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Krebs Cycle Ets

🎓 Class 11 Biology CBSE Theory Ch 12 – Respiration in Plants ⏱ ~14 min
🌐 ભાષા:

આ MCQ મોડ્યુલ આના પર આધારિત છે: Krebs Cycle Ets

આ મૂલ્યાંકન આના પર આધારિત હશે: Krebs Cycle Ets

મૂલ્યાંકન બનાવવામાં તેમની સામગ્રી સામેલ કરવા ચિત્રો, PDF અથવા Word દસ્તાવેજ અપલોડ કરો.

Krebs’ Cycle, the Electron Transport System and Oxidative Phosphorylation

Two molecules of acetyl CoA are now in the mitochondrial matrix, carrying four of the original glucose's six carbons. This part strips those carbons away, banks the energy in reduced coenzymes, and finally cashes the coenzymes in for ATP at the inner membrane — where oxygen is waiting at the end of the line.

12.4.1 Tricarboxylic Acid Cycle

The opening condensation

The TCA cycle starts with the condensation of the acetyl group with oxaloacetic acid (OAA) and water to yield citric acid. The reaction is catalysed by the enzyme citrate synthase, and a molecule of CoA is released. Note the carbon arithmetic: acetyl (2C) + OAA (4C) = citric acid (6C) — a tricarboxylic acid, which is where the cycle's formal name comes from.

The two decarboxylations

Citrate is then isomerised to isocitrate. It is followed by two successive steps of decarboxylation, leading to the formation of α-ketoglutaric acid and then succinyl-CoA. Each decarboxylation removes one carbon as CO₂: citrate/isocitrate (6C) → α-ketoglutaric acid (5C)succinyl-CoA (4C).

The substrate-level phosphorylation

In the remaining steps of the citric acid cycle, succinyl-CoA is oxidised to OAA, allowing the cycle to continue. During the conversion of succinyl-CoA to succinic acid a molecule of GTP is synthesised.

This is a substrate level phosphorylation — the only one in the cycle, and quite distinct from the membrane-linked ATP synthesis of the ETS. In a coupled reaction GTP is converted to GDP with the simultaneous synthesis of ATP from ADP. So the cycle's direct ATP yield comes through GTP, not from any electron transport.

Where the reducing power is generated

There are three points in the cycle where NAD⁺ is reduced to NADH + H⁺ and one point where FAD⁺ is reduced to FADH₂.

What the cycle must be given back. The continued oxidation of acetyl CoA via the TCA cycle requires the continued replenishment of oxaloacetic acid, the first member of the cycle. In addition it also requires regeneration of NAD⁺ and FAD⁺ from NADH and FADH₂ respectively. The second requirement is precisely what the electron transport system does — which is why the cycle cannot run for long without oxygen even though oxygen never enters the cycle itself.
Figure 12.3 — The citric acid (Krebs') cycle Pyruvate (3C) CO₂ out NADH + H⁺ CoA, NAD⁺ in Acetyl coenzyme A (2C) Oxaloacetic acid (4C) Citric acid (6C) α-ketoglutaric (5C) Succinic acid (4C) Malic acid (4C) Fumaric acid (4C) CITRIC ACID CYCLE mitochondrial matrix citrate synthase; + H₂O, CoA released CO₂NADH CO₂NADH GTP → ATP FAD⁺ → FADH₂ NADH ONE TURN GIVES 3 NADH + H⁺ 1 FADH₂ 1 GTP → 1 ATP and 2 CO₂

The summary equation for this phase of respiration may be written as follows:

Pyruvic acid + 4NAD+ + FAD+ + 2H2O + ADP + Pi
—mitochondrial matrix→
3CO2 + 4NADH + 4H+ + FADH2 + ATP
Read that equation carefully — it covers the link reaction too. It starts from pyruvic acid, not acetyl CoA, so the 3CO₂ and the 4 NADH include the one CO₂ and one NADH of the oxidative decarboxylation, plus the two CO₂ and three NADH of the cycle itself. This is exactly the “complete oxidation of pyruvate by the stepwise removal of all the hydrogen atoms, leaving three molecules of CO₂” promised in Part 2. Per glucose, double everything.

