| Understanding Oxidative Stress in Brain with Ultramicroelectrodes: Implications for a Possible Mechanism of Alzheimer Disease Christian Amatore1; 1CNRS & PSL, FRENCH ACAD. OF SCI. AND XIAMEN UNIVERSITY, Paris, France; PAPER: 323/Oxidative/Regular (Oral) SCHEDULED: 12:10/Thu. 24 Oct. 2019/Zeus (55/Mezz. F) ABSTRACT: Oxidative stress is an essential metabolic outcome in aerobic organisms due to the activity of the mitochondria in providing the basic energy of cells or during the operation of several enzymatic pools. It also serves to regulate the size and shape of organs or restructure them during foetal development by apoptosis. Oxidative stress is also indispensable to the immune system by allowing macrophages to eliminate virus, bacteria and impaired or dead cells through phagocytosis [1]. In fact, no aerobic organism could live without oxidative stress: a fact that explains why evolution maintained such unsafe mechanisms in aerobic organisms. They are, however, associated to highly negative issues. Indeed, oxidative stress mechanisms provide a variety of life-harmful radicals and species called generically Reactive Oxygen Species (ROS) and Reactive Nitrogen Species (RNS) whose fluxes need to be finely controlled to avoid the destruction of most organic molecules (e.g., lipids in cell membranes, enzymes, etc.) and biological molecules (DNA, proteins, etc.) in cells. Thus, under normal conditions, a panoply of antioxidants and enzymatic systems ensures a fine homeostatic balance. Rupture of this delicate balance, however, is frequent and may provoke severe damages leading to human pathologies (aging, cancers, AIDS, hearth and brain strokes, Parkinson and Alzheimer’ diseases, etc.). Using platinized carbon fiber ultramicroelectrodes, we could establish the composition of primary oxidative stress in macrophages [1, 2] and characterize the nature of functional hyperemia in the brain [3]. This led us to formulate an alternative hypothesis about the onset of Alzheimer disease when Amyloid-β and ascorbate molecules are present [4, 5]. References: 1. K. Hu, Y. Li, S.A. Rotenberg, C. Amatore, M.V. Mirkin. J. Am. Chem. Soc., 141, 2019, 4564-4568. 2. C Amatore, S. Arbault, M. Guille, F. Lemaître. Chem. Rev., 108, 2008, 2585–2621. 3. C. Amatore, S. Arbault, C. Bouton, K. Coffi, J.-C. Drapier, H. Ghandour, Y. Tong. ChemBioChem, 7, 2006, 653-661. 4. R. Giacovazzi, I. Ciofini, L. Rao, C. Adamo, C. Amatore, Phys. Chem. Phys. Chem. (PCCP), 16, 2014, 10169-10174. 5. L. Lai, C. Zhao, M. Su, X. Li, X. Liu, H. Jiang, C. Amatore, X.M. Wang. Biomater. Sc., 4, 2016, 1085-1091. |
