2014, Número 3
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Med Int Mex 2014; 30 (3)
Estrés oxidativo y nitrosativo como mecanismo de daño al hepatocito producido por el metabolismo del etanol
Hernández-Rodríguez S, Gutiérrez-Salinas J, García-Ortíz L, Mondragón-Terán P, Ramírez-García S, Núñez-Ramos NR
Idioma: Español
Referencias bibliográficas: 56
Paginas: 295-308
Archivo PDF: 534.45 Kb.
RESUMEN
Los radicales libres derivados del oxígeno (ROS) y del nitrógeno (RNS) son
moléculas muy reactivas que pueden reaccionar con las macromoléculas
de la célula y provocarle un daño irreversible. Dentro del hepatocito,
el etanol es oxidado a acetaldehído por medio de tres sistemas:
a) en el
citosol por la enzima alcohol deshidrogenasa (ADH);
b) en el retículo
endoplásmico por el citocromo P450 (CYP2E1), y
c) en los peroxisomas
por la enzima catalasa. El acetaldehído es oxidado en la mitocondria
por la enzima aldehído deshidrogenasa (ALDH) para generar acetato.
Las consecuencias metabólicas de la oxidación por el etanol incluyen
una alteración del equilibrio redox citoplásmico y mitocondrial que
genera alta producción de radicales libres derivados del oxígeno y del
nitrógeno, principalmente en la cadena respiratoria de las mitocondrias.
La producción de éstos puede sobrepasar las defensas antioxidantes y
ocasiona el llamado estrés oxidativo junto con estrés nitrosativo, ambos
capaces de dañar a todos los componentes macromoleculares de la célula
y provocar su muerte al activar el mecanismo de apoptosis.
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