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Complement activation by the hydroxyl radical during intestinal reperfusion

R H Turnage1, J C Magee, K S Guice

  • 1Department of Surgery, University of Texas Southwestern Medical School, Dallas 75235-9031, USA.

Shock (Augusta, Ga.)
|December 1, 1994
PubMed
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Intestinal reperfusion injury activates the complement system, producing C5a. Hydroxyl radical scavengers blocked this complement activation, suggesting a key role for hydroxyl radicals in this process.

Area of Science:

  • Biochemistry
  • Immunology
  • Physiology

Background:

  • Intestinal ischemia-reperfusion (IIR) injury is a significant clinical concern.
  • The complement system plays a crucial role in inflammatory responses.
  • Hydroxyl radical (OH.) generation is implicated in IIR pathophysiology.

Purpose of the Study:

  • To investigate the hypothesis that hydroxyl radical generation during intestinal reperfusion activates the complement system.
  • To determine if complement activation leads to the formation of C5a, a potent chemotaxin.
  • To elucidate the role of hydroxyl radicals in complement activation during IIR.

Main Methods:

  • Anesthetized rats underwent 120 minutes of intestinal ischemia followed by 60 minutes of reperfusion.
  • Complement (C) activation was assessed by measuring total plasma C activity, C5a-related chemotaxis, and leukoaggregation.

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  • Dimethylthiourea and deferoxamine were used to scavenge hydroxyl radicals and chelate iron, respectively.
  • Sham-operated animals served as controls.

    • Main Results:

    • Total plasma C activity was significantly reduced (64% of controls) in IIR animals (p < .05).
    • Plasma from IIR animals induced significantly greater chemotaxis and leukoaggregation compared to sham controls (p < .05).
    • Anti-C5a antibody treatment ameliorated IIR plasma-induced leukoaggregation.
    • Pretreatment with dimethylthiourea and deferoxamine prevented complement activation and inhibited chemotactic activity in IIR animals.

    Conclusions:

    • Intestinal reperfusion injury activates the complement system.
    • Hydroxyl radical generation during reperfusion is a significant mechanism for complement activation in this model.
    • Targeting hydroxyl radical formation may offer a therapeutic strategy for intestinal reperfusion injury.