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Electron Transport Chain – Diagram, Definition, Steps, Products, Importance

Table of Contents

What is the Electron Transport Chain?

  • The Electron Transport Chain (ETC) is a pivotal component in the cellular respiration process. It is a series of intricate reactions that harness the redox energy derived from the oxidation of NADH and FADH2. This energy is then transformed into a proton-motive force, which is instrumental in the synthesis of ATP through a mechanism termed oxidative phosphorylation.
  • Oxidative phosphorylation is the culminating phase of cellular respiration. During this phase, electrons are transferred from organic compounds to oxygen, releasing energy in the process. In the context of aerobic respiration, molecular oxygen serves as the ultimate electron acceptor.
  • However, in anaerobic respiration, other molecules, such as sulfate, assume this role. This sequence of reactions is paramount because it facilitates the breakdown of ATP into ADP and its subsequent reformation into ATP. Remarkably, this cycle enables the body to utilize its finite ATP stores approximately 300 times daily.
  • The progression of electrons occurs through four substantial protein complexes situated in the inner mitochondrial membrane. Collectively, these complexes are referred to as the respiratory chain or the electron-transport chain.
  • This phase is of utmost importance in energy production. This is because all oxidative stages in the breakdown of carbohydrates, fats, and amino acids culminate in this final phase of cellular respiration, where the energy from oxidation propels ATP synthesis.
  • Furthermore, the ETC comprises a sequence of protein complexes and molecules that facilitate the transfer of electrons from electron donors to electron acceptors through redox reactions.
  • This simultaneous reduction and oxidation process is coupled with the transfer of protons (H+ ions) across a membrane. The electrons transferred from NADH and FADH2 traverse through four extensive enzyme complexes and two mobile electron carriers, many of which are embedded within the membrane.
  • The movement of electrons within the ETC is an exergonic process. The energy derived from these redox reactions establishes an electrochemical proton gradient, which is pivotal for the synthesis of ATP. In the realm of aerobic respiration, this electron flow culminates with molecular oxygen serving as the final electron acceptor. Conversely, in anaerobic respiration, alternative electron acceptors like sulfate are employed.
  • The driving force behind these redox reactions in the ETC is the disparity in the Gibbs free energy between reactants and products. The energy liberated during the conversion of higher-energy electron donors and acceptors into their lower-energy counterparts is harnessed by the ETC complexes to establish an electrochemical gradient of ions. This gradient propels the synthesis of ATP by coupling oxidative phosphorylation with ATP synthase.
  • In eukaryotic entities, the ETC and the site of oxidative phosphorylation are localized on the inner mitochondrial membrane. The energy released from the reactions between oxygen and reduced compounds, such as cytochrome c, NADH, and FADH2, is employed by the ETC to pump protons into the intermembrane space.
  • This action generates an electrochemical gradient across the inner mitochondrial membrane. In photosynthetic eukaryotes, the ETC is located on the thylakoid membrane, where light energy propels electron transport, leading to ATP synthesis.
  • In bacteria, the specifics of the ETC can differ among species, but it invariably consists of redox reactions coupled to ATP synthesis through the creation of an electrochemical gradient and oxidative phosphorylation via ATP synthase.
  • Therefore, the Electron Transport Chain is not only a marvel of biological engineering but also a testament to the intricate processes that sustain life at the cellular level.

Electron transport chain Definition

The Electron Transport Chain (ETC) is a series of protein complexes and molecules located in the inner mitochondrial membrane that transfers electrons from electron donors to electron acceptors, facilitating the production of ATP through oxidative phosphorylation.

Electron Transport Chain Animation Video

Fundamentals of Electron Transport Chain 

  • The Electron Transport Chain (ETC) is a crucial component of aerobic cellular respiration, a process that cells employ to generate energy. To understand the fundamentals of the ETC, it’s essential to first grasp the broader context of aerobic cellular respiration.
  • Aerobic cellular respiration can be delineated into three primary stages: glycolysis, the citric acid (or Krebs) cycle, and oxidative phosphorylation. In the initial phase, glycolysis, glucose undergoes metabolism to yield two pyruvate molecules. This process results in the production of ATP and nicotinamide adenine dinucleotide (NADH). Subsequently, each pyruvate molecule undergoes oxidation to form acetyl CoA, generating an additional NADH molecule and releasing carbon dioxide (CO2). This acetyl CoA then enters the citric acid cycle, a sequence of chemical reactions that yield CO2, NADH, flavin adenine dinucleotide (FADH2), and ATP.
  • The culmination of these processes leads to the final stage: oxidative phosphorylation. Here, the accumulated NADH and FADH2 molecules from the preceding stages are utilized to produce water and ATP. This stage can be further divided into two components: the electron transport chain and chemiosmosis.
  • The ETC is a complex assembly of proteins anchored to the inner mitochondrial membrane, along with organic molecules. Electrons traverse this chain through a series of redox reactions, releasing energy in the process. This energy is harnessed to establish a proton gradient. Following this, chemiosmosis comes into play. The proton gradient created is exploited by the protein ATP-synthase to synthesize a significant quantity of ATP.
  • Besides cellular respiration, the concept of an electron transport chain is also pivotal in photosynthesis, a process plants employ to convert light energy into chemical energy in the form of sugars. In the light-dependent reactions of photosynthesis, light energy and water are harnessed to produce ATP, NADPH, and oxygen (O2). The formation of the ATP in this phase is facilitated by a proton gradient established via an electron transport chain. Subsequent to these reactions, in the light-independent phase, sugars are synthesized using the ATP and NADPH generated earlier.
  • Therefore, the electron transport chain is not only integral to cellular respiration but also plays a vital role in photosynthesis. It serves as a bridge, channeling electrons and harnessing their energy for the synthesis of ATP, the primary energy currency of cells. This intricate system underscores the precision and efficiency of cellular processes, emphasizing the importance of the ETC in energy production and utilization.

