Publicaciones 2011-2020

@article{RN364,
title = {Development of an Iron-Selective Antioxidant Probe with Protective Effects on Neuronal Function},
author = { O. Garcia-Beltran and N.P. Mena and P. Aguirre and G. Barriga-Gonz\'{a}lez and A. Gald\'{a}mez and E. Nagles and T. Adasme and C. Hidalgo and M. Nunez},
url = {/brokenurl#<Go to ISI>://WOS:000417648600030},
doi = {10.1371/journal.pone.0189043},
issn = {1932-6203},
year = {2017},
date = {2017-01-01},
journal = {Plos One},
volume = {12},
number = {12},
abstract = {Iron accumulation, oxidative stress and calcium signaling dysregulation are common pathognomonic signs of several neurodegenerative diseases, including Parkinson's and Alzheimer's diseases, Friedreich ataxia and Huntington's disease. Given their therapeutic potential, the identification of multifunctional compounds that suppress these damaging features is highly desirable. Here, we report the synthesis and characterization of N-(1,3-dihydroxy- 2-(hydroxymethyl) propan-2-yl)-2-(7-hydroxy-2-oxo-2H-chromen-4-yl) acetamide, named CT51, which exhibited potent free radical neutralizing activity both in vitro and in cells. CT51 bound Fe2+ with high selectivity and Fe3+ with somewhat lower affinity. Cyclic voltammetric analysis revealed irreversible binding of Fe3+ to CT51, an important finding since stopping Fe2+/Fe3+ cycling in cells should prevent hydroxyl radical production resulting from the Fenton-Haber-Weiss cycle. When added to human neuroblastoma cells, CT51 freely permeated the cell membrane and distributed to both mitochondria and cytoplasm. Intracellularly, CT51 bound iron reversibly and protected against lipid peroxidation. Treatment of primary hippocampal neurons with CT51 reduced the sustained calcium release induced by an agonist of ryanodine receptor-calcium channels. These protective properties of CT51 on cellular function highlight its possible therapeutic use in diseases with significant oxidative, iron and calcium dysregulation.},
keywords = {calcium cells, coumarins, deficiency, fluorescence fluorescence, fragmentation, iron, labile mitochondrial on oxidative parkinsons-disease, probes, sh-sy5y stress},
pubstate = {published},
tppubtype = {article}
}

@article{RN125,
title = {Design, Synthesis and Cellular Dynamics Studies in Membranes of a New Coumarin-Based "Turn-Off" Fluorescent Probe Selective for Fe2+},
author = { O. Garcia-Beltran and N. Mena and O. Yanez and J. Caballero and V. Vargas and M. Nunez and B.K. Cassels},
url = {/brokenurl#<Go to ISI>://WOS:000325121800007},
doi = {10.1016/j.ejmech.2013.06.022},
issn = {0223-5234},
year = {2013},
date = {2013-01-01},
journal = {European Journal of Medicinal Chemistry},
volume = {67},
pages = {60-63},
publisher = {2013 Elsevier Masson SAS.},
abstract = {A new coumarin-based 'turn-off' fluorescent probe, 7-(diethylamino)-N-(1,3-dihydroxy-2-(hydroxymethyl)propan-2-yl)-2-oxo-2H-chromene-3-carboxamide (AGD) was synthesized. This compound is highly selective for ferrous ions (Fe2+) and can reversibly detect them in aqueous medium. The probe localizes to the cell membrane in living cells, where it can detect changes in Fe2+ concentration. Molecular dynamics (MD) simulations indicate that AGD interacts with the lipid bilayer at the level of the glycerol moieties.},
keywords = {cells, chelatable chelators, chemosensor, deficiency, dynamics, fe2+ fe3+ fluorescent ion, iron, labile molecular probes, sensor, turn-off},
pubstate = {published},
tppubtype = {article}
}