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Electron Transport Chain: Complex I and II01:46

Electron Transport Chain: Complex I and II

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...
Mitochondrial Membranes01:45

Mitochondrial Membranes

A single mitochondrion is a bean-shaped organelle enclosed by a double-membrane system. The outer membrane of mitochondria is smooth and contains many porins - the integral membrane transporters. Porins enable free diffusion of ions and small uncharged molecules through the outer mitochondrial membrane but limit the transport of molecules larger than 5000 Daltons. Further, the outer mitochondrial membrane forms a unique structure called membrane contact sites with other subcellular organelles,...
The Electron Transport Chain01:30

The Electron Transport Chain

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 in...

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Related Experiment Video

Updated: May 24, 2026

Experimental Protocol for Detecting Mitochondrial Function in Hepatocytes Exposed to Organochlorine Pesticides
08:39

Experimental Protocol for Detecting Mitochondrial Function in Hepatocytes Exposed to Organochlorine Pesticides

Published on: September 16, 2020

Mitochondrial dysfunction and antioxidant therapy in sepsis.

Milagros Rocha1, R Herance, S Rovira

  • 1University Hospital Doctor Peset Foundation, Valencia, Spain.

Infectious Disorders Drug Targets
|March 17, 2012
PubMed
Summary

Sepsis causes organ damage via excessive reactive oxygen species (ROS) and mitochondrial dysfunction. Mitochondria-targeted antioxidants show promise for treating sepsis by protecting against oxidative stress.

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Last Updated: May 24, 2026

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08:39

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Published on: September 16, 2020

A Preclinical Model of Sepsis-Induced Myopathy with Disuse in Mice
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Published on: June 14, 2024

A Flow Cytometry-based Assay for Measuring Mitochondrial Membrane Potential in Cardiac Myocytes After Hypoxia/Reoxygenation
07:14

A Flow Cytometry-based Assay for Measuring Mitochondrial Membrane Potential in Cardiac Myocytes After Hypoxia/Reoxygenation

Published on: July 13, 2018

Area of Science:

  • Biochemistry
  • Cell Biology
  • Pathophysiology

Background:

  • Sepsis is a leading cause of intensive care unit mortality.
  • Oxidative stress, involving reactive oxygen species (ROS) and nitric oxide (NO), is central to sepsis-induced organ dysfunction.
  • Mitochondrial damage and dysfunction, including impaired respiration and ATP depletion, characterize sepsis.

Purpose of the Study:

  • To review sepsis from a mitochondrial perspective.
  • To discuss the role of ROS in sepsis pathophysiology.
  • To explore strategies for targeted antioxidant delivery to mitochondria for sepsis treatment.

Main Methods:

  • Literature review of cellular metabolism of ROS.
  • Analysis of current antioxidant therapies and their efficacy.
  • Examination of recent advancements in mitochondria-targeted antioxidants.

Main Results:

  • Excessive ROS production overwhelms antioxidant defenses in sepsis.
  • Mitochondrial dysfunction leads to impaired cellular respiration and ATP synthesis.
  • Targeted delivery of antioxidants to mitochondria offers a potential therapeutic strategy.

Conclusions:

  • Mitochondrial-targeted antioxidants represent a promising therapeutic avenue for sepsis.
  • Understanding ROS metabolism and mitochondrial function is crucial for developing effective sepsis treatments.
  • Further research into mitochondria-targeted antioxidants could improve patient outcomes in sepsis.