Red cell regulation of tumor necrosis factor-induced human neutrophil cytostatic activity

H Y Shau1

  • 1Division of Surgical Oncology, UCLA School of Medicine 90024-1782.

Cancer Communications
|September 1, 1991
PubMed

Insights

Red blood cells (RBC) protect tumor cells from tumor necrosis factor (TNF)-activated neutrophil suppression. This protection relies on RBC

Area of Science:

  • Immunology
  • Cell Biology
  • Biochemistry

Background:

  • Tumor necrosis factor (TNF) activates polymorphonuclear neutrophils (PMN) to inhibit tumor cell growth.
  • Red blood cells (RBC) can block this TNF-induced cytostatic activity.
  • Hydrogen peroxide (H2O2) mediates TNF-induced PMN cytostatic activity.

Purpose of the Study:

  • To investigate the role of RBC in protecting tumor cells from TNF-activated PMN-mediated cytostasis.
  • To determine whether RBC's catalase or glutathione redox cycle is responsible for this protective effect.

Main Methods:

  • Utilized 3-amino-1,2,4-triazole (AT), a catalase inhibitor, and N-ethylmaleimide (NE), a glutathione inhibitor.
  • Assessed the impact of RBC treated with AT or NE on the cytostatic activity of TNF-activated PMN against Raji tumor cells.

Main Results:

  • RBC depleted of catalase activity by AT failed to protect Raji tumor cells from PMN-induced cytostasis.
  • RBC with inhibited glutathione redox cycle (using NE) still protected tumor cells.
  • These findings indicate that RBC's catalase, not its glutathione system, is crucial for protection.

Conclusions:

  • Red blood cells protect tumor cells from TNF-activated PMN-mediated cytostatic effects.
  • This RBC-mediated protection is dependent on the catalase enzyme, not the glutathione redox cycle.