Iglesias González, JavierSánchez Iglesias, SofíaBeiras Iglesias, AndrésMéndez Álvarez, EstefaníaSoto-Otero, Ramón2024-02-082024-02-082017Iglesias-González, J., Sánchez-Iglesias, S., Beiras-Iglesias, A. et al. Effects of Aluminium on Rat Brain Mitochondria Bioenergetics: an In vitro and In vivo Study. Mol Neurobiol 54, 563–570 (2017)http://hdl.handle.net/10347/32559This version of the article has been accepted for publication, after peer review (when applicable) and is subject to Springer Nature’s AM terms of use, but is not the Version of Record and does not reflect post-acceptance improvements, or any corrections. The Version of Record is available online at: http://dx.doi.org/10.1007/s12035-015-9650-zNumerous 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.engAluminiumMitochondriaHigh-resolution respirometryParkinson's diseaseOxidative stressRat brainjournal article10.1007/s12035-015-9650-zopen access