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

Ischemia: from acidosis to oxidation

R L Levine1

  • 1Laboratory of Biochemistry, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892.

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology
|October 1, 1993
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

T cell-derived interferon-γ programs stem cell death in immune-mediated intestinal damage.

Science immunology·2019
Same author

Oxidative stress does not mediate heat shock-induced cell damage and apoptosis.

Redox report : communications in free radical research·2016
Same author

Patient-derived xenotransplants can recapitulate the genetic driver landscape of acute leukemias.

Leukemia·2016
Same author

STATISTICAL AND PSYCHOMETRIC INFERENCE IN PRINCIPAL COMPONENTS ANALYSIS.

Multivariate behavioral research·2016
Same author

BRIEF REPORT: SELECTIVE BREEDING FOR PRINCIPAL COMPONENTS AND FACTORS BASED UPON BEHAVIORAL TRAITS.

Multivariate behavioral research·2016
Same author

Dnmt3a regulates myeloproliferation and liver-specific expansion of hematopoietic stem and progenitor cells.

Leukemia·2015

Lactic acidosis does not cause organ damage during ischemia; instead, it is protective. Free radicals generated during reperfusion, not acidosis, are the primary cause of tissue injury.

Area of Science:

  • Biochemistry
  • Pathophysiology
  • Cellular Biology

Background:

  • Organ damage is a rapid consequence of compromised blood flow (ischemia).
  • Lactic acidosis is traditionally, but incorrectly, implicated as the cause of ischemic organ damage.
  • Emerging evidence suggests acidosis may be protective against cellular injury.

Purpose of the Study:

  • To review the literature on hypoxia and ischemia.
  • To evaluate the role of acidosis in organ damage during ischemia and reperfusion.
  • To identify the actual mechanisms of cellular damage during reperfusion.

Main Methods:

  • Literature review of studies on hypoxia, ischemia, and acidosis.
  • Analysis of recent research on cellular damage during reperfusion.

Related Experiment Videos

  • Investigation of reactive species and oxidative modification of proteins.

    • Main Results:

    • Little evidence supports acidosis as a cause of tissue damage in ischemia.
    • Acidosis appears to be protective during reperfusion.
    • Free radicals and reactive species generated during reperfusion are implicated in tissue damage.
    • Metal-catalyzed oxidation, involving iron, contributes to protein damage during reperfusion.

    Conclusions:

    • The traditional view of lactic acidosis causing ischemic organ damage is not supported by current literature.
    • Acidosis may play a protective role in mitigating cellular damage.
    • Reactive oxygen species and oxidative protein modification are key contributors to reperfusion injury.
    • Understanding these mechanisms is crucial for treating conditions like retinopathy of prematurity.