Difference between revisions of "Iglesias-Gonzalez 2016 Mol Neurobiol"
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|tissues=Nervous system | |tissues=Nervous system | ||
|preparations=Isolated mitochondria | |preparations=Isolated mitochondria | ||
|enzymes=Complex I, Complex II;succinate dehydrogenase, Complex IV;cytochrome c oxidase, Complex V;ATP synthase | |enzymes=Complex I, Complex II;succinate dehydrogenase, Complex III, Complex IV;cytochrome c oxidase, Complex V;ATP synthase | ||
|diseases=Alzheimer's, Neurodegenerative, Parkinson's | |diseases=Alzheimer's, Neurodegenerative, Parkinson's | ||
|couplingstates=LEAK, OXPHOS, ETS | |couplingstates=LEAK, OXPHOS, ETS | ||
|substratestates=CI, CII, CI&II | |substratestates=CI, CII, CI&II | ||
|instruments=Oxygraph-2k, TPP | |instruments=Oxygraph-2k, TPP | ||
|additional= | |additional=2016-07 | ||
}} | }} | ||
Revision as of 08:47, 15 September 2016
| Iglesias-González J, Sánchez-Iglesias S, Beiras-Iglesias A, Méndez-Álvarez E, Soto-Otero R (2016) Effects of aluminium on rat brain mitochondria bioenergetics: an in vitro and in vivo study. Mol Neurobiol [Epub ahead of print]. |
Iglesias-Gonzalez J, Sanchez-Iglesias S, Beiras-Iglesias A, Mendez-Alvarez E, Soto-Otero R (2016) Mol Neurobiol
Abstract: Numerous studies have highlighted the potential of aluminium as an aetiological factor for some neurodegenerative disorders, particularly Alzheimer's disease and Parkinson's disease. Our previous studies have shown that aluminium can cause oxidative stress, reduce the activity of some antioxidant enzymes, and enhance the dopaminergic neurodegeneration induced by 6-hydroxydopamine in an experimental model of Parkinson's disease in rats. We now report a study on the effects caused by aluminium on mitochondrial bioenergetics following aluminium addition and after its chronic administration to rats. To develop our study, we used a high-resolution respirometry to test the mitochondrial respiratory capacities under the conditions of coupling, uncoupling, and non-coupling. Our study showed alterations in leakiness, a reduction in the maximum capacity of complex II-linked respiratory pathway, a decline in the respiration efficiency, and a decrease in the activities of complexes III and V in both models studied. The observed effects also included both an alteration in mitochondrial transmembrane potential and a decrease in oxidative phosphorylation capacity when relatively high concentrations of aluminium were added to the isolated mitochondria. These findings contribute to explain both the ability of aluminium to generate oxidative stress and its suggested potential to act as an etiological factor by promoting the progression of neurodegenerative disorders such as Parkinson's disease. • Keywords: Aluminium, High-resolution respirometry, Mitochondria, Oxidative stress, Parkinson’s disease, Rat brain
• O2k-Network Lab: ES Santiago De Compostela Mendez-Alvarez E
Labels: MiParea: Respiration, Pharmacology;toxicology
Pathology: Alzheimer's, Neurodegenerative, Parkinson's
Organism: Rat Tissue;cell: Nervous system Preparation: Isolated mitochondria Enzyme: Complex I, Complex II;succinate dehydrogenase, Complex III, Complex IV;cytochrome c oxidase, Complex V;ATP synthase
Coupling state: LEAK, OXPHOS, ETS"ETS" is not in the list (LEAK, ROUTINE, OXPHOS, ET) of allowed values for the "Coupling states" property.
HRR: Oxygraph-2k, TPP
2016-07
