Characterization of 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one as a heme-site inhibitor of nitric oxide-sensitive guanylyl cyclase.
Mol Pharmacol
; 50(1): 1-5, 1996 Jul.
Article
en En
| MEDLINE
| ID: mdl-8700100
Nitric oxide (NO) binds with high affinity to the heme of soluble guanylyl cyclase (sGC), resulting in accumulation of the second messenger cGMP in many biological systems. 1H-[1,2,4]Oxadiazolo[4,3-a]quinoxalin-1-one (ODQ) was recently described as potent and selective inhibitor of sGC, providing an invaluable tool with which to settle the function of the cGMP pathway in NO-mediated signal transduction [Mol. Pharmacol. 48:184-188 (1995)]. The present study investigated the mechanism of ODQ-induced inhibition of purified bovine lung sGC. The drug induced a rightward shift of the concentration-response curves recorded with two different NO donors and a reduction of maximal sGC activity, pointing to a mixed type of inhibition. The time course of NO-stimulated sGC activity determined in the presence of 0.3 microM ODQ showed that the inhibitory effect was time-dependent (half-time approximately 3 min) and virtually complete after about 10 min. The cyclase did not recover from ODQ-induced inhibition upon extensive dilution, pointing to an apparently irreversible inactivation of the enzyme by the quinoxalin. Light absorbance spectroscopy showed that ODQ (0.3 mM) induced a shift of the Soret band of the heme from 431 nm to 393 nm, indicating that ODQ oxidizes the ferrous form of the enzyme to the ferric species, which is though to exhibit only poor NO sensitivity. Together, our results suggest that inhibition of sGC by ODQ is NO-competitive and results in an apparently irreversible oxidation of the prosthetic heme group.
Buscar en Google
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Oxadiazoles
/
Quinoxalinas
/
Inhibidores Enzimáticos
/
Guanilato Ciclasa
/
Hemo
/
Óxido Nítrico
Tipo de estudio:
Diagnostic_studies
Límite:
Animals
Idioma:
En
Revista:
Mol Pharmacol
Año:
1996
Tipo del documento:
Article
País de afiliación:
Austria
Pais de publicación:
Estados Unidos