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Query: UNIPROT:Q16795 (ubiquinone)
 5,455 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of substances of different nature on the thermodynamic characteristics of dimyristoylphosphatidylcholine (DMPC) phase transition by the differential scanning microcalorimetry has been studied. The substances disposed in hydrophobic part of membrane--alpha-tocopherol, ubiquinone Q10, ionol and vitamin K3 cause the decrease of enthalpy and cooperativity of phase transition. The substances which have the side hydrocarbon chain (tocopherol and ubiquinone Q10) compared with ones without it (ionol and vitamin K3) and reduced quinones (Q10 and vitamin K3) compared with the oxidized ones have stronger influence on the enthalpy and cooperativity of transition. The inclusion of the local anesthetic dicaine disposed mainly in the zone of polar heads of phospholipids into DMPC membranes decreases the temperature of phase transition considerably and practically does not change the cooperativity. A possibility to use the method of differential scanning microcalorimetry to estimate the localization of membrane tropic substances within lipid bilayer is under discussion.
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PMID:[The action of membranotropic compounds with various structures on the parameters of the phase transition of dimyristoylphosphatidylcholine]. 276 95

In uncoupled pig-heart mitochondria the rate of the reduction of duroquinone by succinate in the presence of cyanide is inhibited by about 50% by antimycin. This inhibition approaches completion when myxothiazol is also added or British anti-Lewisite-treated (BAL-treated) mitochondria are used. If mitochondria are replaced by isolated succinate:cytochrome c oxidoreductase, the inhibition by antimycin alone is complete. The reduction of a plastoquinone homologue with an isoprenoid side chain (plastoquinone-2) is strongly inhibited by antimycin with either mitochondria or succinate:cytochrome c reductase. The reduction by succinate of plastoquinone analogues with an n-alkyl side chain in the presence of mitochondria is inhibited neither by antimycin nor by myxothiazol, but is sensitive to the combined use of these two inhibitors. On the other hand, the reduction of the ubiquinone homologues Q2, Q4, Q6 and Q10 and an analogue, 2,3-dimethoxyl-5-n-decyl-6-methyl-1,4-benzoquinone, is not sensitive to any inhibitor of QH2:cytochrome c reductase tested or their combined use, either in normal or BAL-treated mitochondria or in isolated succinate:cytochrome c reductase. It is concluded that quinones with a ubiquinone ring can be reduced directly by succinate:Q reductase, whereas those with a plastoquinone ring can not. Reduction of the latter compounds requires participation of either center i or center o (Mitchell, P. (1975) FEBS Lett. 56, 1-6) or both, of QH2:cytochrome c oxidoreductase. It is proposed that a saturated side chain promotes, while an isoprenoid side chain prevents reduction of these compounds at center o.
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PMID:The effect of ring substituents on the mechanism of interaction of exogenous quinones with the mitochondrial respiratory chain. 301 95

Deuteriated analogues of ubiquinone 10 (Q10) have been dispersed with plasma membranes of Escherichia coli and with the inner membranes of beetroot mitochondria. Orientational order at various deuteriated sites was measured by solid-state deuterium nuclear magnetic resonance (2H NMR). Similar measurements were made, using the compounds dispersed in dimyristoylphosphatidylcholine (DMPC) and egg yolk lecithin and dispersions prepared from the lipid extracts of beetroot mitochondria. In all cases only a single unresolved 2H NMR spectrum (typically 1000-Hz full width at half-height) was observed at concentrations down to 0.02 mol % Q10 per membrane lipid. This result shows that most Q10 is in a mobile environment which is physically separate from the orientational constraints of the bilayer lipid chains. In contrast, a short-chain analogue of Q10, in which the 10 isoprene groups have been replaced by a perdeuteriated tridecyl chain, showed 2H NMR spectra with quadrupolar splittings typical of an ordered lipid that is intercalated into the bilayer. The NADH oxidase activity and O2 uptake in Escherichia coli and in mitochondria were independent of which analogue was incorporated into the membrane. Thus, despite the major difference in their physical association with membranes, or their lipid extracts, the electron transport function of the long- and short-chain ubiquinones is similar, suggesting that the bulk of the long-chain ubiquinone does not have a direct function in electron transporting activity. The physiologically active Q10 may only be a small fraction of the total ubiquinone, a fraction that is below the level of detection of the present NMR equipment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Location and activity of ubiquinone 10 and ubiquinone analogues in model and biological membranes. 332 5

