The Effect of Ca2+ on Reactive Oxygen Species Generation and Elimination in Brain Mitochondria

Abstract

Event Abstract Back to Event The Effect of Ca2+ on Reactive Oxygen Species Generation and Elimination in Brain Mitochondria Zsofia Komary1*, Laszlo Tretter1 and Vera Adam-Vizi1 1 Department of Medical Biochemistry, Semmelweis University, Hungary Mitochondria have an essential role in the intracellular ROS (reactive oxygen species) generation. Mitochondrial ROS production is a significant pathogenic factor both in acute ischemic and in chronic neurodegenerative diseases. Mitochondria however might play a role in the elimination of ROS as well. The purpose of our experiments was to describe the effects of Ca2+ on ROS production/ROS elimination in isolated brain mitochondria. H2O2 was measured by the Amplex red method. Ca2+ in the micromolar range caused permeability transition (PT) of mitochondria respiring on glutamate + malate. Parallel with the PT, ROS generation was reduced and loss of NAD(H) was observed. Inhibition of PT with ADP resulted in an increase of ROS production after addition of Ca2+. Mitochondrial ROS elimination was measured detecting the accumulation of H2O2. Micromolar [Ca2+] did not cause H2O2 accumulation neither in the presence nor in the absence of PT inhibitor ADP. Inhibition of the complexes of the respiratory chain (complex I inhibitor - rotenon, complex III inhibitor – antimycin) resulted in an extensive elevation of ROS generation, however it did not influence the efficacy of ROS elimination. Ca2+ acting in the presence of respiratory inhibitors increased ROS formation and reduced ROS elimination with antimycin, but combination of Ca2+ with rotenone did not influence ROS elimination. It is concluded that a Ca2+-mediated single hit on the mitochondrial metabolism does not prevent ROS elimination. Combination of Ca2+-load with inhibition of the respiratory chain can impair endogenous ROS scavenging. These results contribute to the understanding of the role of mitochondrial components in excitotoxic ROS production. Conference: 12th Meeting of the Hungarian Neuroscience Society, Budapest, Hungary, 22 Jan - 24 Jan, 2009. Presentation Type: Poster Presentation Topic: Pathophysiology and neurology - degenerative disorders Citation: Komary Z, Tretter L and Adam-Vizi V (2009). The Effect of Ca2+ on Reactive Oxygen Species Generation and Elimination in Brain Mitochondria. Front. Syst. Neurosci. Conference Abstract: 12th Meeting of the Hungarian Neuroscience Society. doi: 10.3389/conf.neuro.01.2009.04.160 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 05 Mar 2009; Published Online: 05 Mar 2009. * Correspondence: Zsofia Komary, Department of Medical Biochemistry, Semmelweis University, Budapest, Hungary, komaryzsofia@yahoo.co.uk Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Zsofia Komary Laszlo Tretter Vera Adam-Vizi Google Zsofia Komary Laszlo Tretter Vera Adam-Vizi Google Scholar Zsofia Komary Laszlo Tretter Vera Adam-Vizi PubMed Zsofia Komary Laszlo Tretter Vera Adam-Vizi Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.