Inhibition of NADH oxidation by pyridine derivatives |
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| Authors: | R R Ramsay K A McKeown E A Johnson R G Booth T P Singer |
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| Affiliation: | 1. Shanghai Meteorological Bureau, Shanghai, China;2. Shanghai Key Laboratory of Meteorology and Health, Shanghai, China;3. National Marine Environmental Forecasts Center, State Oceanic Administration, Beijing, China;4. Department of Geography, Michigan State University, East Lansing, MI, USA;5. National Center for Atmospheric Research, Boulder, CO, USA;1. Department of Physics, University of Texas at Austin, Austin, TX 78712, USA;2. Department of Computer Science, Trinity University, San Antonio, TX 79212, USA;3. Department of Chemical Engineering, Texas Tech University, Lubbock, TX 79409, USA;4. Department of Mathematics, Trinity University, San Antonio, TX 78212, USA;5. Department of Physics and Astronomy, Trinity University, San Antonio, TX 78212, USA;6. Department of Physics, Texas Tech University, Lubbock, TX 79409, USA |
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| Abstract: | The neurotoxicity of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, an impurity in an illicit drug, is expressed after its oxidation to 1-methyl-4-phenylpyridinium by monoamine oxidase. The pyridinium is concentrated by carrier-mediated transport into the mitochondria where it inhibits NADH dehydrogenase and, hence, ATP synthesis. Some structurally related compounds have been tested for their effect on the oxidation of NAD+-linked substrates in intact mitochondria, and for the inhibition of the accumulation of the pyridinium into mitochondria and of NADH dehydrogenase activity in a membrane preparation. Some pyridine derivatives are more inhibitory to NADH dehydrogenase than is 1-methyl-4-phenylpyridinium but these are not concentrated into mitochondria by the uptake system. 4-Phenylpyridine, one of the most effective inhibitors, both occurs naturally and is an environmental pollutant. |
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