Among various ubiquinone (Q) isoprenologues tested, only Q7 was more efficient than menadione in promoting the oxidation of 5-methyltetrahydrofolate (CH3FH4) by 5,10-methylenetetrahydrofolate reductase isolated from adult Brugia pahangi, whereas Q10 was the best cofactor in the same reaction catalysed by the analogous enzyme from adult Dirofilaria immitis. Menoctone (3-[1-cyclohexyloctyl] -2-hydroxy-1,4-naphthoquinone) was a strong competitive inhibitor of both these ubiquinone isoprenologues in the respective reactions. When incubated in the presence of D,L-[14C]-mevalonate, adult B. pahangi and D. immitis synthesized radiolabelled Q9 only, in addition to other isoprenoid derivatives in the neutral lipid fraction. In view of the inability of Q9 to promote the oxidation of CH3FH4 by 5,10-methylenetetrahydrofolate reductase from B. pahangi, it seems unlikely that this filaria uses Q9 as a cofactor in this reaction. Conceivably, D. immitis could use Q9 as a cofactor in its enzymatic oxidation of CH3FH4, since in this circumstance, it was a better cofactor than menadione.
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PMID:Synthesis of ubiquinone 9 by adult Brugia pahangi and Dirofilaria immitis: evidence against its involvement in the oxidation of 5-methyltetrahydrofolate. 724 67

Antioxidation activity (AOA) of ubiquinone (Q10), phylloquinone (vitamin K1), menadione as well as of the newly synthesized analogues of vitamin K1--N-derivatives of 2-methyl-3-aminomethyl 1.4-naphthoquinone, producing autocomplexes with intramolecular transfer of electrons, was studied in the model system of the methyl oleate initiated oxidation. The menadione AOA was shown to be 2-fold higher as compared with the inhibitory activity of natural quinones. Activity of AK-40 and AK-49, artificial analogues of vitamin K1, was higher 2.6-fold than that of ubiquinone and phylloquinone and 1.4-fold higher than menadione activity. At the same time, AOA of ubiquinone and phylloquinone was 1.5-fold lower than the tocopherol activity, while naphthoquinones AK-40 and AK-49 were 2-fold more active as compared with tocopherol but their activity was 2-fold lower than ionol. Mechanism of natural and synthetic quinones action as well as properties of their long chain analogues are discussed.
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PMID:[Antioxidant activity of natural and synthetic quinones]. 777 Oct 81

Biotin (0.3 mg/kg per os) and ubiquinone Q10 (50 mg/kg, per os) during chronic administration were found to produce stimulating effects on premature animals. The two drugs contributed to a more rapid development of memory and learning processes in premature new-born rats than in mature ones, normalized the major parameters of carbohydrate and lipid metabolism. Some specific features and differences were ascertained in the stimulating effects of biotin and ubiquinone Q10.
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PMID:[The effect of ubiquinone Q10 and biotin on the growth and development of premature animals]. 831 16

We have used the potent squalene synthase inhibitor squalestatin I to investigate the regulation of isoprenoid metabolism in rat liver Fresh-frozen liver pieces from normal rats and rats infused with squalestatin I at 16 micrograms h-1 for 16 h were assayed for farnesyl pyrophosphate (FPP) and geranylgeranyl pyrophosphate (GGPP) by HPLC after dephosphorylation. Levels of FPP and GGPP were 5.4 +/- 1.6 nmol g-1 and 1.6 +/- 0.7 nmol g-1 (n = 13) wet wt., respectively, in control livers and 110 + 41 nmol g-1 and 3.0 +/- 2.2 nmol g-1 (n = 13) in livers from squalestatin I infused rats. In order to determine the relative level of isopentenyl pyrophosphate, liver slices from normal and squalestatin I infused rats were labeled to steady-state with [3H]acetate. Analysis of isoprenoid pyrophosphate intermediates by radio-HPLC after dephosphorylation indicated that squalestatin I brought about a 20-fold increase in the relative level of FPP (confirming direct analysis) and a 5-fold increase in the relative level of IPP. No change in either of these compounds was observed in livers from cholesterol-fed rats. To determine if squalestatin I altered the synthesis of nonsterol products, rats were subjected to long term subcutaneous infusion. After 14 days of infusion of 15 micrograms h-1, the median chain length of hepatic dolichol and dolichyl phosphate increased from C95 to C115 and the levels of these lipids increased approximately 3-fold. In addition, dolichyl phosphate mannose synthase activity in microsomes from squalestatin I treated rats was increased relative to controls when assayed in the absence of dolichyl phosphate. Squalestatin I affected ubiquinone metabolism to a lesser extent: chain lengths shifted from a Q10/Q9 ratio of 0.118 +/- 0.021 in the normal rat to 0.185 +/- 0.016 in the squalestatin I treated animals, and levels rose by approximately 90%. These results suggest that the isoprenoid pyrophosphate intermediates are shared by the cholesterol, dolichol and ubiquinone pathways and further show that the dolichol and ubiquinone pathways are not saturated. Apparently, under normal conditions, the levels of these intermediates are maintained relatively constant by coordinate enzyme regulation, thereby ensuring a constant rate of synthesis of nonsterols.
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PMID:Squalene synthase inhibition alters metabolism of nonsterols in rat liver. 890 50

