Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:Q8NEX9 (reductase)
 26,410 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Blood samples from 406 cardiac patients were analyzed by a differential assay of the specific activities (s.a.) of the succinate dhydrogenase-coenzyme Q-10 reductase to detect and quantitate existing deficiencies of coenzyme Q-10. 87/406, or ca. 20%, showed a mean lower basal S.A. and a mean higher per cent deficiency than a control group; both differences were significant (p is less than 0.001). The remaining 319 patients (80%) showed a negligible deficiency, but a mean low basal S.A., significant by p is less than 0.001. Cardiac patients may show low S.A.'s (sub-normal) of this CoQ-10-enzyme with or without a deficiency of CoQ-10. The desirable state for the patient is a normal level of the enzyme for bioenergetics and no deficiency of CoQ-10. Previously, a deficiency of CoQ-10 was found for cardiac biopsies from surgery; now, blood samples reveal the same deficiency. Frequent correlation between deficiencies in the blood and cardiac tissue is expected. This CoQ-10-enzyme in blood can aid patient selection for the clinical administration of CoQ-10 to cardiac patients.
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PMID:Bioenergetics in clinical medicine XIV. Studies on an apparent deficiency of coenzyme Q-10 in patients with cardiovascular and related diseases. 27 62

The previously observed alterations in the energy transducing system of rat liver mitochondria during 3'-methyl-4-(dimethylamino)azobenzene (3'-Me-DAB) carcinogenesis were investigated using aliphatic dicarbonyl compounds as molecular probes and the effect of temperature on the membrane-linked NADH-indophenol reductase. The vicinal diketone, diacetyl, uncouples oxidative phosphorylation in normal rat liver mitochondria while the higher diketones, acetylacetone and acetonylacetone, are increasingly less effective in that order; diacetyl totally abolishes respiratory control with substrates the oxidation of which involves the NADH leads to CoQ segment, but only partially with succinate which bypasses this segment. Diacetyl, likewise, uncouples oxidative phosphorylation in liver mitochondria from rats fed 3'-Me-DAB, but the mitochondria are most resistant to this uncoupling (in terms of the P/O ratio) at the time period when the respiratory control index (determined in the absence of diacetyl) is at the dye-induced minmum. This time period is at 3 to 4 weeks of dye administration, representing the cumulative dose for tumorigenesis threshold. At this threshold period of feeding 3'-Me-DAB, discontinuities in the Arrhenius plot of the mitochondrial membrane-localized NADH-indophenol reductase appear, with a return toward the control state (no break) at 8 weeks, only to reappear in the plot of the enzyme from tumor mitochondria, suggesting sequential membrane phase transitions in the mitochondria during azo dye carcinogenesis.
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PMID:Mitochondrial membrane-linked reactions in carcinogenesis: change in steroselective uncoupling of oxidative phosphorylation by aliphatic dicarbonyls and in the Arrhenius plot of NADH-indophenol reductase. 40 68

The effect of ubiquinones with different length of their chain (CoQ0, CoQ1, CoQ2, CoQ6, CoQ9) and their synthetic analogues (analogues of ubiquinone-1, hexahydroubiquinone-4, monophytylquinone, diphytylquinone, triphytylquinone) on the activity of ubiquinone dependent enzyme systems was studied in mitochondrial fractions from the yeast Candida guilliermondii. All of the ubiquinone homologues studied activated these systems. The synthetic analogues of ubiquinone nonspecifically inhibited the activity of NADH2-oxidase system. The inhibition was reversible when CoQ0 and CoQ1, but not CoQ6 and CoQ9, were added to the system. In the succinate-CoQ-reductase system, the inhibition caused by the analogues of ubiquinone was eliminated when all of the tested homologues were added to the system. In contrast to other analogues of ubiquinone, hexahydroubiquinone-4 was an inhibitor for the NADH2-oxidase system and an activator for the succinate-CoQ-reductase system, and eliminated the inhibiting action of other ubiquinone analogues in this system. Similar action of ubiquinone homologues was shown in the elimination of the inhibition of ubiquinone dependent systems caused by the specific inhibitors of electron transport, viz. rotenone and antimycin A.
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PMID:[Effect of ubiquinones and their analogs on the respiratory chain enzyme activity of Candida guilliermondii yeasts]. 53 Jan 41

