Search results for "Ubiquinone"
showing 6 items of 26 documents
ENDOR Spectroscopic and Molecular Orbital Study of the Dynamical Properties of the Side Chain in Radical Anions of Ubiquinones Q-1, Q-2, Q-6, and Q-10
2000
Abstract The dynamics of the side chain of the radical anions of ubiquinones Q-1 (2,3-dimethoxy-5-methyl-6-[3-methyl-2-butenyl]-1,4-benzoquinone), Q-2, Q-6, and Q-10 have been investigated using electron nuclear double-resonance (ENDOR) spectroscopy. When radicals are produced in the liquid phase, secondary radicals are also formed. The EPR spectra of these additional radicals overlap with the radical of interest. ENDOR spectroscopy was found to be capable for studying the dynamical properties of such conditions. The temperature dependence of the isotropic hyperfine coupling constants of the β- and γ-protons of the side chain was measured. The activation energy of the rotation and other dyn…
Mitochondrial complex I: new insights from inhibitor assays
2000
The NADH:ubiquinone oxidoreductase (complex I) of the mitochondrial respiratory chain is by far the most complicated of the proton-translocating enzymes involved in the oxidative phosphorylation. Many clues regarding both electron transfer and proton translocation are still unknown. In this sense, inhibitor assays are relevant and useful pieces for elaborating a suitable model to explain the elusive bioenergetic mechanism of this enzyme. This short review presents the most recent advances in inhibitor studies and highlights the major controversies.
Kinetic characterization of mitochondrial complex I inhibitors using annonaceous acetogenins
1999
The NADH:ubiquinone oxidoreductase (complex I) of the mitochondrial respiratory chain is by far the largest and most complicated of the proton-translocating enzymes involved in the oxidative phosphorylation. Many clues regarding the electron pathways from matrix NADH to membrane ubiquinone and the links of this process with the translocation of protons are highly controversial. Different types of inhibitors become valuable tools to dissect the electron and proton pathways of this complex enzyme. Therefore, further knowledge of the mode of action of complex I inhibitors is needed to understand the underlying mechanism of energy conservation. This study presents for the first time a detailed …
Effects of vitamin A deficiency on mitochondrial function in rat liver and heart.
2000
The aim of this study was to investigate comparative effects of vitamin A deficiency on respiratory activity and structural integrity in liver and heart mitochondria. Male rats were fed a liquid control diet (control rats) or a liquid vitamin A-deficient diet (vitamin A-deficient rats) for 50 days. One group of vitamin-A deficient rats was refed a control diet for 15 days (vitamin A-recovered rats). To assess the respiratory function of mitochondria the contents of coenzyme Q (ubiquinone, CoQ), cytochrome c and the activities of the whole electron transport chain and of each of its respiratory complexes were evaluated. Chronic vitamin A deficiency promoted a significant increase in the endo…
A Deficiency in Respiratory Complex I in Heart Mitochondria from Vitamin A-Deficient Rats Is Counteracted by an Increase in Coenzyme Q
1997
Defects of NADH:coenzyme Q oxidoreductase (complex I) of mitochondria have been described in many congenital and acquired diseases. Administration of coenzyme Q (CoQ, ubiquinone) has been shown to benefit patients with some of these diseases. However, the mechanisms by which CoQ exerts the therapeutic effects are not clearly understood. A reason could be the lack of saturation of CoQ, in kinetic terms, for complex I activity. However, this hypothesis has not been proved in vivo because of the difficulty to incorporate CoQ into the mitochondrial membranes. We have found a deficiency in respiratory complex I in heart mitochondria from vitamin A-deficient rats which was accompanied by high CoQ…
Inhibition of xanthine oxidase to prevent statin-induced myalgia and rhabdomiolysis
2015
Although statins remain the cornerstone of lipid-lowering therapy for reducing the burden of atherosclerotic vascular disease, their administration has been associated with muscle-related adverse effects, including myalgia and rhabdomyolysis. Such adverse events are probably due to reduced antioxidant defenses associated with fewer intermediate metabolites in the cholesterol synthesis pathway. We hypothesize that the concomitant inhibition of xanthine oxidase via coadministration of allopurinol with statins could diminish reactive oxygen species (ROS)-related muscle damage, which would have in turn have positive effects on both the incidence of muscle-related adverse events and cardiovascul…