Jove
Visualize
Contact Us
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 Videos

Modulation of mitochondrial function by hydrogen peroxide.

A C Nulton-Persson1, L I Szweda

  • 1Department of Physiology and Biophysics, Case Western Reserve University, Cleveland, Ohio 44106-4970, USA.

The Journal of Biological Chemistry
|April 3, 2001
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

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

Sort by
Same author

Neurofilaments are the major neuronal target of hydroxynonenal-mediated protein cross-links.

Free radical research·2013
Same author

Identification of ATP synthase as a lipid peroxide protein adduct in pancreatic islets from humans with and without type 2 diabetes mellitus.

The Journal of clinical endocrinology and metabolism·2013
Same author

The glial glutamate transporter, GLT-1, is oxidatively modified by 4-hydroxy-2-nonenal in the Alzheimer's disease brain: the role of Abeta1-42.

Journal of neurochemistry·2001
Same author

Oxidative modification and inactivation of the proteasome during coronary occlusion/reperfusion.

The Journal of biological chemistry·2001
Same author

Free radicals alter maximal diaphragmatic mitochondrial oxygen consumption in endotoxin-induced sepsis.

Free radical biology & medicine·2001
Same author

Caloric restriction of rhesus monkeys lowers oxidative damage in skeletal muscle.

FASEB journal : official publication of the Federation of American Societies for Experimental Biology·2000
Same journal

Wanted and unwanted modifications of mRNA, and their effect on gene expression and signaling.

The Journal of biological chemistry·2026
Same journal

TGF-β2 drives lipid droplet accumulation in chondrocytes through the TβRI/p-Smad3/Fabp5 axis.

The Journal of biological chemistry·2026
Same journal

Macrophage-specific targeting of histone demethylases with small-molecule inhibitors suppresses inflammatory response in vivo.

The Journal of biological chemistry·2026
Same journal

Substrate and target selectivity of 4'-fluoroadenosine against viral and host polymerases.

The Journal of biological chemistry·2026
Same journal

Correction: Characterization of Mast2 kinase defines structural features, regulation, and substrates.

The Journal of biological chemistry·2026
Same journal

Isotope-Edited ESEEM: A New Method for Probing Copper Binding Sites in Neurodegenerative Proteins.

The Journal of biological chemistry·2026
See all related articles

Hydrogen peroxide (H2O2) temporarily inactivates key mitochondrial enzymes, including alpha-ketoglutarate dehydrogenase and succinate dehydrogenase. Enzyme activity recovers when mitochondria remain intact, suggesting H2O2 may regulate these enzymes.

Area of Science:

  • Mitochondrial biochemistry
  • Cellular metabolism
  • Oxidative stress

Background:

  • Mitochondrial electron transport produces superoxide and hydrogen peroxide (H2O2).
  • H2O2 can modify cellular components, necessitating understanding mitochondrial responses.
  • Elevated H2O2 occurs in various physiological and pathological states.

Purpose of the Study:

  • To investigate the effects of H2O2 on isolated rat heart mitochondria.
  • To identify specific mitochondrial targets of H2O2-induced damage and recovery.
  • To explore the regulatory potential of H2O2 in mitochondrial function.

Main Methods:

  • Treatment of isolated rat heart mitochondria with H2O2.
  • Measurement of state 3 NADH-linked respiration.

Related Experiment Videos

  • Assessment of electron transport chain complexes and Krebs cycle enzyme activities.
  • Analysis of NADH levels and enzyme recovery.
  • Main Results:

    • H2O2 caused a decline and subsequent recovery in state 3 respiration.
    • Alpha-ketoglutarate dehydrogenase (KGDH), succinate dehydrogenase (SDH), and aconitase were inactivated by H2O2.
    • KGDH and SDH activity recovered concurrently with respiration.
    • Enzyme inactivation was not due to direct H2O2 interaction; intact mitochondria were required for recovery.

    Conclusions:

    • H2O2 reversibly inactivates KGDH and SDH within intact mitochondria.
    • Mitochondrial integrity is crucial for the recovery of enzyme activity.
    • H2O2 may play a regulatory role in KGDH and SDH function.