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Related Concept Videos

Electron Transport Chains01:28

Electron Transport Chains

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The final stage of cellular respiration is oxidative phosphorylation that consists of two steps: the electron transport chain and chemiosmosis. The electron transport chain is a set of proteins found in the inner mitochondrial membrane in eukaryotic cells. Its primary function is to establish a proton gradient that can be used during chemiosmosis to produce ATP and generate electron carriers, such as NAD+ and FAD, that are used in glycolysis and the citric acid cycle.
The ETC is comprised of...
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The Electron Transport Chain01:30

The Electron Transport Chain

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The electron transport chain or oxidative phosphorylation is an exothermic process in which free energy released during electron transfer reactions is coupled to ATP synthesis. This process is a significant source of energy in aerobic cells, and therefore inhibitors of the electron transport chain can be detrimental to the cell's metabolic processes.
Inhibitors of the electron transport chain
Rotenone, a widely used pesticide, prevents electron transfer from Fe-S cluster to ubiquinone or Q...
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Electron Transport Chain: Complex I and II01:46

Electron Transport Chain: Complex I and II

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The mitochondrial electron transport chain (ETC) is the main energy generation system in the eukaryotic cells. However, mitochondria also produce cytotoxic reactive oxygen species (ROS) due to the large electron flow during oxidative phosphorylation. While Complex I is one of the primary sources of superoxide radicals, ROS production by Complex II is uncommon and may only be observed in cancer cells with mutated complexes.
ROS generation is regulated and maintained at moderate levels necessary...
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Electron Transport Chain Components01:29

Electron Transport Chain Components

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The electron transport chain (ETC) is a crucial metabolic pathway that facilitates energy conversion in prokaryotic and eukaryotic cells. In eukaryotes, the ETC comprises four membrane-associated protein complexes in the inner mitochondrial membrane. In prokaryotes, the ETC in the plasma membrane can vary in composition, with fewer or different complexes depending on the organism and environmental conditions. These complexes transfer electrons from electron donors, such as NADH and FADH2, to...
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Electron Transport Chain: Complex III and IV01:43

Electron Transport Chain: Complex III and IV

9.3K
During the electron transport chain, electrons from NADH and FADH2 are first transferred to complexes I and II, respectively. These two complexes then transfer the electrons to ubiquinol, which carries them further to complex III. Complex III passes the electrons across the intermembrane space to Cyt c, which carries them further to complex IV. Complex IV donates electrons to oxygen and reduces it to water. As electrons pass through complexes I, III, and IV, the energy released aids the pumping...
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Secondary Active Transport01:55

Secondary Active Transport

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One example of how cells use the energy contained in electrochemical gradients is demonstrated by glucose transport into cells. The ion vital to this process is sodium (Na+), which is typically present in higher concentrations extracellularly than in the cytosol. Such a concentration difference is due, in part, to the action of an enzyme “pump” embedded in the cellular membrane that actively expels Na+ from a cell. Importantly, as this pump contributes to the high concentration of...
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Related Experiment Video

Updated: Jan 30, 2026

Analyzing Supercomplexes of the Mitochondrial Electron Transport Chain with Native Electrophoresis, In-gel Assays, and Electroelution
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Analyzing Supercomplexes of the Mitochondrial Electron Transport Chain with Native Electrophoresis, In-gel Assays, and Electroelution

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Isoniazid Bactericidal Activity Involves Electron Transport Chain Perturbation.

Sheng Zeng1, Karine Soetaert2, Faustine Ravon1

  • 1Microbiology, Bioorganic and Macromolecular Chemistry Research Unit, Faculté de Pharmacie, Université Libre de Bruxelles, Brussels, Belgium.

Antimicrobial Agents and Chemotherapy
|January 16, 2019
PubMed
Summary
This summary is machine-generated.

Isoniazid (INH) killing of tuberculosis bacteria is linked to energy production disruption, not just target inhibition. Respiratory changes help bacteria survive INH stress.

Keywords:
Mycobacterium tuberculosisQ203bedaquilineelectron transport chainisoniazidpersistence

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Characterizing Electron Transport through Living Biofilms
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Related Experiment Videos

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Analyzing Supercomplexes of the Mitochondrial Electron Transport Chain with Native Electrophoresis, In-gel Assays, and Electroelution
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A High-throughput Shigella-specific Bactericidal Assay
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Area of Science:

  • Microbiology
  • Biochemistry
  • Drug Discovery

Background:

  • Isoniazid (INH) is a crucial first-line tuberculosis drug.
  • Its known mechanism, inhibiting mycolic acid synthesis, doesn't fully explain its bactericidal activity, especially under stress.
  • Stress conditions like hypoxia and starvation impair INH efficacy.

Purpose of the Study:

  • To investigate the link between isoniazid's bactericidal activity and cellular energy metabolism.
  • To explore the role of the electron transport chain (ETC) in isoniazid's mechanism of action.
  • To identify mechanisms of bacterial survival against isoniazid under stress.

Main Methods:

  • Measuring ATP levels and oxygen consumption in Mycobacterium bovis BCG treated with isoniazid.
  • Using specific inhibitors targeting cytochrome bc1, F0F1 ATP synthase, NADH dehydrogenases (NDHs), and succinate dehydrogenases (SDHs).
  • Assessing the impact of antioxidants (NAC, TEMPOL) and membrane potential changes.
  • Utilizing a culture settling model to evaluate bacterial recovery during INH challenge.

Main Results:

  • Isoniazid rapidly increased cellular ATP levels and oxygen consumption in M. bovis BCG.
  • Inhibitors of cytochrome bc1 and F0F1 ATP synthase, as well as NDHs and SDHs, compromised INH's ATP-boosting and bactericidal effects.
  • The antioxidant N-acetylcysteine (NAC) abrogated INH-induced ATP increase and killing.
  • Isoniazid treatment dissipated the mycobacterial membrane potential.
  • Inhibition of cytochrome bd oxidase reduced bacterial recovery under INH stress.

Conclusions:

  • Isoniazid's bactericidal activity is significantly linked to perturbations in the mycobacterial electron transport chain (ETC) and energy metabolism (ATP production).
  • The electron transport chain components, including NDHs, SDHs, cytochrome bc1, and F0F1 ATP synthase, are implicated in INH's killing mechanism.
  • Mycobacteria reprogram their respiration to utilize cytochrome bd oxidase to survive isoniazid treatment, particularly under stress conditions.