So far, then: glucose has been broken down to release CO₂, and eight molecules of NADH + H⁺ and two of FADH₂ have been synthesised, besides just two molecules of ATP in the TCA cycle. Neither O₂ nor the promised large number of ATP has yet appeared. What is the role of all this NADH + H⁺ and FADH₂?

📐 Activity 12.3 — Audit the eight NADH of one glucose

What to do. On paper, list every step in this chapter so far that reduces NAD⁺ to NADH + H⁺, write how many times each occurs per glucose, and add them up. Do the same for FADH₂ and for ATP made directly (substrate-level). Then check your total against the sentence above.

Predict: before adding, guess how the eight NADH split between glycolysis, the link reaction and the cycle.
StepTimes per glucoseNADHFADH₂ATP (direct)
Glycolysis: PGAL → BPGA22
Glycolysis: BPGA → PGA and PEP → pyruvate2 each4 gross, 2 net
Link reaction: pyruvate → acetyl CoA22
TCA cycle: three NAD⁺ points2 turns × 36
TCA cycle: one FAD⁺ point2 turns × 12
TCA cycle: succinyl-CoA → succinic acid (GTP)22

Totals. NADH from glycolysis 2, from the link reaction 2, from the cycle 6 — that is 10, of which the chapter's phrase “eight molecules of NADH + H⁺” counts the mitochondrial ones (2 from the link reaction + 6 from the cycle), since it is describing what happens after glucose enters the mitochondrion. Add the 2 from glycolysis and the full tally per glucose is 10 NADH, 2 FADH₂, 2 ATP net from glycolysis and 2 ATP from the cycle. Keep this table — Part 4 turns it into the respiratory balance sheet.

The point of the audit. Notice that almost nothing has been made as ATP. The energy of glucose is at this stage stored almost entirely as reduced coenzymes, and cashing them in is the job of the electron transport system.

12.4.2 Electron Transport System (ETS) and Oxidative Phosphorylation

The following steps in the respiratory process are to release and utilise the energy stored in NADH + H⁺ and FADH₂. This is accomplished when they are oxidised through the electron transport system and the electrons are passed on to O₂, resulting in the formation of H₂O.

The electron transport system (ETS) is the metabolic pathway through which the electron passes from one carrier to another, and it is present in the inner mitochondrial membrane.

The carriers, complex by complex

  • Complex I — NADH dehydrogenase. Electrons from NADH produced in the mitochondrial matrix during the citric acid cycle are oxidised by an NADH dehydrogenase (complex I), and electrons are then transferred to ubiquinone located within the inner membrane.
  • Complex II. Ubiquinone also receives reducing equivalents via FADH₂ (complex II) that is generated during oxidation of succinate in the citric acid cycle. Note that FADH₂ enters later than NADH, bypassing complex I — the reason its ATP yield is lower.
  • Complex III — cytochrome bc₁. The reduced ubiquinone (ubiquinol) is then oxidised with the transfer of electrons to cytochrome c via the cytochrome bc₁ complex (complex III).
  • Cytochrome c. A small protein attached to the outer surface of the inner membrane, acting as a mobile carrier for transfer of electrons between complex III and IV.
  • Complex IV — cytochrome c oxidase. This refers to the cytochrome c oxidase complex containing cytochromes a and a₃, and two copper centres.
  • Complex V — ATP synthase. When the electrons pass from one carrier to another via complex I to IV in the electron transport chain, they are coupled to ATP synthase (complex V) for the production of ATP from ADP and inorganic phosphate.
Figure 12.4 — The Electron Transport System (ETS) INTERMEMBRANE SPACE protons accumulate here inner mitochondrial membrane MATRIX Complex INADHdehydrogenase Complex II(FADH₂) Complex IIIcytochromebc₁ Complex IVcyt c oxidasecyt a, a₃, 2 Cu Complex VATP synthaseF₁ – F₀ UQ ubiquinone cyt c NADH + H⁺ FADH₂ (succinate) ½O₂ + 2H⁺ → H₂O ADP + Pi → ATP 4H⁺ per ATP NADH enters at complex I and yields 3 ATP; FADH₂ enters later at complex II and yields 2 ATP. Oxygen acts only at the very end — as the final hydrogen acceptor.

