Mechanism of product release in NO detoxification from Mycobacterium tuberculosis truncated hemoglobin N.
J Am Chem Soc
; 130(5): 1688-93, 2008 Feb 06.
Article
em En
| MEDLINE
| ID: mdl-18189394
The capability of Mycobacterium tuberculosis to rest in latency in the infected organism appears to be related to the disposal of detoxification mechanisms, which converts the nitric oxide (NO) produced by macrophages during the initial growth infection stage into a nitrate anion. Such a reaction appears to be associated with the truncated hemoglobin N (trHbN). Even though previous experimental and theoretical studies have examined the pathways used by NO and O2 to access the heme cavity, the eggression pathway of the nitrate anion is still a challenging question. In this work we present results obtained by means of classical and quantum chemistry simulations that show that trHbN is able to release rapidly the nitrate anion using an eggression pathway other than those used for the entry of both O2 and NO and that its release is promoted by hydration of the heme cavity. These results provide a detailed understanding of the molecular basis of the NO detoxification mechanism used by trHbN to guarantee an efficient NO detoxification and thus warrant survival of the microorganism under stress conditions.
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Hemoglobinas Anormais
/
Mycobacterium tuberculosis
/
Óxido Nítrico
Idioma:
En
Revista:
J Am Chem Soc
Ano de publicação:
2008
Tipo de documento:
Article
País de afiliação:
Argentina
País de publicação:
Estados Unidos