2015 |
Mena, N P; Garcia-Beltran, O; Lourido, F; Urrutia, P J; Mena, R; Castro-Castillo, V; Cassels, B K; Nunez, M The Novel Mitochondrial Iron Chelator 5-((Methylamino)Methyl)-8-Hydroxyquinoline Protects against Mitochondrial-Induced Oxidative Damage and Neuronal Death Artículo de revista Biochemical and Biophysical Research Communications, 463 (4), pp. 787-792, 2015, ISSN: 0006-291x. Resumen | Enlaces | BibTeX | Etiquetas: brain chelation, contributes, degeneration, disease, diseases, homeostasis, hydroxyquinolines, in-vivo, inhibition iron iron, mitochondria, neurodegenerative parkinson's parkinsons-disease, substantia-nigra @article{RN243, title = {The Novel Mitochondrial Iron Chelator 5-((Methylamino)Methyl)-8-Hydroxyquinoline Protects against Mitochondrial-Induced Oxidative Damage and Neuronal Death}, author = { N.P. Mena and O. Garcia-Beltran and F. Lourido and P.J. Urrutia and R. Mena and V. Castro-Castillo and B.K. Cassels and M. Nunez}, url = {/brokenurl#<Go to ISI>://WOS:000358455300051}, doi = {10.1016/j.bbrc.2015.06.014}, issn = {0006-291x}, year = {2015}, date = {2015-01-01}, journal = {Biochemical and Biophysical Research Communications}, volume = {463}, number = {4}, pages = {787-792}, publisher = {2015 Elsevier Inc.}, abstract = {Abundant evidence indicates that iron accumulation, oxidative damage and mitochondrial dysfunction are common features of Huntington's disease, Parkinson's disease, Friedreich's ataxia and a group of disorders known as Neurodegeneration with Brain Iron Accumulation. In this study, we evaluated the effectiveness of two novel 8-OH-quinoline-based iron chelators, Q1 and Q4, to decrease mitochondrial iron accumulation and oxidative damage in cellular and animal models of PD. We found that at sub-micromolar concentrations, Q1 selectively decreased the mitochondrial iron pool and was extremely effective in protecting against rotenone-induced oxidative damage and death. Q4, in turn, preferentially chelated the cytoplasmic iron pool and presented a decreased capacity to protect against rotenone-induced oxidative damage and death. Oral administration of Q1 to mice protected substantia nigra pars compacta neurons against oxidative damage and MPTP-induced death. Taken together, our results support the concept that oral administration of Q1 is a promising therapeutic strategy for the treatment of NBIA.}, keywords = {brain chelation, contributes, degeneration, disease, diseases, homeostasis, hydroxyquinolines, in-vivo, inhibition iron iron, mitochondria, neurodegenerative parkinson's parkinsons-disease, substantia-nigra}, pubstate = {published}, tppubtype = {article} } Abundant evidence indicates that iron accumulation, oxidative damage and mitochondrial dysfunction are common features of Huntington's disease, Parkinson's disease, Friedreich's ataxia and a group of disorders known as Neurodegeneration with Brain Iron Accumulation. In this study, we evaluated the effectiveness of two novel 8-OH-quinoline-based iron chelators, Q1 and Q4, to decrease mitochondrial iron accumulation and oxidative damage in cellular and animal models of PD. We found that at sub-micromolar concentrations, Q1 selectively decreased the mitochondrial iron pool and was extremely effective in protecting against rotenone-induced oxidative damage and death. Q4, in turn, preferentially chelated the cytoplasmic iron pool and presented a decreased capacity to protect against rotenone-induced oxidative damage and death. Oral administration of Q1 to mice protected substantia nigra pars compacta neurons against oxidative damage and MPTP-induced death. Taken together, our results support the concept that oral administration of Q1 is a promising therapeutic strategy for the treatment of NBIA. |
2015 |
The Novel Mitochondrial Iron Chelator 5-((Methylamino)Methyl)-8-Hydroxyquinoline Protects against Mitochondrial-Induced Oxidative Damage and Neuronal Death Artículo de revista Biochemical and Biophysical Research Communications, 463 (4), pp. 787-792, 2015, ISSN: 0006-291x. |