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

Postischemic hyperoxia reduces hippocampal pyruvate dehydrogenase activity.

Erica M Richards1, Robert E Rosenthal, Tibor Kristian

  • 1Department of Anesthesiology, University of Maryland, Baltimore, MD 21201, USA.

Free Radical Biology & Medicine
|May 24, 2006
PubMed
Summary

Hyperoxic reperfusion worsens pyruvate dehydrogenase complex (PDHC) loss in the hippocampus after cardiac arrest, indicating oxidative stress targets this key enzyme in cerebral energy metabolism.

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

Pentose Phosphate Pathway Is Critical for Providing Energy by Bypassing 6-Phosphofructo-1-Kinase (PFK1) During Increased Neuronal Activity.

Metabolites·2026
Same author

Embracing Scientific Debate in Brain Metabolism.

Journal of neurochemistry·2025
Same author

Characterization of a Ferret Model of Traumatic Brain Injury due to Under-Vehicle Blast, Controlled Cortical Impact, or Blast Plus Impact.

Journal of neuroscience research·2025
Same author

Longitudinal Brain Structural, Neurochemical, and Behavioral Changes Following Traumatic Brain Injury in Immature Rat Brain with ALCAR Treatment.

Neurochemical research·2025
Same author

Acute Changes in Rat Tissue Gene Expression Following Exposure to Flight Relevant Hypobaria.

Scientific data·2025
Same author

Metabolic Imaging of Hyperpolarized [1-<sup>13</sup>C]Pyruvate in a Ferret Model of Traumatic Brain Injury.

International journal of molecular sciences·2025

Area of Science:

  • Biochemistry
  • Neuroscience
  • Cellular Metabolism

Background:

  • The pyruvate dehydrogenase complex (PDHC) is crucial for cerebral energy metabolism, linking anaerobic and aerobic pathways.
  • Previous research suggests oxidative damage to PDHC during cerebral ischemia and reperfusion.
  • The role of hyperoxia in exacerbating PDHC dysfunction remains unclear.

Purpose of the Study:

  • To investigate if hyperoxic reperfusion increases the loss of PDHC activity.
  • To determine if tyrosine nitration or S-nitrosation mediates this effect.
  • To identify PDHC as a potential target of oxidative stress.

Main Methods:

  • Utilized a canine cardiac arrest model with ventricular fibrillation.
  • Animals were resuscitated and ventilated with either hyperoxic (100% O2) or normoxic (21-30% O2) conditions.

Related Experiment Videos

  • Brain tissue was analyzed for PDHC activity, immunoreactivity, and 3-nitrotyrosine levels post-reperfusion.

    • Main Results:

    • Hyperoxic reperfusion significantly decreased hippocampal PDHC activity and increased 3-nitrotyrosine immunoreactivity.
    • Normoxic reperfusion did not alter PDHC activity or 3-nitrotyrosine levels.
    • In vitro studies showed peroxynitrite dose-dependently reduces PDHC activity and increases nitrotyrosine.

    Conclusions:

    • Hyperoxic reperfusion exacerbates the loss of hippocampal PDHC activity following cerebral ischemia.
    • Oxidative stress, specifically via peroxynitrite, likely contributes to PDHC dysfunction.
    • PDHC is identified as a significant target of oxidative damage in the hippocampus during reperfusion injury.