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Formación de oxidantes inflamatorios derivados del óxido nítrico por la mieloperoxidasa en los neutrófilos

J P Eiserich¹, M Hristova, C E Cross

¹Department of Internal Medicine, University of California, Davis 95616, USA. jason.eiserich@ccc.uab.edu

|February 5, 1998

Resumen

El nitrito (NO2-) contribuye a la inflamación mediante la formación de especies reactivas de nitrógeno a través de la mieloperoxidasa en los neutrófilos. Este proceso conduce a la nitratación y cloración de la tirosina, afectando la función celular y contribuyendo potencialmente al daño oxidativo in vivo.

Área de la Ciencia:

La bioquímica es la bioquímica.
Inmunología Inmunología.
Biología celular Biología celular.

Sus antecedentes:

El óxido nítrico (.NO) está implicado en enfermedades inflamatorias e infecciosas.
Peroxynitrite (ONOO-), formado por .NO y superóxido, es un presunto mediador de la toxicidad de .NO.
La evidencia de la actividad de ONOO in vivo a menudo se basa en la detección de 3-nitrotirosina.

Objetivo del estudio:

Para investigar el papel del nitrito (NO2-) en los procesos inflamatorios.
Para dilucidar los mecanismos por los cuales el NO2- promueve la nitratación de tirosina.
Para determinar si los neutrófilos polimorfonucleares (PMN) median la nitratación dependiente del NO2.

Principales métodos:

Estudió la reacción del NO2- con el ácido hipocloroso (HOCl) o la mieloperoxidasa (MPO).
Se ha investigado la conversión de NO2 a cloruro de nitrilo (NO2Cl) y dióxido de nitrógeno (.NO2) por PMNs humanos activados.
Nitración y cloración cuantificada de tirosina utilizando NO2 etiquetado con 15N y efectos evaluados sobre la actividad de la enzima convertidora de angiotensina (ECA).

Principales resultados:

Las PMN humanas activadas convierten NO2- en NO2Cl y .NO2 a través de vías dependientes de MPO.
La nitratación y la cloración mediadas por PMN de los residuos de tirosina fueron mejoradas por NO2- y .NO.
15NO2- confirmó su papel en la nitratación mediada por PMN, y la inactivación mediada por PMN exacerbada por NO2- de la célula endotelial ACE.

Conclusiones:

NO2- puede regular los procesos inflamatorios a través de mecanismos oxidativos que involucran a los PMNs.
El NO2Cl y .NO2 derivados del PMN contribuyen a la nitratación y cloración de la tirosina.
Estas vías pueden explicar las observaciones in vivo de nitratación y cloración de tirosina en condiciones inflamatorias.

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