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Related Concept Videos

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...
Mitochondria01:37

Mitochondria

Mitochondria are eukaryotic cellular organelles that are known to produce energy through a process called oxidative phosphorylation. Besides their primary function, mitochondria are involved in various cellular processes, including cell growth, differentiation, signaling, metabolism, and senescence. Age-related changes cause a decline in mitochondrial quality and integrity due to increased mitochondrial mutations and oxidative damage. Thus, aging can severely impact mitochondrial functions,...
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,...
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 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...
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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Assessing Mitochondrial Function in Sciatic Nerve by High-Resolution Respirometry
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Published on: May 5, 2022

Mitochondrial superoxide radicals differentially affect muscle activity and neural function.

Tanja Godenschwege1, Renée Forde, Claudette P Davis

  • 1Department of Biological Sciences, Florida Atlantic University, Boca Raton, Florida 33431, USA.

Genetics
|June 24, 2009
PubMed
Summary

Mitochondrial superoxide radicals (O(2)(-)) cause degenerative diseases. This study found muscles are more sensitive to superoxide attack than neurons, with muscle-specific SOD2 expression improving mobility and lifespan in mutants.

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Measurement of Mitochondrial Respiration in Human and Mouse Skeletal Muscle Fibers by High-Resolution Respirometry
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Measurement of Mitochondrial Respiration in Human and Mouse Skeletal Muscle Fibers by High-Resolution Respirometry

Published on: October 4, 2024

Area of Science:

  • Cellular biology
  • Mitochondrial metabolism
  • Neuroscience

Background:

  • Cellular superoxide radicals (O(2)(-)) are primarily generated during mitochondrial oxygen metabolism.
  • Superoxide dismutase (SOD) enzymes catalyze O(2)(-) into other reactive oxygen species (ROS), and mitochondrial ROS overproduction is linked to degenerative diseases.
  • Loss of mitochondrial SOD2 function in model systems results in movement disorders and reduced lifespan.

Purpose of the Study:

  • To investigate the differential sensitivity of muscles and neurons to mitochondrial superoxide radicals.
  • To determine the role of SOD2 in mitigating ROS-induced damage in these tissues.
  • To explore therapeutic strategies targeting SOD2 for degenerative conditions.

Main Methods:

  • Utilized a mitochondrial SOD2 loss-of-function mutant (Sod2(n283)) in model organisms.
  • Measured neural outputs from motor and sensory neurons and analyzed neural circuitry.
  • Performed ultrastructural analysis of muscles and assessed muscle ATP production.
  • Investigated the effects of targeted SOD2 expression in muscles and neurons.

Main Results:

  • Neurons showed no overt defects or sensitivity to elevated mitochondrial superoxides, even with neuronal SOD2 expression failing to rescue phenotypes.
  • Muscle ultrastructural analysis revealed fewer mitochondria and reduced ATP production in Sod2(n283) mutants.
  • Targeting SOD2 expression specifically to muscles ameliorated the early mortality phenotype and improved mobility in Sod2(n283) mutants.

Conclusions:

  • Muscles are significantly more sensitive to mitochondrial superoxide attack compared to neurons.
  • The observed phenotypes in SOD2-deficient animals are primarily attributable to muscle dysfunction.
  • Muscle-specific SOD2 expression represents a potential therapeutic avenue for mitigating ROS-related degenerative diseases.