This study investigated the effects of oral supplementation with ubiquinone-10 (Q10) (n = 9) compared with a placebo (n = 9) on aerobic and anaerobic physical performance over 22 days of supplementation. The supplementation period included 5 days of high intensity anaerobic training between days 11 and 14. The results demonstrated, that on an anaerobic (10 x 10 s) cycling test, the placebo group showed a significantly greater improvement than the Q10-group after a supplementation and training period (P < 0.001). Further, the Q10 group had a significantly lower increase in total work performed during the seven training sessions (15 x 10 s) compared with the placebo group (P < 0.001). There was a significant increase in maximal blood lactate accumulation during cycling in the both groups, when compared with levels before the training and recovery period. There was no significant difference between the groups, either in VO2max determined during running, or in submaximal and peak VO2, Rate of Perceived Exertion, respiratory quotient, blood lactate concentration or heart rate determined during submaximal and maximal cycling. Although insignificant (P = 0.1-0.3), there was evidence of higher submaximal VO2 (55-80% of VO2peak) during cycling in the Q10-group compared with the placebo group after training and recovery. It is concluded that with high intensity anaerobic training, there was a significantly greater increase in anaerobic performance in the placebo group compared with the Q10 group. The results suggest less increase in physical performance with Q10 supplement and high intensity anaerobic training, compared with placebo.
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PMID:Effects of ubiquinone-10 supplementation and high intensity training on physical performance in humans. 940 91

Study of the incorporation of 13C-labelled glucose or pyruvate into the isoprenoids of tobacco BY-2 cells allowed the biosynthetic origin of isopentenyl diphosphate to be determined. Sterols synthesized in the cytoplasm and the prenyl chain of ubiquinone Q10 located in mitochondria were derived from the same isopentenyl diphosphate pool, synthesized from acetyl-CoA through mevalonate, whereas the prenyl chain of plastoquinone was obtained from the mevalonate-independent glyceraldehyde 3-phosphate/pyruvate route, like all chloroplast isoprenoids from higher plants. These results are in accord with the compartmentation and complete enzymic independence of the biosynthesis of long-chain all-trans polyprenols in mitochondria and chloroplasts.
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PMID:Mevalonate-derived isopentenyl diphosphate is the biosynthetic precursor of ubiquinone prenyl side chain in tobacco BY-2 cells. 953 5

The effect of lifelong oral supplementation with ubiquinone Q10 (10 mg/kg/day) was examined in Sprague-Dawley rats and C57/B17 mice. There were no significant differences in survival or life-span found in either rats or mice. Histopathologic examination of different rat tissues showed no differences between the groups. In Q10 supplemented rats, plasma and liver Q10 levels were 2.6 to 8.4 times higher at all age points than in control rats. Interestingly, in supplemented rats the Q9 levels also were significantly higher (p<0.05) in plasma and liver at ages 18 and 24 months. Neither Q9 nor Q10 levels were affected by supplementation in kidney, heart, or brain tissues. In spite of the significant changes in plasma and liver ubiquinone concentrations, lifelong Q10 supplementation did not prolong or shorten the lifespan of either rats or mice.
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PMID:The effects of lifelong ubiquinone Q10 supplementation on the Q9 and Q10 tissue concentrations and life span of male rats and mice. 958 86


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