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Related Experiment Videos

DNA fragmentation in mouse organs during endotoxic shock

I Bohlinger1, M Leist, F Gantner

  • 1Department of Biochemical Pharmacology, Faculty of Biology, University of Konstanz, Germany.

The American Journal of Pathology
|October 1, 1996
PubMed
Summary

Systemic inflammatory response syndrome can lead to organ failure. This study shows endotoxin causes DNA fragmentation in multiple organs, but hepatocyte apoptosis is minimal in high-dose endotoxic shock.

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Area of Science:

  • Pathophysiology
  • Immunology
  • Toxicology

Background:

  • Systemic inflammatory response syndrome (SIRS) has unpredictable outcomes, often resulting in multiple organ failure.
  • Pathophysiological mechanisms involve cytokine-induced organ damage from host response overactivation.
  • Understanding organ failure in septic shock is crucial for effective treatment.

Purpose of the Study:

  • To investigate organ damage mechanisms in experimental septic shock.
  • To examine apoptotic and necrotic tissue damage following endotoxin administration.
  • To elucidate the role of cytokines and nitric oxide in endotoxin-induced organ failure.

Main Methods:

  • Mice were injected with a lethal dose of endotoxin.
  • Biochemical, histological, and ultrastructural analyses were performed to assess tissue damage.

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  • DNA fragmentation patterns were analyzed in liver, lung, kidney, and intestine.

    • Main Results:

    • Endotoxin induced oligonucleosomal and random DNA fragmentation across multiple organs.
    • Liver DNA fragmentation occurred in both hepatocytes and nonparenchymal cells.
    • Tumor necrosis factor mediated DNA fragmentation, while nitric oxide attenuated it.

    Conclusions:

    • Endotoxin triggers cytokine-mediated DNA fragmentation in various organs.
    • High-dose endotoxic shock in mice is characterized by single-cell necrosis and nonparenchymal cell damage.
    • Hepatocyte apoptosis plays a minor role in liver failure during high-dose endotoxic shock.