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Síndrome de Abstinencia Alcohólica: Resultado del estrés oxidativo y desequilibrio neuronal. Estado del arte
Resumen
El alcoholismo constituye una enfermedad crónica que conlleva a afectaciones conductuales que se prolongan durante la abstinencia. El consumo de etanol incrementa la acumulación de Acetaldehído y Especies Reactivas de Oxígeno provocando daño a nivel cerebral. Dos importantes neurotransmisores involucrados en el daño neuronal son el Ácido γ-Amino butírico (GABA,) un neurotransmisor inhibitorio y el glutamato el más importante neurotransmisor excitatorio, las afectaciones del receptor GABAérgico contribuyen a la tolerancia y dependencia al etanol y síntomas de hiperexcitabilidad en la abstinencia mientras que las afectaciones del receptor NMDA glutamatérgico contribuyen a la tolerancia y dependencia al etanol así como al establecimiento de los síntomas de abstinencia. Las afectaciones en el metabolismo del Etanol desencadenan alteraciones conductuales ya que la disfunción de la enzima Acetaldehído deshidrogenasa provoca acumulación a nivel cerebral de Acetaldehído responsable en gran medida del daño cerebral ocasionado durante el alcoholismo. En el presente trabajo se revisa de forma sistemática y organizada por temáticas, en orden lógico y partiendo de conceptos básicos, la literatura experimental existente en bases de datos como PubMed y Medline, acerca de los elementos protagonistas en la relación entre estrés oxidativo y desequilibrio neuronal que constituyen la base de las afectaciones conductuales en el desarrollo de la adicción y durante la abstinencia. Nuestro objetivo es contribuir a clarificar el conocimiento existente acerca de las relaciones entre determinados factores biológicos (como neurotransmisores e indicadores de desbalance redox) y los efectos del alcohol, poniendo de manifiesto la importancia de algunos factores de riesgo para el desarrollo del alcoholismo.
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