Electron Transport Chain Diagram

Electron Transport Chain Diagram
Electron Transport Chain Diagram

Equation of Electron Transport Chain 

The Electron Transport Chain (ETC) is a fundamental component in the realm of cellular respiration, playing a pivotal role in energy production. At its core, the ETC is a sequence of oxidation-reduction reactions that facilitate the release of energy. These reactions are meticulously orchestrated, ensuring the efficient conversion of molecules and the subsequent production of ATP, the cell’s primary energy currency.

To elucidate further, the equation representing the reactions within the electron transport chain is as follows:

NADH+21​O2​+H++ADP+PiNAD++ATP+H2​O

Breaking down this equation:

  • NADH is oxidized, releasing electrons that are then channeled through the ETC. In the process, NADH is converted back to its oxidized form, NAD+.
  • Molecular oxygen (O2​), serving as the final electron acceptor in the chain, is reduced by accepting electrons and protons to form water (H2​O).
  • Concurrently, the energy released during these reactions is harnessed to combine DP (adenosine diphosphate) and Pi (inorganic phosphate) to synthesize ATP (adenosine triphosphate), the primary energy molecule in cells.

Therefore, this equation succinctly encapsulates the series of reactions that transpire within the ETC. Besides the primary reactants and products, it’s essential to understand that several protein complexes and coenzymes are involved in facilitating these reactions. These complexes, embedded in the inner mitochondrial membrane, ensure the smooth flow of electrons, culminating in the production of ATP.

In essence, the electron transport chain is a marvel of biological precision, ensuring that cells have a consistent and efficient means of producing energy. The aforementioned equation provides a concise yet comprehensive overview of the processes and molecules involved, emphasizing the functions and transformations that occur within this critical pathway.

Electron Transport Chain Location – Where does the Electron Transport Chain take Place?

  • The Electron Transport Chain (ETC) is a pivotal component in cellular respiration, and its location is integral to its function. In eukaryotic cells, the ETC is situated within the mitochondria, a specialized double-membraned organelle often dubbed the “powerhouse” of the cell.
  • The mitochondrion is characterized by its unique double-membrane structure. The outer membrane is permeable to ions and encompasses enzymes vital for the citric acid cycle. In contrast, the inner membrane is impermeable to many ions and houses the electron transport chain, along with enzymes essential for ATP synthesis. This inner membrane is intricately folded into structures known as cristae, which increase the surface area, thereby enhancing the efficiency of energy production.
  • Within the mitochondrion, there are two distinct compartments: the matrix and the intermembrane space. The matrix is rich in essential enzymes and molecules, including ATP, ADP, AMP, NAD, NADP, and various ions like Ca^2+ and Mg^2+. The intermembrane space, on the other hand, contains enzymes such as adenylate kinase.
  • The number of electron transport chains within the mitochondria can vary based on the cell’s location and function. For instance, liver mitochondria house approximately 10,000 sets of electron transport chains. In contrast, heart mitochondria, given their heightened energy demands, possess nearly three times this number.
  • During the ETC’s operation, protons are actively pumped from the mitochondrial matrix into the intermembrane space. This action establishes a proton gradient, often termed the “proton motive force.” This gradient is instrumental in driving ATP production through a mechanism known as the chemiosmotic mechanism. Essentially, the ATP produced is directly proportional to the number of protons shuttled across the inner mitochondrial membrane.
  • The ETC itself comprises a series of redox reactions facilitated by protein complexes. These complexes transfer electrons from a donor molecule to an acceptor molecule. As a result of these reactions, the aforementioned proton gradient is established. This gradient effectively converts mechanical work into chemical energy, culminating in ATP synthesis. These complexes are firmly embedded within the cristae of the inner mitochondrial membrane in eukaryotes. It’s worth noting that while the ETC is predominantly found in the mitochondria of eukaryotes, it also exists in the thylakoid membrane of chloroplasts in photosynthetic eukaryotes and, with certain modifications, in prokaryotes.
  • The ETC utilizes by-products from various metabolic pathways, including the citric acid cycle, amino acid oxidation, and fatty acid oxidation. The overarching redox reaction of the ETC can be summarized as:
    2H++2e−+21​O2​→H2​O+ENERGY
  • In this exothermic reaction, energy is liberated as electrons traverse the complexes, producing three ATP molecules. The matrix’s phosphate is imported via the proton gradient, contributing to further ATP synthesis. This ATP generation process, powered by the oxidation of hydrogen, is termed oxidative phosphorylation. The ATP molecules synthesized subsequently fuel a myriad of cellular reactions essential for life.
  • Therefore, the Electron Transport Chain’s location within the mitochondria is not a mere coincidence but a testament to the intricate design of cellular machinery, ensuring optimal energy production and utilization.

