, inhibited ATP synthase

A. I > II > III

B. I > III > II

C. II > I > III

D. III > I > II

A. I > II > III

high ADP with functioning ATP synthase (I) provides maximum drive for oxidative phosphorylation. low ADP (II) slows the process through respiratory control. inhibited ATP synthase (III) blocks proton flow entirely, stopping oxidative phosphorylation regardless of ADP levels due to back-pressure from accumulated pmf.

a researcher develops a new rug that specifically prevents the γ subunit from rotating. the immediate effect would be

A. Increased ATP synthesis

B. Increased proton pumping

C. Decreased ATP synthesis and eventual inhibition of electron transport

D. Increased heat production

C. decreased ATP synthesis and eventual inhibition of electron transport

blocking γ rotation prevents ATP synthesis, causing ADP and Pi to accumulate while ATP cannot be regenerated. the pmf would build to maximum as protons accumulate in the intermembrane space, eventually creating enough back-pressure to inhibit the proton pumps in the ETC complexes.

true/false: acceptor control ensures that oxidative phosphorylation only occurs when the cell actually needs ATP, making it an efficient regulatory mechanism

true

acceptor control, where ADP availability regulates oxidative phosphorylation rate, is elegantly efficient. when ATP Sis abundant (low ADP), oxidative phosphorylation slows automatically. when cells consume ATP (high ADP), the process accelerates. this demand-driven regulation prevents wasteful ATP overproduction.

which combination would result in the most efficient ATP production from cytoplasmic NADH?

A. Muscle tissue using glycerol-3-phosphate shuttle

B. Heart tissue using malate-aspartate shuttle

C. Brain tissue using glycerol-3-phosphate shuttle

D. All options are equally efficient

B. heart tissue using malate

heart tissue expresses the malate-aspartate shuttle, which delivers electrons to complex I for maximum ATP yield (2.5 ATP per NADH vs. 1.5 for glyerol-3-phosphate). the high energy demands of cardiac muscle make this efficiency critical for sustaining continuous contractile work.

two 170 lb volunteers undergo separate interventions

• Volunteer A ingests a sub-lethal dose of 2,4-dinitrophenol (DNP).

• Volunteer B is cooled to 15 °C, triggering norepinephrine-mediated activation of uncoupling protein-1 (UCP-1) in brown adipose tissue.

Which statement most accurately compares the metabolic consequences of the two interventions?

A. Both volunteers show similar increases in whole-body oxygen consumption, but only Volunteer A experiences a rise in core temperature.

B. Volunteer A displays a systemic rise in oxygen consumption and potentially dangerous hyperthermia, whereas Volunteer B limits heat production to brown adipose tissue, keeping core temperature within a safe range.

C. Volunteer A’s ATP synthesis rate increases because the electron-transport chain accelerates, while Volunteer B’s ATP synthesis rate falls owing to proton leak through UCP-1.

D. Proton-motive force collapses completely in both volunteers, preventing any ATP re-synthesis until the interventions stop.

B. volunteer A displays a systemic rise in oxygen consumption and potentially dangerous hypothermia, whereas volunteer B limits heart production to brown adipose tissue, keeping core temperature within a safe range

DNP is an uncoupler that affects all mitochondria systemically, leading to dangerous whole-body heat generation and hyperthermia. UCP-1 in contrast, is tissue-specific to brown adipose tissue, providing controlled, localized thermogenesis that maintains core temperature homeostasis. this distinction explains why DNP is lethal while CP-1 is a natural, safe thermogenic mechanism

consider the complete oxidation of one glucose molecule. if all cytoplasmic NADH used the glycerol-3-phosphate shuttle instead of the malate-aspartate shuttle, the total ATP yield would be:

