noc-18 and nitrosylprotoheme

noc-18 has been researched along with nitrosylprotoheme* in 1 studies

Other Studies

1 other study(ies) available for noc-18 and nitrosylprotoheme

Article	Year
Effects of nitric oxide on the eosinophil survival in vitro. A role for nitrosyl-heme. FEBS letters, 1999, Jan-22, Volume: 443, Issue:1 In a previous paper we showed that the nitric oxide (NO) donors azide and hydroxylamine inhibited eosinophil apoptosis. Azide and hydroxylamine generate a nitrosyl-heme complex - due to endogenous catalase activity - which activates soluble guanylate cyclase. In contrast, in the present paper, we show that NO donors (SNAP, SIN-1, S-nitroso-L-cysteine, NOC-18) which spontaneously release NO in physiological solutions did not support the survival of eosinophils and induced apoptosis or necrosis. However, the addition of hematin (the ferric form of heme) together with low doses of NO (SNAP 10 microM) promoted eosinophil survival. In conclusion, we propose that NO and heme (e.g. from heme-containing enzymes such as peroxidase or catalase), both released in inflammation sites, could form nitrosyl-heme and thus promote eosinophilic inflammation. Topics: Apoptosis; Cell Survival; Cysteine; Cytokines; Eosinophils; Guanylate Cyclase; Heme; Hemin; Humans; Interleukin-5; Nitric Oxide; Nitric Oxide Donors; Nitroso Compounds; Penicillamine; S-Nitroso-N-Acetylpenicillamine; S-Nitrosothiols	1999

Article

Year

Effects of nitric oxide on the eosinophil survival in vitro. A role for nitrosyl-heme.

FEBS letters, 1999, Jan-22, Volume: 443, Issue:1

In a previous paper we showed that the nitric oxide (NO) donors azide and hydroxylamine inhibited eosinophil apoptosis. Azide and hydroxylamine generate a nitrosyl-heme complex - due to endogenous catalase activity - which activates soluble guanylate cyclase. In contrast, in the present paper, we show that NO donors (SNAP, SIN-1, S-nitroso-L-cysteine, NOC-18) which spontaneously release NO in physiological solutions did not support the survival of eosinophils and induced apoptosis or necrosis. However, the addition of hematin (the ferric form of heme) together with low doses of NO (SNAP 10 microM) promoted eosinophil survival. In conclusion, we propose that NO and heme (e.g. from heme-containing enzymes such as peroxidase or catalase), both released in inflammation sites, could form nitrosyl-heme and thus promote eosinophilic inflammation.

Topics: Apoptosis; Cell Survival; Cysteine; Cytokines; Eosinophils; Guanylate Cyclase; Heme; Hemin; Humans; Interleukin-5; Nitric Oxide; Nitric Oxide Donors; Nitroso Compounds; Penicillamine; S-Nitroso-N-Acetylpenicillamine; S-Nitrosothiols

1999