More articles from Volume 1, Issue 1, 2024
REDOX AND METABOLIC REPROGRAMMING OF BREAST CANCER CELLS AND ASSOCIATED ADIPOSE TISSUE - THE CORNERSTONES OF ADAPTIVE TUMOUR BEHAVIOUR
INSULIN MODULATES MITOCHONDRIAL STRUCTURAL AND FUNCTIONAL MOSAICISM IN BROWN ADIPOCYTES
NITRITE MITIGATES OXIDATIVE BURST IN ISCHEMIA/REPERFUSION IN BRAIN SLICES
NITRIC OXIDE, SUPEROXIDE AND PEROXYNITRITE – REDOX REGULATION OF THE CARDIOVASCULAR SYSTEM BY NITRO-OXIDATIVE STRESS AND S-NITROS(YL)ATION
DIETARY NITRATE AS PIVOT ON THE GUT MICROBIOTA-HOST REDOX COMMUNICATION
EFFECT OF SUCCINATE DEHYDROGENASE DEFICIENCY ON MITOCHONDRIAL FUNCTION
Laboratory of Bioenergetics, Czech Academy of Sciences, Institute of Psychology, Brno, Czechia
Faculty of Science, Charles University, Prague, Czechia
Laboratory of Bioenergetics, Institute of Physiology, Czech Academy of Sciences, Prague, Czechia
Laboratory of Bioenergetics, Institute of Physiology, Czech Academy of Sciences, Prague, Czechia
Laboratory of Bioenergetics, Institute of Physiology, Czech Academy of Sciences, Prague, Czechia
Laboratory of Translational Metabolism, Institute of Physiology, Czech Academy of Sciences, Prague, Czechia
Laboratory of Metabolism of Bioactive Lipids, Institute of Physiology, Czech Academy of Sciences, Prague, Czechia
Laboratory of Bioenergetics, Institute of Physiology, Czech Academy of Sciences, Prague, Czechia
Laboratory of Bioenergetics, Institute of Physiology, Czech Academy of Sciences, Prague, Czechia
Editor: Bato Korac
Published: 29.08.2024.
Short oral presentations
Volume 1, Issue 1 (2024)
Abstract
Succinate dehydrogenase (SDH) connects the tricarboxylic acid (TCA) cycle and the respiratory chain. Mutations in SDH subunits have been associated with tumorigenesis and mitochondrial disease. In this project, we focused on subunit A of SDH (SDHA), primarily associated with inherited mitochondrial disease, and investigated the consequences of its loss or re-expression of mutant variants in HEK cells (SDHA KO). Lack of SDHA led to a downregulation of all SDH subunits and a secondary downregulation of the majority of mitochondrial complex I and IV subunits. Cellular respiratory capacity was severely decreased in the model, SDH-dependent respiration completely abolished and complex I-dependent respiration attenuated, reflecting the downregulation of respiratory chain complexes in general. Finally, the NAD+/NADH ratio was increased in SDHA KO, indicating complex rearrangement of the TCA. It resulted in higher glycolytic activity and lipid accumulation.
Supported by Czech Science Foundation (21-18993S), Grant Agency of Charles University (283423) and Czech Health Research Council (NU22-01-00499).
Citation
Copyright
This work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License.
Article metrics
The statements, opinions and data contained in the journal are solely those of the individual authors and contributors and not of the publisher and the editor(s). We stay neutral with regard to jurisdictional claims in published maps and institutional affiliations.