CONGRESOS, CURSOS Y CONFERENCIAS
Seminarios INMA - Junior
El próximo miércoles 3 de marzo a las 12:00h darán comienzo los primeros Seminarios INMA Junior.
La sesión contará con las charlas de dos jóvenes investigadores del Instituto de Nanociencia y Materiales de Aragón, INMA (CSIC-Unizar) y se podrá seguir a través de Zoom ( https://us02web.zoom.us/j/82452333200?pwd=dVhBSEVCUVRSWTJ2QU5VR3VZMWpOdz09 ) y a través del canal de Youtube del INMA ( https://www.youtube.com/channel/UCEEolwQroau-y9pRAUbPXpg ) .
Ponente 1: Javier Bonet Aletá
Título: The chemistry of tumors as new tool for alternative therapies using catalytic nanoparticles
Resumen de la charla: New strategies in cancer therapy focus on combining different catalytic processes: the depletion of key metabolites such as Glutathione (GSH) or Glucose, and the in situ generation of harmfully Reactive Oxygen Species (ROS) species via Fenton reaction. GSH is a natural antioxidant which maintains the cytosol concentration of ROS (e.g. H2O2, O2·- or ·OH) below cytotoxic levels. Glucose, as the major source of energy in cells, is required to ensure ATP levels, particularly in cancer cells. Thus, the design of new nanomaterials showing the ability to alter these species under tumor microenviroment (herein, TME) chemical conditions are particularly interesting to control cancer growth. In this work, we present a nanoplatform based on Cu(II) and Fe(III) (CuFe) with the capability of triggering a cascade reaction specifically in TME conditions.
Due to its own metabolism, cytosol GSH/H2O2 levels in cancer cells are abnormally large. GSH can be oxidized by CuFe yielding GSSG and Cu(I)/Fe(II) species which are highly active in Fenton reaction. As a consequence of the depletion of GSH in cell, more H2O2 is available to increase ·OH hydroxyl levels via Fenton-process. Moreover, the remarked acidity of TME also favors Fenton reaction. High reactivity of ·OH radicals is responsible for oxidizing glucose, DNA, amino acids or membrane-lipids, causing critical cell damage entailing cell apoptosis. In this way, CuFe is able both of depleting antioxidant and increase ROS in TME conditions, generating selective cytotoxicity to cancer cells.
Ponente 2: Alfonso Toro Córdova