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The nitric oxide donors, azide and hydroxylamine, inhibit the programmed cell death of cytokine‐deprived human eosinophils
Author(s) -
Beauvais Francis,
Michel Laurence,
Dubertret Louis
Publication year - 1995
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(95)00188-f
Subject(s) - nitric oxide , hydroxylamine , chemistry , in vitro , pharmacology , eosinophil , programmed cell death , phosphodiesterase , guanylate cyclase , phosphodiesterase inhibitor , biochemistry , cytokine , azide , immunology , enzyme , biology , apoptosis , asthma , organic chemistry
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.