How much ATP per coenzyme?

The number of ATP molecules synthesised depends on the nature of the electron donor. Oxidation of one molecule of NADH gives rise to 3 molecules of ATP, while that of one molecule of FADH₂ produces 2 molecules of ATP.

The role of oxygen — small but indispensable

Although the aerobic process of respiration takes place only in the presence of oxygen, the role of oxygen is limited to the terminal stage of the process. Yet the presence of oxygen is vital, since it drives the whole process by removing hydrogen from the system. Oxygen acts as the final hydrogen acceptor.

Why this matters more than it looks. Oxygen touches only the last complex, and yet withdraw it and everything upstream stops within seconds — ETS, Krebs' cycle, the link reaction, all of it. The reason is the chain of dependencies you have been building: the cycle needs NAD⁺ and FAD⁺ regenerated, only the ETS regenerates them, and the ETS can only keep passing electrons if something takes them off the end. Remove the final acceptor and the queue backs up all the way to pyruvate — which is exactly when the cell falls back on fermentation.

Why it is called oxidative phosphorylation

Unlike photophosphorylation, where it is the light energy that is utilised for the production of the proton gradient required for phosphorylation, in respiration it is the energy of oxidation-reduction utilised for the same process. It is for this reason that the process is called oxidative phosphorylation.

ATP synthase — F₁ and F₀

You have already studied the mechanism of membrane-linked ATP synthesis as explained by the chemiosmotic hypothesis in the earlier chapter. The energy released during the electron transport system is utilised in synthesising ATP with the help of ATP synthase (complex V), which consists of two major components, F₁ and F₀.

  • The F₁ headpiece is a peripheral membrane protein complex and contains the site for synthesis of ATP from ADP and inorganic phosphate.
  • F₀ is an integral membrane protein complex that forms the channel through which protons cross the inner membrane.

The passage of protons through the channel is coupled to the catalytic site of the F₁ component for the production of ATP. And the precise stoichiometry is worth memorising: for each ATP produced, 4H⁺ pass through F₀ from the intermembrane space to the matrix down the electrochemical proton gradient.

Photophosphorylation versus oxidative phosphorylation
FeaturePhotophosphorylation (Chapter 11)Oxidative phosphorylation (Chapter 12)
Membrane involvedThylakoid membrane of the chloroplastInner mitochondrial membrane
Energy source for the gradientLight energyEnergy of oxidation–reduction
Where protons accumulateThylakoid lumenIntermembrane space
Enzyme partsCF₀ (channel) and CF₁ (facing stroma)F₀ (channel) and F₁ (headpiece, catalytic site)
Terminal electron acceptorNADP⁺O₂ — the final hydrogen acceptor, reduced to H₂O
Proton cost per ATP4H⁺ through F₀

🎯 Interactive: Follow an electron down the chain

What it does: Oxidises NADH from the matrix

Electrons from NADH produced in the mitochondrial matrix during the citric acid cycle are oxidised by NADH dehydrogenase and then transferred to ubiquinone, located within the inner membrane. Because NADH enters at the very first complex, its oxidation yields 3 ATP.

🎯 Competency-Based Questions

Scenario: Isolated plant mitochondria are supplied with pyruvate, ADP, inorganic phosphate and oxygen, and ATP production is measured. Three treatments are then applied in separate flasks: (i) an inhibitor that blocks cytochrome c oxidase; (ii) an uncoupler that makes the inner membrane freely permeable to protons; (iii) malonate, which blocks the oxidation of succinate.