In a detailed study focused on the methodological problems in dehydrogenase histochemistry [e.g., fixation, diffusion of enzymes and of reduced inermediates, conversion of NADPH and NADP to NADH and NAD, respectively, penetration of tetrazolium salt and formazan substantivity, 'nothing dehydrogenase' reaction, use of exogenous CoQ10 and of flavoprotein substitute (PMS)], the distribution and activity of succinate dehydrogenase, NAD(P)H-tetrazolium reductase, glucose-6-phosphate dehydrogenase, lactate dehydrogenase (H and M types), and of L-glutamate dehydrogenase (E.C.1.4.1.2 and E.C.1.4.1.3) have been investigated in the rat cerebellum. It was evident from the study that reliable results could only be obtained if all the aforementioned factors had been considered. The image of actual concentration of SDH in the neuropil of the molecular layer could only be recorded by adding CoQ10, while other structures exhibited greater balance between SDH and endogenous mitochondrial CoQ. Contrary to previous studies, a reversed localization of the activity of G-6-PDH and LDH was noticed. The elements of molecular and Purkinje layers were rich in G-6-PDH, while the granular layer was nearly depleted. The actual level of LDH could only be recorded if NADH-tetrazolium reductase was bypassed with PMS. The H and M types of LDH coexisted in the three cortical layers, the H type being prevalent and the M type attaining its highest level in synaptic glomeruli followed by the structures of the molecular layer and the Purkinje cells. High activity of GDH was noticed in Bergmann glia followed by synaptic glomeruli, while most other structures showed weak to moderate activity. The two GDH types coexisted in all structures showing activity, except for Bergmann cells, which only showed presence of the E.C. 1.4.1.3 type. Furthermore, Bergmann glia was exceptional by showing no activity of SDH and LDH, but strong activity of G-6-PDH and NADPH-tetrazolium reductase. The granular cells were exceptional by showing weak or no activity of all enzymes in question.
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PMID:Methodological aspects of the histochemical localization and activity of some cerebellar dehydrogenases. 66 87

The activity of ubiquinone-dependent enzyme systems was studied in mitochondrial fractions of the yeast Candida guilliermondii cultivated on the medium containing carbohydrates of hydrocarbons as a source of carbon. The activity of NADH2-oxidase and succinate-CoQ-reductase was higher in systems with mitochondrial fractions from the cells grown on the medium with n-paraffins than in mitochondrial fractions from the cells cultivated on the medium with glucose. About 30% of intracellular ubiquinone is located in the mitochondrial fraction of hydrocarbon oxidizing yeast cells; however, the activity of enzymes was stimulated upon introduction of exogeneous ubiquinones into the systems. Therefore, exogeneous ubiquinones may be involved in the electron transport chain during oxidation of reduced substrates. Both ubiquinone-dependent enzyme systems are resistant to storage.
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PMID:[Localization of ubiquinone-9 in electron transport chain of Candida guilliermondii]. 100 42

Eight patients under routine care for periodontitis received oral treatment with a form of coenzyme Q (7 / CoQ10 and 1 / hexahydrocoenzyme Q4). An unchanged plaque score showed the patients cooperated and were under plaque control. The periodontal score decreased (p less than 0.01) on CoQ treatment. Unexpectedly, the periodontal pocket depth decreased (P less than 0.05) on CoQ treatment since all patients were considered candidates for surgical intervention. Healing was so excellent 5-7 days post-biopsy that the biopsy sites were difficult to locate. The healing was viewed as extraordinarily effective. The mean value of the specific activities of the succinate dehydrogenase-coenzyme Q10 reductase of gingival biopsies increased (P less than 0.05) during treatment which could correlate with the extraordinarily healing. Treatment of periodontitis with coenzyme Q should be considered as adjunctive treatment with current dental practice.
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PMID:Bioenergetics in clinical medicine. II. Adjunctive treatment with coenzyme Q in periodontal therapy. 110 47