A. 28 ATP

B. 30 ATP

C. 32 ATP

D. 36 ATP

B. 30 ATP

Using the glycerol-3-phosphate shuttle costs 2 ATP compared to malate-aspartate (1.5 ATP × 2 cytoplasmic NADH = 3 ATP instead of 2.5 × 2 = 5 ATP). Starting from the standard 32 ATP with malate-aspartate shuttle, you lose 2 ATP, yielding 30 ATP total. This demonstrates how shuttle choice affects overall glucose ATP yield.

a patient has a genetic defect preventing pyruvate dehydrogenase complex function. which of the following would you expect

A. Normal ATP production from glucose

B. Reduced ATP production, but fatty acid oxidation unaffected

C. Complete loss of all ATP synthesis

D. Enhanced gluconeogenesis

B. reduced ATP production, but fatty acid oxidation unaffected

without PDH, pyruvate cannot enter the TCA cycle, severely limiting ATP from glucose (only glycolysis yields 2 ATP net). however, fatty acids bypass PDH and feed acetyl-CoA directly into the TCA cycle via β-oxidation, maintaining some oxidative phosphorylation capacity. this explains why PDH deficiency patients may benefit from high-fat diets.

true or false: if complex I of the electron transport chain were completely inhibited, the malate-aspartate shuttle would become useless for ATP production from cytoplasmic NADH.

true

the malate-aspartate shuttle regenerates matrix NADH, which must donate electrons to complex I. if complex I is blocked, this NADH cannot enter the ETC, making the shuttle’s effort futile. in contrast, the glycerol-3-phosphate shuttle feeds complex II and would still function — an important metabolic flexibility.

during gluconeogenesis from lactate, the cytoplasmic NADH produced must be reoxidized. which shuttle system would have a higher operational cost for the cell?

A. Glycerol-3-phosphate shuttle

B. Malate-aspartate shuttle

C. Both are equally expensive

D. Neither has a metabolic cost

B. malate-aspartate shuttle

consider that the malate-aspartate shuttle is reversible and normally imports reducing equivalents into mitochondria. during gluconeogenesis, what direction must it operate? think about what energy might be required to drive the shuttle “backward” against its normal direction. the glycerol-3-phosphate shuttle is irreversible — how does this affect its operational cost?

a cell that is actively performing gluconeogenesis, fatty acid synthesis, and protein synthesis would most likely have:

A. No relationship between energy charge and oxidative phosphorylation

B. Low energy charge and rapid oxidative phosphorylation

C. Incorrect: High energy charge and slow oxidative phosphorylation

D. Variable energy charge depending on substrate availability

B. low energy charge and rapid oxidative phosphorylation

consider the ATP requirements of each process mentioned. are the ATP-producing (catabolic) or ATP-consuming (anabolic)? when cell is building large molecules, what happens to its ATP;ADP ratio, and how does this affect oxidative phosphorylation rate through acceptor control?

match each metabolic state with its expected effect on oxidative phosphorylation rate:

1. active glycolysis with high ATP demand

2. gluconeogenesis from amino acids

3. resting state with high ATP/ADP ratio

1. rapid rate

2. rapid rate

3. slow rate

Active glycolysis with high ATP demand depletes ATP (high ADP), stimulating rapid oxidative phosphorylation. Gluconeogenesis is ATP-intensive, also driving rapid oxidative phosphorylation. The resting state with high ATP/ADP ratio exhibits respiratory control—limited ADP availability slows oxidative phosphorylation. You've correctly identified how energy charge regulates oxidative phosphorylation rate.

true or false: if both the glycerol-3-phosphate shuttle and complex II where simultaneously inhibited, a cell could still produce ATP from glucose catabolism

true

the cell would lose the contribution from the glycerol-3-phosphate shuttle and complex II (including succinate oxidation in the TCA cycle), but the malate-aspartate shuttle could still deliver cytoplasmic NADH to complex I. additionally, NADH from the TCA cycle would still feed complex I, and glycolysis would still produce substrate-level phosphorylation ATP. total ATP would be reduced, but not eliminated.