Q1. Predict the effect of treatment (i) on ATP production and on the Krebs' cycle. L4 Analyse

ATP production by oxidative phosphorylation stops, and the Krebs' cycle stops too. Complex IV is cytochrome c oxidase, the point at which electrons are finally handed to oxygen. Block it and electrons cannot leave the chain, so every carrier upstream stays reduced. NAD⁺ and FAD⁺ are no longer regenerated, and since the continued oxidation of acetyl CoA via the TCA cycle requires regeneration of NAD⁺ and FAD⁺, the cycle halts. Only substrate-level phosphorylation (the GTP step) could continue briefly, and only until the coenzymes run out.

Q2. In treatment (ii) electron transport continues and oxygen is consumed, yet no ATP is made. Explain. L4 Analyse

Because ATP synthesis is membrane-linked, not directly chemical. The ETS does not make ATP itself; it builds a proton gradient, and for each ATP produced, 4H⁺ pass through F₀ from the intermembrane space to the matrix down the electrochemical proton gradient. If protons can leak across the membrane freely, no gradient develops, so nothing drives the catalytic site of F₁. Electron flow and oxygen consumption are unaffected because they do not depend on the gradient — which is precisely why such substances are called uncouplers: they separate oxidation from phosphorylation.

Q3. Fill in the blanks: Oxidation of one NADH yields ______ ATP while one FADH₂ yields ______ ATP, because FADH₂ enters the chain at complex ______ and therefore bypasses complex ______. L2 Understand

3; 2; II; I. Both donors reduce the same ubiquinone, but FADH₂ joins the chain further along, so fewer energy-releasing transfers lie ahead of its electrons.

Q4. Malonate in treatment (iii) blocks succinate oxidation. Which single entry into the ETS is lost, and by how much does the theoretical ATP yield per glucose fall? L3 Apply

The FADH₂ entry at complex II is lost, since ubiquinone receives reducing equivalents via FADH₂ generated during oxidation of succinate in the citric acid cycle. Per glucose the cycle turns twice and so makes 2 FADH₂, each worth 2 ATP — a loss of 4 ATP. In practice the loss is far worse, because blocking a step of the cycle also stops the regeneration of oxaloacetic acid, and the continued oxidation of acetyl CoA requires the continued replenishment of OAA, the first member of the cycle. The whole cycle would seize up, not merely lose one branch.

Q5. “Since oxygen acts only at the terminal stage, its role in respiration is minor.” Evaluate this statement. L5 Evaluate

The statement's premise is true but its conclusion is wrong, and the chapter says so in almost these words. Yes — the role of oxygen is limited to the terminal stage of the process; oxygen appears nowhere in glycolysis, nowhere in the link reaction and nowhere in the Krebs' cycle. But the presence of oxygen is vital, since it drives the whole process by removing hydrogen from the system. Oxygen acts as the final hydrogen acceptor. The mistake is to equate “acts at one point” with “matters little”. A chain of carriers can only keep accepting electrons if something is taking them off the far end; with no final acceptor, every carrier stays reduced, NAD⁺ and FAD⁺ are not regenerated, the cycle stops for want of them, and the cell is thrown back on fermentation with its net two ATP and under seven per cent energy release. A better formulation: oxygen's participation is positionally minimal but functionally decisive — it is the drain that lets the whole pipeline flow.

🧠 Assertion–Reason Questions

For each pair choose: (A) Both A and R are true and R is the correct explanation of A. (B) Both A and R are true but R is not the correct explanation of A. (C) A is true but R is false. (D) A is false but R is true.

Assertion (A): Oxidation of FADH₂ yields fewer ATP than oxidation of NADH.

Reason (R): FADH₂ passes its reducing equivalents to ubiquinone via complex II, bypassing complex I.

Answer: A. Both are true and the reason explains the assertion: fewer energy-releasing transfers remain downstream, so FADH₂ gives 2 ATP against NADH's 3.

Assertion (A): The GTP formed in the Krebs' cycle is an example of oxidative phosphorylation.

Reason (R): GTP is formed during the conversion of succinyl-CoA to succinic acid and is converted to GDP with the simultaneous synthesis of ATP from ADP.

