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The interaction of citrate and calcium in regulating the oxidation of exogenous NADH in plant mitochondria |
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| Affiliation: | 1. Nestlé Institute of Health Sciences, Nestlé Research, EPFL Innovation Park, CH-1015 Lausanne, Switzerland;2. Molecular Nutritional Medicine, Else Kröner Fresenius Center for Nutritional Medicine, Technische Universität München, 85354 Freising, Germany;3. Department of Biochemistry and Molecular Biology, University of Valladolid, Unidad de Excelencia Instituto de Biología y Genética Molecular (IBGM), 47003 Valladolid, Spain;4. Healthy Longevity Translational Research Programme, Yong Loo Lin School of Medicine, National University of Singapore, 119228, Singapore;5. Department of Biochemistry, Yong Loo Lin School of Medicine, National University of Singapore, 117596, Singapore |
| Abstract: | Plant mitochondria oxidize exogenous NADH via an external NADH dehydrogenase; little is known about the regulation of this dehydrogenase. Data presented here show that citrate caused a non-competitive inhibition of NADH oxidation. This inhibition can be reversed by Ca2+. It is postulated that citrate causes the inhibition by extracting Ca2+ from the NADH-ubiquinone reductase. Citrate caused a more powerful effect if added before rather than after the NADH. This suggests that the Ca2+ is less easily removed in the presence of NADH due to a conformational change in the membrane. Experimentals using a series of electron acceptors suggest that citrate prevents electron transfer between the flavoprotein and the ubiquinone. It is suggested that calcium facilitates electron flux between these components by binding the flavoprotein to the membrane. |
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