The nitric oxide donors, azide and hydroxylamine, inhibit the programmed cell death of cytokine-deprived human eosinophils

FEBS Lett. 1995 Mar 20;361(2-3):229-32. doi: 10.1016/0014-5793(95)00188-f.


Azide and hydroxylamine release nitric oxide (NO) enzymatically in biological conditions. We observed that both compounds were able to inhibit in vitro the programmed cell death of human eosinophils from peripheral blood. This protective effect could be mimicked by permeable cGMP analogs and by the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine. Moreover, the soluble guanylate cyclase inhibitor LY-83583 inhibited in a dose-response manner the effects of the NO donors. Consequently, via the increase of eosinophil survival, NO could contribute to the amplification of inflammatory and allergic processes. This effect appears to be mediated, at least in part, by the soluble guanylate pathway.

Publication types

  • Comparative Study

MeSH terms

  • 1-Methyl-3-isobutylxanthine / pharmacology
  • Aminoquinolines / pharmacology
  • Apoptosis / drug effects*
  • Azides / pharmacology*
  • Cell Survival / drug effects
  • Cells, Cultured
  • Dibutyryl Cyclic GMP / pharmacology
  • Dose-Response Relationship, Drug
  • Eosinophils / cytology
  • Eosinophils / drug effects
  • Eosinophils / physiology*
  • Guanylate Cyclase / antagonists & inhibitors
  • Humans
  • Hydroxylamine
  • Hydroxylamines / pharmacology*
  • Kinetics
  • Nitric Oxide / pharmacology*


  • Aminoquinolines
  • Azides
  • Hydroxylamines
  • Hydroxylamine
  • Nitric Oxide
  • Dibutyryl Cyclic GMP
  • 6-anilino-5,8-quinolinedione
  • Guanylate Cyclase
  • 1-Methyl-3-isobutylxanthine