Components/ Electron carriers of Electron Transport Chain

Ubiquinone to Ubiquinol
Ubiquinone to Ubiquinol

The Electron Transport Chain (ETC) is a meticulously orchestrated sequence of reactions that facilitate the transfer of electrons from one molecule to another. Central to this process are the electron carriers, which play a pivotal role in ensuring the smooth progression of these reactions. These carriers are specialized molecules that accept and donate electrons, driving the chain forward.

  1. FMN (Flavin Mononucleotide) At the onset of the electron transport chain, electrons derived from NADH are relayed to Flavin Mononucleotide (FMN). This transfer results in the reduction of FMN to FMNH2, as depicted by the equation: NAD+H++FMNNAD+FMNH2 This electron transfer is facilitated by the enzyme NADH dehydrogenase. Subsequently, these electrons are conveyed to a series of iron-sulfur complexes (Fe-S), which exhibit a heightened affinity for electrons.
  2. Ubiquinone (Co-enzyme-Q) Positioned between the flavoproteins and cytochromes are the ubiquinones, often referred to as UQ. Distinctively, ubiquinone stands out as the sole electron carrier in the respiratory chain that isn’t tethered to a protein. This unique characteristic grants ubiquinone the mobility to oscillate between flavoproteins and cytochromes. As electrons transition from FMNH2 through the Fe-S centers to ubiquinone, it is transformed into its reduced form, UQH2. Concurrently, the oxidized form of flavoprotein, FMN, is liberated. This process can be summarized as: FMNH2+UQFMN+UQH2
  3. Cytochromes Following ubiquinone in the electron transport sequence are the cytochromes. These are pigmented proteins, discernible by their red or brown hue, endowed with a heme group that facilitates the electron transfer from ubiquinone to molecular oxygen. It’s imperative to note that each cytochrome, akin to the Fe-S centers, transfers a singular electron. In contrast, other carriers like FMN and ubiquinone relay two electrons. There exists a spectrum of cytochromes, each classified as a, b, c, and so forth. Their nomenclature is rooted in their light absorption properties. For instance, cytochrome a absorbs the longest wavelength, followed by b, and so on.
Electron CarrierDescriptionFunction
FMN (Flavin Mononucleotide)At the beginning of the electron transfer chain, accepts electrons from NADH.Transfers electrons to Fe-S centers. Reaction: NAD + H+ + FMN → NAD + FMNH2
Ubiquinone (Co-enzyme-Q)An electron carrier between flavoproteins and cytochromes. Not bound to a protein, allowing it to move between flavoproteins and cytochromes.Accepts electrons from FMNH2 via the Fe-S centers. Reaction: FMNH2 + UQ → FMN + UQH2
CytochromesRed or brown colored proteins containing a heme group. Types include a, b, c, etc., based on their light absorption properties.Carry electrons in a sequence from ubiquinone to molecular oxygen. Each cytochrome transfers a single electron, unlike other carriers which transfer two.
Fe-S centersIron-sulfur complexes that have a higher relative affinity towards electrons.Facilitate the transfer of electrons within the chain, especially from FMN to ubiquinone.

Therefore, the electron carriers within the ETC are not mere passive participants but are instrumental in driving the chain forward. Each carrier, whether it be FMN, ubiquinone, or the various cytochromes, plays a distinct and crucial role in ensuring the efficient transfer of electrons. Their collective function underscores the precision and intricacy of the Electron Transport Chain, emphasizing its significance in cellular respiration and energy production.

Electron Transport Chain Complexes

The Electron Transport Chain (ETC) is a sophisticated series of enzyme complexes that play a pivotal role in cellular respiration, particularly in the process of oxidative phosphorylation. These complexes are strategically positioned within the inner mitochondrial membrane and are responsible for the transfer of electrons from one molecule to another, ultimately leading to the production of ATP. Let’s delve into the specifics of these complexes:

