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El estrés oxidativo y la activación plaquetaria en la homocistinuria homocigótica
G Davì1, G Di Minno, A Coppola
1Center of Excellence on Aging, Department of Biomedical Sciences, University of Chieti G. D'Annunzio, Chieti, Italy. gdavi@unich.it
Circulation
|September 6, 2001
Resumen
La hiperhomocisteinemia grave (CbetaSD) aumenta el daño oxidativo, lo que lleva a una mayor activación plaquetaria. La suplementación con vitamina E redujo los marcadores de este daño y la activación en los pacientes.
Área de la Ciencia:
- La bioquímica es la bioquímica.
- Medicina Cardiovascular La medicina cardiovascular es una especialidad de la salud.
- Trastornos metabólicos Los trastornos metabólicos son trastornos metabólicos que se producen en el cuerpo.
Sus antecedentes:
- La hiperhomocisteinemia severa, causada por la deficiencia de cistationina beta-sintasa (CbetaSD), está relacionada con la enfermedad vascular atero-trombótica prematura.
- La homocisteína está implicada en el daño vascular a través de mecanismos de estrés oxidativo.
Objetivo del estudio:
- Investigar si la formación in vivo de 8-iso-prostaglandina F ((2alfa) está elevada en pacientes con CbetaSD.
- Para determinar si esta elevación se correlaciona con la activación plaquetaria in vivo, medida por la excreción del metabolito del tromboxano.
- Para evaluar el efecto de la suplementación de vitamina E en estos marcadores.
Principales métodos:
- Se recogieron muestras de orina y sangre de 13 pacientes homocigotos con CbetaSD y controles sanos.
- Se midió la excreción urinaria de 8-iso-PGF ((2alfa) y 11-dehidro-TXB ((2).
- Se evaluaron los niveles plasmáticos de homocisteína y vitamina E.
- Se administró vitamina E (600 mg/día durante 2 semanas) y se volvieron a medir los marcadores.
Principales resultados:
- Los pacientes con CbetaSD mostraron una excreción urinaria significativamente mayor de 8-iso-PGF(2alfa) y 11-dehidro-TXB(2) en comparación con los controles.
- Ambos marcadores se correlacionaron con la homocisteína plasmática y entre sí.
- La suplementación con vitamina E aumentó significativamente los niveles plasmáticos de vitamina E y redujo la excreción de 8-iso-PGF ((2alfa) y 11-dehidro-TXB ((2).
- Se observó una fuerte correlación inversa entre los niveles urinarios de 8-iso-PGF y los niveles plasmáticos de vitamina E.
Conclusiones:
- La peroxidación mejorada del ácido araquidónico a los F(2)-isoprostanos puede vincular la hiperhomocisteinemia y la activación plaquetaria en CbetaSD.
- Estos hallazgos apoyan una mayor investigación sobre la suplementación de vitamina E para pacientes con CbetaSD.
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