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Related Concept Videos

Electron Transport Chain: Complex III and IV01:43

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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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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.
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Electron Transport Chain: Complex I and II01:46

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Related Experiment Video

Updated: Sep 29, 2025

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Identifying Site-Specific Superoxide and Hydrogen Peroxide Production Rates From the Mitochondrial Electron Transport

Quynh V Duong1, Yan Levitsky2, Maria J Dessinger2

  • 1Department of Biochemistry and Molecular Biology, Michigan State University, East Lansing, Michigan 48824, USA.

Function (Oxford, England)
|March 25, 2022
PubMed
Summary

Mitochondrial reactive oxygen species (ROS) production was modeled, revealing complex I as a major source during pathological conditions. Understanding ROS sources is key to addressing oxidative stress and cell death.

Keywords:
Electron transport system (ETS)computational biologyenzyme kineticsforward electron transportischemia/reperfusion injurymitochondriaoxidative stressreactive oxygen speciesreverse electron transport

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Area of Science:

  • Biochemistry
  • Cellular Biology
  • Physiology

Background:

  • Mitochondrial reactive oxygen species (ROS) are crucial for cellular signaling but dysregulated in conditions like ischemia/reperfusion (I/R) injury, leading to cell death.
  • A quantitative framework to pinpoint mitochondrial ROS sources and regulatory mechanisms is lacking, hindering therapeutic development for oxidative stress-induced damage.

Purpose of the Study:

  • To develop a kinetic model of mitochondrial ROS homeostasis, focusing on electron transport chain (ETC) complexes I, II, and III.
  • To quantitatively assess the contributions of specific ETC redox sites to mitochondrial ROS production under varying conditions.

Main Methods:

  • Developed a thermodynamically consistent, mass-and-charge balanced kinetic model of mitochondrial ROS homeostasis.
  • Focused the model on redox sites of ETC complexes I, II, and III.
  • Calibrated and corroborated the model using comprehensive ROS homeostasis data sets.

Main Results:

  • The model predicts complex I ROS production dominates under high membrane potential, elevated NADH, and QH2 levels.
  • Complex I significantly contributes to ROS under pathological conditions, while complexes II and III produce basal ROS, especially with high QH2.
  • Complex I hydrogen peroxide production explains the non-linear ROS-O2 relationship at low oxygen concentrations.

Conclusions:

  • The model quantifies individual ETC redox site contributions to mitochondrial ROS emission.
  • Highlights the necessity of quantifying scavenging system activity for a complete understanding of mitochondrial ROS homeostasis.
  • Provides a framework for investigating ROS production in various respiratory states and workloads.