  1. Complex I (Mitochondrial complex I) Complex I, also known as NADH dehydrogenase, is the initial complex in the ETC. Comprising NADH dehydrogenases and Fe-S centers, it catalyzes the transfer of two electrons from NADH to ubiquinone (UQ). Concurrently, it translocates four H+ ions across the membrane, establishing a proton gradient. The reaction can be represented as: NADH+H++CoQNAD++CoQH2 Initially, NADH undergoes oxidation to NAD^+, reducing FMN to FMNH2. Subsequently, FMNH2 is oxidized back to FMN, with the electrons being relayed first to Fe-S centers and then to ubiquinone.
  2. Complex II (Mitochondrial complex II) Complex II, encompassing succinic dehydrogenase, FAD, and Fe-S centers, facilitates the transfer of electrons from other donors, such as fatty acids and glycerol-3 phosphate, to ubiquinone via FAD and Fe-S centers. Notably, while it operates parallel to Complex I, it does not translocate H+ ions across the membrane. The reaction can be summarized as: Succinate+FADH2+CoQFumarate+FAD++CoQH2
  3. Complex III (Mitochondrial complex III) This complex, composed of cytochrome b, c, and a specific Fe-S center, is integral for the transfer of two electrons from the reduced CoQH2 to two molecules of cytochrome c. During this process, protons from ubiquinone are released across the membrane, contributing to the proton gradient. The reaction is represented as: CoQH2+2cytcc(Fe3+)→CoQ+2cytcc(Fe2+)+4H+
  4. Complex IV (Mitochondrial complex IV) Often referred to as cytochrome oxidase, Complex IV is the terminal complex in the ETC. It comprises cytochrome a and a3 and is responsible for transferring two electrons from cytochrome c to molecular oxygen (O2), culminating in the formation of water. Simultaneously, four protons are shuttled across the membrane, further bolstering the proton gradient. The reaction can be depicted as: 4cytcc(Fe2+)+O2→4cytcc(Fe3+)+H2O
Complex NameComponentsFunction
Complex INADH dehydrogenases, Fe-S centersCatalyzes the transfer of two electrons from NADH to ubiquinone (UQ) and translocates four H+ ions across the membrane. Reaction: NADH + H+ + CoQ → NAD+ + CoQH2
Complex IISuccinic dehydrogenase, FAD, Fe-S centersFacilitates the transfer of electrons from donors like fatty acids to ubiquinone via FAD and Fe-S centers. Reaction: Succinate + FADH2 + CoQ → Fumarate + FAD+ + CoQH2
Complex IIICytochrome b, c, specific Fe-S centerTransfers two electrons from reduced CoQH2 to two molecules of cytochrome c. Protons from ubiquinone are released. Reaction: CoQH2 + 2 cytc c (Fe3+) → CoQ + 2 cytc c (Fe2+) + 4H+
Complex IVCytochrome a, a3 (cytochrome oxidase)Transfers two electrons from cytochrome c to molecular oxygen (O2), forming water. Reaction: 4 cytc c (Fe 2+) + O2 → 4cytc c (Fe3+) + H2O

Therefore, these enzyme complexes are the linchpins of the Electron Transport Chain, ensuring the seamless transfer of electrons and the establishment of a proton gradient. This gradient is instrumental in driving ATP synthesis, emphasizing the significance of these complexes in energy production within cells.

Electron Transport Chain Steps (Mitochondrial Electron Transport Chain)

Electron Transport Chain Steps
Electron Transport Chain Steps

The mitochondrial electron transport chain (ETC) is a crucial component of cellular respiration, responsible for the production of ATP, the primary energy currency of the cell. The ETC is a series of sequential steps where electrons are transferred from one molecule to another, ultimately leading to the production of water and ATP. Here are the detailed steps of the Electron Transport Chain:

Complex I inhibitors
Complex I inhibitors

1. Transfer of Electrons from NADH to Ubiquinone (UQ)

  • NADH, generated from various metabolic pathways such as the TCA cycle, β-oxidation of fatty acids, and other oxidation reactions, donates its electrons.
  • Within the mitochondrial matrix, NADH transfers its electrons to Flavin Mononucleotide (FMN) in the intermembrane space through Complex I, also known as NADH dehydrogenase.
  • FMN then relays these electrons to a series of Iron-Sulfur (Fe-S) centers.
  • The Fe-S centers sequentially transfer the electrons to Coenzyme Q (CoQ), forming ubiquinol in the process.
  • This electron transfer releases energy, which is harnessed to pump protons across the inner mitochondrial membrane, establishing a proton gradient.
  • The protons then flow back into the matrix through ATP synthase, driving the synthesis of ATP.
Complex I of Electron Transport Chain
Complex I of Electron Transport Chain

2. Transfer of Electrons from FADH2 to CoQ

  • The oxidation of succinate to fumarate in the TCA cycle produces FADH2.
  • Electrons from FADH2 enter the ETC at Complex II, known as succinate dehydrogenase.
  • These electrons are then passed to CoQ via a series of Fe-S centers.
  • Unlike Complex I, Complex II does not pump protons across the membrane.
Complex II of Electron Transport Chain
Complex II of Electron Transport Chain

3. Transfer of Electrons from CoQH2 to Cytochrome c

  • Reduced CoQH2 donates its electrons through a series of cytochromes, specifically cytochrome b and c1, eventually reaching cytochrome c.
  • This process is catalyzed by Complex III, or cytochrome reductase.
  • As electrons are transferred, the Fe3+ ion in cytochrome c is reduced to Fe2+.
  • Energy released during this electron transfer pumps protons across the membrane, further contributing to the proton gradient.
  • As before, the return flow of these protons through ATP synthase facilitates ATP production.
Complex III of Electron Transport Chain
Complex III of Electron Transport Chain