The specific activities (S.A.) of the succinate dehydrogenase-coenzyme Q10 (CoQ10) reductase of a control group of 65 Japanese adults and 59 patients having essential hypertension were determined. The mean S.A. of the hypertensive group was significantly lower (p less than 0.001) and the mean % deficiency of enzyme activity was significantly higher (p less than 0.001) than the values for the control group. These data on Japanese in Osaka agree with data on Americans in Dallas. Some patients showed no CoQ10-deficiency, and others showed definite deficiencies. Emphasizing the CoQ10-enzyme for patient selection, CoQ10 was administered to hypertensive patients. Four individuals showed significant but partial reductions of blood pressure. Monitoring the CoQ10-enzyme before, during, and after administration of CoQ10 indicated responses. The maintenance of high blood pressure could be primarily due to contraction of the arterial wall. Contraction or relaxation of an arterial wall is dependent upon bioenergetics, which also provide the energy for biosynthesis of angiotensin II, renin, aldosterone, and the energy for sodium and potassium transport. A clinical benefit from administration of CoQ10 to patients with essential hypertension could be based upon correcting a deficiency in bioenergetics, and point to possible combination treatments with a form of CoQ and anti-hypertensive drugs.
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PMID:Bioenergetics in clinical medicine. Studies on coenzyme Q10 and essential hypertension. 115 73

A thirty-two year old female had chronic progressive external ophthalmoplegia (CPEO), exertional fatigue, dysarthria, dysphagia, and bilateral hearing impairment. Histochemical stains, obtained from the right vastus lateralis, showed ragged-red fibers and wide-spread abnormalities in the number, size, and the structure of mitochondria under electronomicroscopic examination. A biochemical analysis showed a low activity of NADH-cytochrome C reductase, NADH dehydrogenase and a normal activity of succinate cytochrome C reductase and cytochrome C oxidase. This data suggests a specific defect in the NADH dehydrogenase of complex I (NADH CoQ reductase). We believe that this is the first biochemically defined mitochondrial myopathy reported in Taiwan and provides additional evidence for the existence of biochemical heterogeneity in mitochondrial disorders of CPEO.
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PMID:Chronic progressive external ophthalmoplegia with NADH-CoQ reductase deficiency: report of a case. 132 93

Ubiquinone (UQ) reductase activity which reduces UQ to ubiquinol (UQH2) in rat tissues was roughly proportional to the UQH2/total UQ ratio in respective tissues. The highest activity was found in the liver, showing the highest UQH2/total UQ ratio. A greater part of liver UQ reductase activity was located in the cytosol. Within a week, the liver UQ reductase activity decreased by 80% even at -20 degrees C. The DT-diaphorase activity was stable. UQ reductase required NADPH as the hydrogen donor and was not inhibited by a less than 1 microM concentration of dicoumarol. There was no stimulation of UQ reductase in the presence of bovine serum albumin nor in Triton X-100. Yet, both stimulated DT-diaphorase. As a result, UQ reductase appeared to be a novel NADPH-UQ oxidoreductase and responsible for the UQ redox state in liver.
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PMID:A novel ubiquinone reductase activity in rat cytosol. 146 65

There is increasing evidence that defective function of the mitochondrial enzyme NADH CoQ reductase (complex I) is involved not only in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) toxicity, but also in idiopathic Parkinson's disease (PD). Complex I deficiency has been identified in PD substantia nigra and appears to be disease-specific and selective for the substantia nigra within the central nervous system. We describe a method for preparation of an enriched mitochondrial fraction from 60 mL blood. Using this technique, we analyzed respiratory chain function in 25 patients with PD and 15 matched control subjects. We confirm a previous report of a specific complex I deficiency in PD platelet mitochondria. Although there was a statistically significant decrease in complex I activity in the PD group compared with the control group (p = 0.005), the defect was mild (16%); it was not possible to distinguish PD from control values on an individual basis. This deficiency is not detectable in platelet whole-cell homogenates, presumably reflecting the relative insensitivity of this preparation and the limited decrease in complex I activity in PD. The presence of a mild complex I defect in platelets together with a more severe defect in substantia nigra suggests either that the pharmacological characteristics shared by these two tissues render them susceptible to a particular toxin or toxins, or that the defect is widely distributed and other biochemical events enhance the deficiency in substantia nigra.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Platelet mitochondrial function in Parkinson's disease. The Royal Kings and Queens Parkinson Disease Research Group. 147 69


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