The Electron Transport Chain

A set of flashcards designed to review key concepts regarding the Electron Transport Chain and its significance in metabolism and ATP production.

What happens to protons during the process of oxidative phosphorylation?

Protons are pumped across the inner mitochondrial membrane, creating a proton gradient that is then used to drive ATP synthesis when protons flow back into the mitochondrial matrix.

What is the total maximum ATP yield from glucose metabolism via glycolysis, TCA cycle, and oxidative phosphorylation?

The total maximum ATP yield is typically 36 to 38 ATP, depending on the shuttle used for transferring NADH to the mitochondrion.

How do defects in oxidative phosphorylation relate to clinical conditions?

Defects can lead to diseases like Parkinsonros and Alzheimerrs due to their significance in tissues with high ATP demands.

What consequences arise from inhibition of the Electron Transport Chain?

Inhibition of any complex in the Electron Transport Chain can lead to decreased ATP synthesis and can ultimately result in cell death.

What is the primary function of Complex I in the electron transport chain?

To transfer electrons from NADH to coenzyme Q (ubiquinone).

What are the intermediate electron carriers found in Complex I?

FMN and Fe-S (iron-sulfur) centers.

From which metabolic pathways does the NADH utilized by Complex I primarily originate?

The TCA cycle and glycolysis.

By what other name is Complex II known?

Succinate dehydrogenase.

What is the main function of Complex II in the electron transport chain?

It transfers electrons from FADH₂ to coenzyme Q.

What reduction is directly linked to the oxidation of succinate to fumarate in Complex II?

The reduction of FAD to FADH₂.

Describe the dual role of succinate dehydrogenase (Complex II).

It functions in both the TCA cycle (oxidizing succinate to fumarate) and the electron transport chain (transferring electrons to coenzyme Q).

What is the primary function of Complex III (Cytochrome bc₁ complex)?

To transfer electrons from ubiquinol to cytochrome c.

What are the intermediate electron carriers in Complex III?

Cytochrome b and Fe-S (iron-sulfur) centers.

How is ubiquinol best described in the context of the electron transport chain?

It is the reduced form of ubiquinone.

By what other name is Complex IV known?

Cytochrome c oxidase.

What is the main role of Complex IV?

To transfer electrons from cytochrome c to molecular oxygen.

What are the intermediate electron carriers found in Complex IV?

Cytochrome a and copper centers.

During the ETC, electrons move from:

Higher to lower energy states, releasing free energy

The free energy released by redox reactions in the ETC is used to:

Pump protons across the inner mitochondrial membrane

The series of reactions in the ETC are best described as:

Oxidation-reduction (redox) reactions

The redox reactions in the ETC are:

Exergonic and release free energy

The free energy released during electron transfer in the ETC is primarily used to:

Pump protons across the inner mitochondrial membrane

During oxidative phosphorylation, protons are pumped:

From the mitochondrial matrix into the intermembrane space

The chemiosmotic hypothesis explains:

How free energy from electron transport produces ATP

According to the chemiosmotic hypothesis, what occurs first?

Proton pumping across the inner mitochondrial membrane

The inner mitochondrial membrane is:

Impermeable to protons, maintaining a proton gradient

The proton gradient across the inner mitochondrial membrane creates:

An electrochemical potential (proton motive force)

How many proton pumping complexes are there in the ETC?

3

Proton pumping by ETC complexes results in

An electrochemical gradient with high [H⁺] in the intermembrane space

Complex V (ATP synthase) consists of:

Fo and F1 subunits

The Fo unit of ATP synthase functions as:

The proton channel in the inner mitochondrial membrane

The F1 unit of ATP synthase:

Synthesises ATP from ADP and Pi

What mechanical event drives ATP synthesis in ATP synthase?

Rotation of the Fo unit

How many ATP molecules are produced per NADH molecule during oxidative phosphorylation?

3

How many ATP molecules are produced per FADH₂ molecule?

2

The maximum theoretical yield of ATP per glucose molecule is:

36-38

The variation in total ATP yield (36 or 38 ATP) depends on:

The type of shuttle system used to transfer cytosolic NADH electrons

The malate–aspartate shuttle produces a total of:

38 ATP

The glycerol-3-phosphate shuttle produces a total of:

36 ATP

In most cells, GTP formed in the TCA cycle is:

Instantly converted to ATP

Defects in oxidative phosphorylation are most commonly due to mutations in:

Mitochondrial DNA (mtDNA)

The mutation rate of mitochondrial DNA (mtDNA) is approximately how much greater than that of nuclear DNA?

10X

Tissues most affected by oxidative phosphorylation defects are those with:

High ATP requirement

Which tissues are most commonly affected by defects in oxidative phosphorylation?

Central nervous system, skeletal muscle, and heart muscle

Impaired oxidative phosphorylation is implicated in which of the following diseases?

Parkinson’s disease and Alzheimer’s disease

Mitochondrial DNA mutations are inherited:

Maternally only

Leber hereditary optic neuropathy is caused by point mutations in genes encoding subunits of which complexes of the ETC?

I, III, and IV

The major clinical manifestation of Leber hereditary optic neuropathy is:

Sudden onset of blindness in young adults

In Leber hereditary optic neuropathy, the inheritance pattern means that:

Only mothers transmit the disease to all their children

The optic nerve is particularly affected in LHON because it:

Relies almost entirely on oxidative phosphorylation for energy

The underlying mechanism of vision loss in LHON is:

Impaired electron flow and decreased ATP production

Inhibition of any ETC complex ultimately leads to:

Inhibition of ATP synthesis and cell death

Riboflavin (vitamin B₂) deficiency primarily affects which ETC complexes?

Complex I and II

The reason riboflavin deficiency affects Complex I and II is because:

Flavin (FMN and FAD) is derived from riboflavin

Which vitamin deficiency also affects electron transport due to its role in NAD synthesis?

Vitamin B3 (niacin)

The poison rotenone inhibits which ETC complex?

Complex I

Doxorubicin inhibits which ETC component, leading to cardiotoxicity?

Coenzyme Q (ubiquinone)

The cardiotoxicity of doxorubicin as a chemotherapy drug is due to:

Inhibition of coenzyme Q in cardiac mitochondria

Iron deficiency can impair which ETC complexes?

Complexes I–III

Why does iron deficiency inhibit multiple ETC complexes?

Iron is needed for cytochrome and Fe–S centres