4. Transfer of Electrons from Cytochrome c to Molecular Oxygen

  • The final electron recipients in the ETC are molecular oxygen molecules.
  • Electrons from cytochrome c are transferred to oxygen through Complex IV, also known as cytochrome oxidase.
  • For every NADH oxidized, half an oxygen molecule is reduced to form water.
  • The oxidation of Fe2+ in cytochrome c back to Fe3+ occurs simultaneously.
  • The energy from this electron transfer is again used to pump protons across the membrane, further driving ATP synthesis.

Therefore, the Electron Transport Chain is a meticulously coordinated series of reactions that harness the energy from electron transfers to pump protons and drive ATP synthesis, powering the cell’s various functions.

Complex IV of Electron Transport Chain
Complex IV of Electron Transport Chain

Electron Transport Chain Products

The Electron Transport Chain (ETC) is a pivotal component of cellular respiration, responsible for the majority of ATP production in eukaryotic cells. The ETC, through a series of redox reactions, harnesses the energy stored in electron carriers and converts it into a form usable by the cell: ATP. Here’s a detailed breakdown of the products generated by the ETC and associated processes:

1. Glycolysis

  • Direct Products: Glycolysis, which occurs in the cytoplasm, directly produces 2 ATP molecules.
  • Ultimate ATP Yield: The net gain from glycolysis is 2 ATP.
  • Additional Products: Besides ATP, glycolysis also results in the production of 2 NADH molecules.
  • ATP Equivalent: These 2 NADH molecules, when shuttled into the mitochondria and processed through the ETC, can produce an additional 3-5 ATP, depending on the shuttle mechanism used.

2. Pyruvate Oxidation

  • Direct Products: As pyruvate enters the mitochondria, it undergoes oxidation, producing 2 NADH molecules.
  • Ultimate ATP Yield: These 2 NADH molecules can be further processed in the ETC to yield a total of 5 ATP.

3. Citric Acid Cycle (TCA or Krebs Cycle)

  • Direct Products: The citric acid cycle, which takes place in the mitochondrial matrix, directly produces 2 ATP or GTP molecules.
  • Ultimate ATP Yield: The net ATP gain from this cycle is 2 ATP.
  • Additional Products: Throughout the cycle, 6 NADH and 2 FADH2 molecules are produced.
  • ATP Equivalent: The 6 NADH molecules can generate 15 ATP when processed through the ETC. The 2 FADH2 molecules, on the other hand, contribute to the production of 3 ATP.
StageDirect Products (net)Ultimate ATP Yield (net)
Glycolysis2 ATP + 2 NADH2 ATP (from glycolysis) + 3-5 ATP (from NADH)
Pyruvate Oxidation2 NADH5 ATP
Citric Acid Cycle (TCA or Krebs Cycle)2 ATP/GTP + 6 NADH + 2 FADH22 ATP + 15 ATP (from NADH) + 3 ATP (from FADH2)
Total30-32 ATP

Therefore, when considering the entire process of cellular respiration, from glycolysis to the citric acid cycle and through the ETC, a total of 30-32 ATP molecules are produced. Besides ATP, the electron transport chain also results in the formation of water, with 44 moles of H2O being produced as a by-product. This water formation occurs when molecular oxygen (O2) acts as the final electron acceptor in the ETC, getting reduced to form water. This not only serves as a crucial step in energy production but also plays a role in maintaining cellular homeostasis.

Formation of Reactive Oxygen Species (ROS) 

During the transfers of electrons through the ETC different highly reactive free radicals are generated which can damage the cells. 

The passage of electrons from complex I to QH2 and QH2 to Complex III leads to the formation of an intermediate called Ubiquinol. Ubiquinol with low probability can pass an electron to the O2 and lead to the formation of Superoxide free radical.

This superoxide free radical can form more reactive hydroxyl free radicals which can damage the cells. To prevent the oxidative damage by these radicals the cell releases an enzyme called superoxide dismutase which converts the superoxide into H2O2.

Now H2O2 is converted into H2O with the help of an enzyme called glutathione peroxidase. The glutathione reductase recycles the oxidized glutathione to reduce glutathione with the help of NADPH, which is generated from the pentose phosphate pathway.