Answer: D. The assertion is false — this is a substrate level phosphorylation, not oxidative phosphorylation, since it needs no membrane, no proton gradient and no electron transport. The reason correctly states where and how the GTP arises.

Assertion (A): The process at the inner mitochondrial membrane is called oxidative phosphorylation.

Reason (R): The energy of oxidation–reduction, rather than light energy, is used to produce the proton gradient required for phosphorylation.

Answer: A. Both are true and the reason is precisely the naming logic the chapter gives, contrasting it with photophosphorylation in the chloroplast.
Coming next. Part 4 takes up Sections 12.5 to 12.7 — the respiratory balance sheet with the four assumptions it rests on and the figure of 38 ATP, why the respiratory pathway is amphibolic rather than merely catabolic, and the respiratory quotient with its values for carbohydrates, fats and proteins.

Frequently Asked Questions - Krebs Cycle, ETS and Oxidative Phosphorylation

How does the Krebs cycle begin?
With the condensation of the acetyl group with oxaloacetic acid and water to yield citric acid, catalysed by citrate synthase, with a molecule of CoA released. Acetyl CoA contributes 2 carbons and OAA 4, giving the 6-carbon tricarboxylic acid that names the cycle.
How many NADH, FADH2 and ATP does one turn of the Krebs cycle give?
There are three points where NAD+ is reduced to NADH + H+ and one point where FAD+ is reduced to FADH2. One GTP is synthesised during the conversion of succinyl-CoA to succinic acid, and in a coupled reaction that GTP gives one ATP. Two CO2 are released per turn.
What is substrate level phosphorylation in respiration?
It is ATP formation that does not depend on a membrane or a proton gradient. In the Krebs cycle, GTP is synthesised during the conversion of succinyl-CoA to succinic acid, and this GTP is converted to GDP with the simultaneous synthesis of ATP from ADP.
What does the Krebs cycle need replenished to keep running?
Oxaloacetic acid, the first member of the cycle, must be continually replenished, and NAD+ and FAD+ must be regenerated from NADH and FADH2. The second requirement is met by the electron transport system, which is why the cycle stops without oxygen.
What is the electron transport system and where is it located?
It is the metabolic pathway through which the electron passes from one carrier to another, present in the inner mitochondrial membrane. NADH and FADH2 are oxidised through it and the electrons are passed on to O2, resulting in the formation of water.
Name the complexes of the ETS and what each does.
Complex I is NADH dehydrogenase, which oxidises NADH and passes electrons to ubiquinone. Complex II brings in reducing equivalents from FADH2. Complex III is the cytochrome bc1 complex, which oxidises ubiquinol and passes electrons to cytochrome c, a mobile carrier on the outer surface of the inner membrane. Complex IV is cytochrome c oxidase with cytochromes a and a3 and two copper centres. Complex V is ATP synthase.
How many ATP are formed from one NADH and one FADH2?
Oxidation of one molecule of NADH gives rise to 3 molecules of ATP, while that of one molecule of FADH2 produces 2 molecules of ATP. The difference arises because FADH2 enters the chain at complex II, bypassing complex I.
What exactly is the role of oxygen in respiration?
Its role is limited to the terminal stage, where it acts as the final hydrogen acceptor and is reduced to water. Yet its presence is vital, because by removing hydrogen from the system it drives the whole process, keeping the carriers free to accept more electrons and allowing NAD+ and FAD+ to be regenerated.
Why is it called oxidative phosphorylation?
Because unlike photophosphorylation, where light energy is used to produce the proton gradient needed for phosphorylation, in respiration it is the energy of oxidation and reduction that is used for the same purpose.
What are F1 and F0 in mitochondrial ATP synthase?
F1 is a peripheral membrane protein complex forming the headpiece, and it contains the site for synthesis of ATP from ADP and inorganic phosphate. F0 is an integral membrane protein complex forming the channel through which protons cross the inner membrane. For each ATP produced, 4H+ pass through F0 from the intermembrane space to the matrix.
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