Jove
Visualize
Contact Us

Related Concept Videos

Electron Transport Chain: Complex III and IV01:43

Electron Transport Chain: Complex III and IV

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...
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...
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...
The Supercomplexes in the Crista Membrane01:41

The Supercomplexes in the Crista Membrane

The mitochondrial cristae membrane is the primary site for the oxidative phosphorylation (OXPHOS) process of energy conversion mediated through respiratory complexes I to V. These complexes have been widely studied for decades, and it has been proven that they form supramolecular structures called respiratory supercomplexes (SC). These higher-order complexes may be crucial in maintaining the biochemical structure and improving the physiological activity of the individual complexes while...
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,...
Redox Reactions01:27

Redox Reactions

Redox reactions are vital biochemical processes that underpin energy metabolism in cells. These reactions involve the transfer of electrons between molecules, occurring in tandem as oxidation and reduction. Oxidation refers to the loss of electrons, while reduction denotes their gain. This coupling ensures the seamless flow of electrons through metabolic pathways. For example, in bacterial metabolism, glucose undergoes oxidation to carbon dioxide, while oxygen is simultaneously reduced to...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Alcohol-induced CYP2E1, mitochondrial dynamics and retrograde signaling in human hepatic 3D organoids.

Free radical biology & medicine·2020
Same author

Dysregulation of RyR Calcium Channel Causes the Onset of Mitochondrial Retrograde Signaling.

iScience·2020
Same author

Mitochondria-targeted paraquat and metformin mediate ROS production to induce multiple pathways of retrograde signaling: A dose-dependent phenomenon.

Redox biology·2020
Same author

YY1 control of mitochondrial-related genes does not account for regulation of immunoglobulin class switch recombination in mice.

European journal of immunology·2020
Same author

Esophageal 3D organoids of <i>MPV17</i> mouse model of mitochondrial DNA depletion show epithelial cell plasticity and telomere attrition.

Oncotarget·2019
Same author

Mitochondrially targeted cytochrome P450 2D6 is involved in monomethylamine-induced neuronal damage in mouse models.

The Journal of biological chemistry·2019
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Video

Updated: May 20, 2026

Visualization of Mitochondrial Respiratory Function using Cytochrome C Oxidase / Succinate Dehydrogenase (COX/SDH) Double-labeling Histochemistry
06:53

Visualization of Mitochondrial Respiratory Function using Cytochrome C Oxidase / Succinate Dehydrogenase (COX/SDH) Double-labeling Histochemistry

Published on: November 23, 2011

Cytochrome c oxidase dysfunction in oxidative stress.

Satish Srinivasan1, Narayan G Avadhani

  • 1Department of Animal Biology, School of Veterinary Medicine, University of Pennsylvania, 3800 Spruce Street, Philadelphia, PA 19104, USA.

Free Radical Biology & Medicine
|July 31, 2012
PubMed
Summary

Cytochrome c oxidase (CcO) regulates cellular respiration and ATP synthesis. Its dysfunction is linked to diseases and increased reactive oxygen species production, impacting cellular toxicity.

More Related Videos

Defining Hsp33's Redox-regulated Chaperone Activity and Mapping Conformational Changes on Hsp33 Using Hydrogen-deuterium Exchange Mass Spectrometry
10:24

Defining Hsp33's Redox-regulated Chaperone Activity and Mapping Conformational Changes on Hsp33 Using Hydrogen-deuterium Exchange Mass Spectrometry

Published on: June 7, 2018

Cellular Redox Profiling Using High-content Microscopy
11:37

Cellular Redox Profiling Using High-content Microscopy

Published on: May 14, 2017

Related Experiment Videos

Last Updated: May 20, 2026

Visualization of Mitochondrial Respiratory Function using Cytochrome C Oxidase / Succinate Dehydrogenase (COX/SDH) Double-labeling Histochemistry
06:53

Visualization of Mitochondrial Respiratory Function using Cytochrome C Oxidase / Succinate Dehydrogenase (COX/SDH) Double-labeling Histochemistry

Published on: November 23, 2011

Defining Hsp33's Redox-regulated Chaperone Activity and Mapping Conformational Changes on Hsp33 Using Hydrogen-deuterium Exchange Mass Spectrometry
10:24

Defining Hsp33's Redox-regulated Chaperone Activity and Mapping Conformational Changes on Hsp33 Using Hydrogen-deuterium Exchange Mass Spectrometry

Published on: June 7, 2018

Cellular Redox Profiling Using High-content Microscopy
11:37

Cellular Redox Profiling Using High-content Microscopy

Published on: May 14, 2017

Area of Science:

  • Biochemistry
  • Cellular Biology
  • Mitochondrial Function

Background:

  • Cytochrome c oxidase (CcO) is the terminal enzyme of the mitochondrial electron transport chain, crucial for cellular respiration.
  • This enzyme, composed of mitochondrially and nuclearly encoded subunits, contains heme and copper centers essential for its catalytic activity.
  • CcO plays a key role in managing molecular oxygen (O2) and is considered a pace-setter for oxidative metabolism and ATP synthesis.

Purpose of the Study:

  • To review the multimodal regulation of CcO activity by various physiological and pathological factors.
  • To examine the direct and indirect roles of CcO in the production of reactive oxygen species (ROS).

Main Methods:

  • Literature review of scientific publications.
  • Analysis of studies on CcO structure, function, and regulation.
  • Synthesis of evidence regarding CcO's role in ROS production.

Main Results:

  • CcO activity is influenced by a wide array of regulatory factors.
  • CcO dysfunction is associated with numerous diseases, including cancer, neurodegenerative disorders, and diabetes.
  • Evidence suggests a link between CcO dysfunction, increased mitochondrial ROS production, and cellular toxicity.

Conclusions:

  • CcO is a highly regulated enzyme critical for cellular energy production.
  • Dysfunctional CcO contributes to various pathologies through mechanisms potentially involving ROS overproduction.
  • Further research into CcO regulation and its role in ROS generation is warranted.