Formation of Reactive Oxygen Species (ROS)
Formation of Reactive Oxygen Species (ROS)

Anaerobic Respiration

  • In anaerobic respiration Nitrate, Sulfate, Co2 functions as a final electron acceptor in ATC.
  • Anaerobic respiration produces less energy or ATP as compared to aerobic respiration.
  • The aerobic respiration is performed by few bacteria, archaea, and some eukaryotic microbes.
  • Paracoccus denitrificans performs both anaerobic respiration in presence of O2 and anaerobic respiration in absence of O2.
  • The anaerobic respiration carried out different enzymes such as nitrate reductase (Nar), nitrite reductase (Nir), nitric oxide reductase (Nor), and nitrous oxide reductase (Nos) for the formation of gaseous Nitrogen from Nitrate.
  • Nitrite is reduced to nitric oxide (NO) by the periplasmic enzyme nitrite reductase. Nitric oxide reductase catalyzes the formation of nitrous oxide (N20) from NO. It is part of the membrane-bound cytochrome b complex. Finally, the periplasmic enzyme nitrous oxide reductase catalyzes the formation of N2 from N20.
Anaerobic Respiration
Anaerobic Respiration

Why is the energy yield or ATP yield in Anaerobic respiration is Low?

The final electron acceptor of anaerobic respiration is nitrate, which has a low positive reduction potential as compared to oxygen(electron acceptor of aerobic respiration). The difference in standard reduction potential of NADH and Nitrate is lower than the difference of reduction potential between the NADH and O2. 

That’s why the energy yield of anaerobic respiration is low, because the energy yield is directly related to the magnitude of reduction potential difference.

Alternative Respiratory Pathways of Plants

  • The plant mitochondria contain an alternative pathway for the transfer of electrons from ubiquinone to O2.
  • They contain an alternative NADH dehydrogenase, it is insensitive to the complex I inhibitor rotenone that’s why it is called rotenone insensitive NADH dehydrogenase complex. This complex transfers the electrons from NADH to Ubiquinone directly.
  • Except alternative NADH dehydrogenase, the plant contains another NADH dehydrogenase at the external face of the inner membrane, which functions the transfer of electrons from the NADPH or NADH to the matrix and then to Ubiquinone.
  • Both these external NADH dehydrogenase and alternative NADH dehydrogenase bypass the complex I.
  • Now the electron is transferred to O2 via the cyanide-resistant alternative oxidase and generates H2O. In this process energy is not conserved as ATP but is released as heat.
  • A skunk cabbage can use the heat to melt snow, produce a foul stench, or attract beetles or flies.
Alternative Respiratory Pathways of Plants
Alternative Respiratory Pathways of Plants

ATP Synthase Definition

  • The synthesis of ATP is accomplished by the ATP synthase. ATP synthase is made of two structural subunits called F1 and F0.
  • These ATP synthases are found in mitochondria, chloroplasts, and bacteria.
  • The F1 complex is spherical in shape and attached on the mitochondria inner membrane with the help of stalk.
  • F1 complex is composed of three α subunits which are alternate with three β subunits, and it also contains a γ subunit which is located at the center.
  • The γ subunit is extended from the F1 to F0 complex and it can rotate.
  • A stalk (γ and ε subunit) connects the F1 complex and F0 complex and serves as a proton channel.
  • The F0 complex is composed of one a subunit, two b sunits and 8 -12 c subunits.
  • A stator arm is embedded within the membrane and also attached with the F1 complex. This stator arm is made of one a subunit, two b sunit and δ subunit.
  • A ring of c subunits in F0 is connected with the stalk (γε). When the ring turns it results in the rotation of Shaft or stalk (γε).
ATP Synthase Diagram
ATP Synthase Diagram

Binding-change model for ATP synthase/ How does ATP synthase produce ATP?

  • The binding change mechanism is a widely accepted model of ATP synthesis. This simplified drawing of the model shows the three catalytic β subunits and the γ subunit, which is located at the center of the F1 complex.
  • The β subunit contains three catalytic sites such as βE, βDP, and βTP. The βE site is open conformation which does not bind with the nucleotides.
  • When the γ subunit rotates it results in conformational change in catalytic sites of β subunits. In one turn of  γ subunit the βE is changed to βHC as a result the ADP and Pi bind to this catalytic site.
  • The 2nd turn of γ subunit results in a three conformational change in catalytic site of β subunits.
    • The βTP is changed to βE as a result the ATP is released from the ATP synthase.
    • The βDP is changed into The βTP as results the ATP is generated.
    • The βHC is changed to The βDP, where ADP is bounded.
Binding-change model for ATP synthase
Binding-change model for ATP synthase

Inhibitors of Oxidative Phosphorylation 

Oxidative phosphorylation is a vital cellular process that produces ATP, the primary energy currency of the cell. This process occurs within the mitochondria and involves a series of protein complexes known as the electron transport chain (ETC). However, certain substances can inhibit the function of these complexes, disrupting ATP production and potentially leading to cellular damage. This article provides a detailed and sequential explanation of various inhibitors of oxidative phosphorylation.

