Posibilidades Terapéuticas con Antioxidantes Mitocondriales

Antioxidantes Mitocondriales Por cuanto el daño oxidativo es parte de la patogenia de la diabetes, es lógico que los antioxidantes tengan potencial terapéutico.

Los compuestos naturales tales como el atocoferol, el ascorbato, la coenzima Q y el ácido lipoico, no tienen una definida acción, aunque administrados en dosis altas hayan demostrado efectividad en otras entidades.

Experimentalmente demuestran que tanto la vitamina E como la coenzima Q protegen a la mitocondria contra la toxicidad del O2 y que la acumulación de los mismos por el organelo aislado aumentan la eficacia de su acción44.

Se ha comprobado que el compuesto alquiltrifenilfosfonio atraviesa las dos capas de la membrana mitocondrial, sin requerir transportadores o moléculas de acoplamiento45.

Así mismo el metil-trifenil-fosfonio no se acumula y es depurado. Ha sido cuantificado en otros tejidos: cerebro, miocardio e hígado en el ratón y desaparece de la circulación una vez suspendida su administración.

Es importante decir que las concentraciones de estos componentes en la mitocondria, es centenares de veces superior, de las cantidades presentes en el citosol.

Hasta el presente diversos protocolos estudian in vivo los compuesto antioxidantes en modelos experimentales con daño mitocondrial.

Conclusiones

En conclusión, el propósito de esta revisión ha sido presentar un aspecto optimista para quienes ven a la diabetes como una enfermedad con un pronóstico cada vez menos próximo a la curación y a la prevención.

Pero el progreso no puede detenerse.

Gracias a que el mundo científico está cada vez más concentrado en la investigación básica y a la aplicación de sus resultados, diversas oportunidades se pueden ofrecer al enfermo.

Como resumen se analizaron los estudios epidemiológicos, la patogénesis, las bases químicas y los mecanismos biomoleculares. Llevan al daño vascular prematuro en la intolerancia a la glucosa. Cuando aún no se ha detectado en el individuo una glicemia que lo catalogue como diabético tipo 2, a saber:

  • Las alteraciones micro vasculares en la intolerancia a la glucosa en dos estudios controlados.
  • El estrés oxidativo por la hiperglicemia y sus consecuencias sobre el daño celular.
  • Los mecanismos en las vías del poliol y la hexosamina en la generación de radicales de oxígeno tóxicos.
  • La participación y modo de acción de los productos de glicosilación avanzada (AGEs) en el daño micro vascular.
  • La activación de la proteína-cinasa C por el diacil-glicerol en la alteración de la curva de tolerancia a la glucosa y los mecanismos que conducen a una serie de eventos bio-moleculares.
  • La participación de la mitocondria en la producción de O2 y la utilización de antioxidantes en este proceso.
  • Las posibles intervenciones y progresos en el período anterior a la aparición de la diabetes 2.
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