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Tumor necrosis factor-alpha-mediated decrease in glutathione increases the sensitivity of pulmonary vascular

Y Ishii1, C A Partridge, P J Del Vecchio

  • 1Department of Physiology and Cell Biology, Albany Medical College of Union University, New York 12208.

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Tumor necrosis factor-alpha (TNF alpha) increases endothelial cell susceptibility to hydrogen peroxide (H2O2) by reducing glutathione (GSH). This mechanism may contribute to vascular injury in sepsis.

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Area of Science:

  • Endothelial cell biology
  • Oxidative stress
  • Inflammation

Background:

  • Tumor necrosis factor-alpha (TNF alpha) is a key inflammatory cytokine.
  • Endothelial cells form the barrier of blood vessels.
  • Hydrogen peroxide (H2O2) can increase endothelial permeability.

Purpose of the Study:

  • To investigate how TNF alpha affects endothelial cell permeability induced by H2O2.
  • To elucidate the role of glutathione (GSH) and catalase in this process.
  • To explore potential mechanisms of TNF alpha-mediated vascular injury.

Main Methods:

  • Bovine pulmonary microvascular endothelial cells (BPMVEC) were cultured on microporous filters.
  • 125I-albumin clearance rate was measured to assess transendothelial permeability.
  • Intracellular GSH, oxidized GSH, and catalase activity were quantified.
  • Effects of GSH repletion and xanthine oxidase (XO) inhibition were tested.

Main Results:

  • TNF alpha pretreatment enhanced H2O2-induced endothelial permeability over threefold.
  • TNF alpha decreased intracellular GSH content and increased oxidized GSH, without altering catalase activity.
  • GSH repletion inhibited the increased sensitivity to H2O2.
  • Xanthine oxidase inhibition attenuated the synergistic effect of TNF alpha and H2O2.

Conclusions:

  • Reduced intracellular GSH content, leading to decreased oxidant buffering capacity, mediates TNF alpha-induced hypersensitivity to H2O2.
  • This mechanism contributes to oxidant-dependent vascular endothelial injury.
  • Findings suggest a role in septicemia-associated vascular damage.