  • Rotenone and Complex I Inhibition Rotenone is a substance that inhibits complex I, specifically the coenzyme Q binding site. Therefore, it prevents the transfer of electrons between the Fe-S clusters and ubiquinone. Besides its role as an inhibitor, rotenone is also used as a pesticide and piscicide. Although rotenone is not easily absorbed through the skin, intentional ingestion can be fatal.
  • Carboxin and Complex II Inhibition Carboxin, a fungicide, targets complex II by interfering with the coenzyme Q binding site, similar to rotenone. However, carboxin is no longer in widespread use due to the availability of newer agents with broader spectrums.
  • Doxorubicin’s Theoretical Impact on Coenzyme Q Doxorubicin, a chemotherapy drug, may impair electron transfer by coenzyme Q, leading to the formation of reactive oxygen species in myocardial tissue. This mechanism could explain the drug’s well-known side effect of dilated cardiomyopathy.
  • Antimycin A and Complex III Inhibition Antimycin A, a piscicide, binds to the Qi binding site of cytochrome C reductase, inhibiting complex III. This action prevents the Q cycle from recycling ubiquinol (CoQH2) through the Q cycle.
  • Carbon Monoxide and Complex IV Inhibition Carbon monoxide (CO) disrupts the ETC by binding to and inhibiting complex IV, cytochrome C oxidase. Besides its impact on the ETC, CO also binds to hemoglobin, preventing oxygen delivery to tissues. Common sources of CO include paint strippers, house fires, and wood-burning stoves. Treatment for CO poisoning involves providing supplemental oxygen or hyperbaric oxygen.
  • Cyanide’s Effect on Complex IV Cyanide also inhibits complex IV by binding to cytochrome C oxidase. Exposure to cyanide can lead to tissue hypoxia, with symptoms including an almond-scented breath. Treatment options for cyanide poisoning include the use of nitrites, hydroxocobalamin, and thiosulfate.
  • Oligomycin and ATP-synthase Inhibition Lastly, oligomycin, a macrolide antibiotic synthesized by Streptomyces species, inhibits the F0 unit of ATP-synthase, preventing ATP production. It is primarily used for research purposes.

In conclusion, oxidative phosphorylation is a crucial process for cellular energy production. However, various substances can inhibit its function, leading to potential cellular damage. Understanding these inhibitors and their mechanisms of action is essential for both research and clinical applications.

Uncoupling Agents

The electron transport chain (ETC) is a fundamental cellular mechanism responsible for the production of adenosine triphosphate (ATP), the primary energy currency of the cell. However, certain agents, termed uncoupling agents, can disrupt this process, leading to profound metabolic consequences. This article provides a comprehensive examination of these agents and their implications.

  1. Mechanism of Action: Uncoupling agents function by decoupling the electron transport process from the phosphorylation of ADP to ATP by ATP-synthase. They induce alterations in the phospholipid bilayer of cellular membranes, rendering them more permeable to protons. This increased proton permeability diminishes the electrochemical gradient across the membrane. Consequently, protons re-enter the mitochondrial matrix without passing through ATP-synthase, resulting in no ATP production.
  2. Metabolic Implications: As ATP production is halted, cells become energy-deprived. In response, the ETC intensifies its activity, attempting to restore ATP levels. However, this futile cycle only leads to excessive heat production due to the increased electron transfer within the ETC. Furthermore, cells shift their metabolic pathway to fermentation, mimicking anaerobic conditions. This metabolic shift can lead to type B lactic acidosis in affected individuals.
  3. Salicylic Acid (Aspirin): Salicylic acid acts as an uncoupling agent. In cases of salicylate toxicity, individuals may exhibit symptoms such as tinnitus. Initially, there is a respiratory alkalosis, which eventually transitions into a combined metabolic acidosis and respiratory alkalosis. Immediate interventions for salicylate poisoning include the administration of activated charcoal if presented within an hour of ingestion or sodium bicarbonate for later presentations.
  4. Thermogenin (UCP1): Thermogenin, or uncoupling protein 1 (UCP1), is predominantly found in brown adipose tissue. Unlike white adipose tissue, which contains a single lipid droplet, brown adipose tissue is characterized by multiple small lipid droplets and a high mitochondrial concentration, giving it its distinctive brown hue. Brown adipose tissue is notably present in hibernating animals and neonates, who rely on it for thermogenesis due to their underdeveloped neurological thermoregulatory mechanisms. The mitochondria in brown fat are enriched with thermogenin, facilitating enhanced disruption of the inner mitochondrial membrane and increased proton leakage.

Importance of the Electron Transport Chain

The electron transport chain (ETC) holds paramount importance in the realm of cellular respiration. This complex system is responsible for several crucial functions that sustain life at the cellular level.

Primary Functions of the ETC

  1. ATP Production: The ETC is instrumental in the synthesis of the majority of ATP molecules during oxidative phosphorylation. These ATP molecules are indispensable, serving as the primary energy currency for various cellular processes, including the biosynthesis of complex macromolecules.
  2. Oxidation of NADH and FADH2: The ETC ensures the complete oxidation of NADH and FADH2. This oxidation process replenishes the cellular metabolic pool with essential cofactors and substrates, namely NAD+ and FAD+. Both play pivotal roles in diverse catabolic and anabolic pathways, contributing significantly to cellular energy metabolism.
  3. Yielding ATP: Depending on the specific complexes involved, the ETC utilizes FADH2, NADH, and H+ to produce either 30 or 32 ATP molecules.

