5-demethoxyubiquinone-9 and ubiquinone-9

5-demethoxyubiquinone-9 has been researched along with ubiquinone-9* in 2 studies

Other Studies

2 other study(ies) available for 5-demethoxyubiquinone-9 and ubiquinone-9

ArticleYear
β-RA reduces DMQ/CoQ ratio and rescues the encephalopathic phenotype in
    EMBO molecular medicine, 2019, Volume: 11, Issue:1

    Coenzyme Q (CoQ) deficiency has been associated with primary defects in the CoQ biosynthetic pathway or to secondary events. In some cases, the exogenous CoQ supplementation has limited efficacy. In the

    Topics: Animals; Brain; Disease Models, Animal; Energy Metabolism; Histocytochemistry; Hydroxybenzoates; Mice; Mitochondrial Encephalomyopathies; Neuroprotective Agents; Salicylic Acid; Survival Analysis; Treatment Outcome; Ubiquinone

2019
Mitochondrial oxidative phosphorylation is defective in the long-lived mutant clk-1.
    The Journal of biological chemistry, 2004, Dec-24, Volume: 279, Issue:52

    The long-lived mutant of Caenorhabditis elegans, clk-1, is unable to synthesize ubiquinone, CoQ(9). Instead, the mutant accumulates demethoxyubiquinone(9) and small amounts of rhodoquinone(9) as well as dietary CoQ(8). We found a profound defect in oxidative phosphorylation, a test of integrated mitochondrial function, in clk-1 mitochondria fueled by NADH-linked electron donors, i.e. complex I-dependent substrates. Electron transfer from complex I to complex III, which requires quinones, is severely depressed, whereas the individual complexes are fully active. In contrast, oxidative phosphorylation initiated through complex II, which also requires quinones, is completely normal. Here we show that complexes I and II differ in their ability to use the quinone pool in clk-1. This is the first direct demonstration of a differential interaction of complex I and complex II with the endogenous quinone pool. This study uses the combined power of molecular genetics and biochemistry to highlight the role of quinones in mitochondrial function and aging.

    Topics: Animals; Ascorbic Acid; Caenorhabditis elegans; Electron Transport Complex I; Electron Transport Complex II; Glutamic Acid; Hydroquinones; Malates; Mitochondria; Mutation; Oxidative Phosphorylation; Pyruvic Acid; Quinones; Substrate Specificity; Tetramethylphenylenediamine; Time Factors; Ubiquinone

2004