Consequences of Disturbed ETC Activities However, the ETC’s significance is further underscored when its function is compromised. Both excessive and deficient ETC activities can lead to mitochondrial stress and dysfunction. Some notable consequences include:

  1. Depleted Cellular ATP: Overactivity of the ETC, as seen in cases of salicylic acid or aspirin overdose, can lead to a significant reduction in cellular ATP. This scenario forces the ETC to work overtime, producing excessive heat and elevating body temperature. In extreme situations, the scarcity of cellular ATP can trigger lactate fermentation in certain tissues, potentially leading to type-b lactic acidosis due to elevated lactate levels in the bloodstream.
  2. Inhibition of Complex I Activity: Chemicals such as rotenone and barbiturates can inhibit Complex I activity, resulting in incomplete electron transport. This disruption reduces oxidative phosphorylation, leading to decreased cellular ATP production. Furthermore, the incomplete ETC can generate harmful radicals like reactive oxygen species, damaging the mitochondria and further hampering cellular metabolism. Over time, this can suppress cell proliferation and even induce apoptosis.
  3. Genetic Implications: Mutations in genes encoding for succinate dehydrogenase can hinder electron flow, increasing oxygen toxicity. In humans, such mutations can lead to various clinical manifestations, including encephalomyopathy, tumors, and optic atrophy, commonly observed in Leigh syndrome.

In conclusion, the electron transport chain is a cornerstone of cellular metabolism, playing a pivotal role in energy production and other vital cellular processes. Understanding its function and potential disruptions is crucial for both basic biological research and clinical applications.

Quiz

FAQ

Where does the electron transport chain take place?

It occurs in mitochondria in both cellular respiration and photosynthesis.

What is the electron transport chain?

An electron transport chain is a series of protein complexes and other molecules that transfer electrons from electron donors to electron acceptors via redox reactions and couples this electron transfer with the transfer of protons across a membrane.

Where is the electron transport chain located?

mitochondria

Where are the proteins of the electron transport chain located

The proteins of the electron transport chain are located in the inner mitochondrial membrane of eukaryotic cells. In prokaryotic cells, such as bacteria, these proteins are found in the plasma membrane. The inner mitochondrial membrane houses the protein complexes (Complex I, II, III, IV, and ATP synthase) that are involved in the electron transport chain and oxidative phosphorylation.

What is the final electron acceptor in the electron transport chain?

The final electron acceptor is oxygen (O2). Oxygen has a high electronegativity; thus, oxygen’s high affinity for electrons makes it an ideal acceptor for low-energy electrons. With the electrons, hydrogen is added to oxygen forming water as the final product.

how many atp are produced in the electron transport chain?

34 ATP molecules are produced in the electron transport chain if we consider that one molecule of NADH produces 3 molecules of ATP and one molecule of FADH2 gives rise to 2 molecules of ATP.

what does the electron transport chain produce?

The electron transport chain produces an electrochemical gradient that drives the synthesis of ATP by chemiosmosis. The end products of the electron transport chains are ATP and water.

What is the purpose of the electron transport chain?

The main purpose of the electron transport chain is to build up a surplus of hydrogen ions (protons) in the intermembrane space sp that there will be a concentration gradient compared to the matrix of the mitochondria. This will drive ATP synthase.

Where does the electron transport chain get its electrons from?

All of the electrons that enter the transport chain come from NADH and FADH 2

in the electron transport chain the final electron acceptor is

In the electron transport chain, the final electron acceptor is oxygen (O₂). Oxygen accepts the electrons after they have passed through the chain and combines with hydrogen ions (protons) to form water (H₂O).

References

  1. Kumari, Asha (2018). Sweet Biochemistry || Electron Transport Chain. , (), 13–16. doi:10.1016/B978-0-12-814453-4.00003-0
  2. Aerts, L. (2017). Parkinson’s Disease || Electron Transport Chain. , (), 41–75. doi:10.1016/B978-0-12-803783-6.00002-X
  3. Nicholls, David G. (2013). Bioenergetics || Respiratory Chains. , (), 91–157. doi:10.1016/B978-0-12-388425-1.00005-1
  4. Engelking, Larry R. (2015). Textbook of Veterinary Physiological Chemistry || Oxidative Phosphorylation. , (), 219–224. doi:10.1016/b978-0-12-391909-0.50036-0
  5. Jain JL, Jain S, and Jain N (2005). Fundamentals of Biochemistry. S. Chand and Company.
  6. Nelson DL and Cox MM. Lehninger Principles of Biochemistry. Fourth Edition.
  7. Berg JM et al. (2012) Biochemistry. Seventh Edition. W. H Freeman and Company.

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What is Karyotyping? What are the scope of Microbiology? What is DNA Library? What is Simple Staining? What is Negative Staining? What is Western Blot? What are Transgenic Plants? Breakthrough Discovery: Crystal Cells in Fruit Flies Key to Oxygen Transport What is Northern Blotting? What is Southern Blotting?
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