Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.3.5.1 (succinate dehydrogenase)
 8,177 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Rabbits were injected with adriamycin 3 days/week/7 weeks. Heart tissues of treated rabbits showed myocardial degeneration, but the tissues of controls were normal. The deficiency in the activity of the succinate dehydrogenase-coenzyme Q10 reductase in the heart tissues of the rabbits treated with adriamycin was higher (0.001 less than P less than 0.01) than that for control tissues. These data indicate a correlation of at least a part of the cardiotoxicity of adriamycin in cancer patients to inhibition of CoQ10-enzymes, since coenzyme Q10 is indispensable to bioenergetics in the myocardium of both humans and rabbit.
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PMID:Effect of adriamycin on the activity of the succinate dehydrogenase-coenzyme Q10 reductase of the rabbit myocardium. 100 20

The activity of the succinate dehydrogenase-coenzyme Q10 reductase from 120 diabetic patients was significantly lower (P less than 0.001) and the per cent deficiency was significantly higher (P less than 0.001) than that of the controls. The diabetes of 37 patients was controlled by diet; the enzyme activity was lower (P less than 0.001) and the deficiency was higher (P less than 0.02) than for controls. In decreasing effectiveness, Dymelor, Glyburide, Phenformin and Tolazamide inhibited the COQ10-enzyme, NADH-oxidase. Tolbutamide, Glypizide, and Chlorpropamide were noninhibitory to succinoxidase and NADH-oxidase. Patients receiving Tolazamide and Phenformin showed a higher incidence (P less than 0.001 to P less than 0.05) of COQ10-deficiency than patients controlled by diet or normal controls. Certain diabetic patients controlled by diet may have a deficiency of COQ10 which may be enhanced by the inhibition by certain commonly used antidiabetic drugs of COQ10-enzymes. A deficiency of COQ10 in the pancreas could impair bioenergetics, the generation of ATP, and the biosynthesis of insulin.
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PMID:Bioenergetics in clinical medicine. XI. Studies on coenzyme Q and diabetes mellitus. 107 May 15

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

When incubated in an air atmosphere, solubilized succinate dehydrogenase (succinate:(acceptor) oxidoreductase, EC 1.3.99.1) quickly loses the capability to recombine with membrane components to catalyze mitochondrial related electron transport activities. At 0 degrees the loss in reconstitution capability is a first-order process; the half-life of the enzyme is 1.6 hr at this temperature. The enzyme is stabilized by recombining it with submitochondrial particles or with a cytochrome b preparation-phospholipid mixture. The presence of the cytochrome b preparation in the succinate dehydrogenase-cytochrome b-phospholipid complex is obligatory, indicating that protein-protein interactions between succinate dehydrogenase and other membrane components are important in stabilizing the capability of the flavoprotein to transfer electrons to other respiratory components. Treatment of this complex with phospholipase C results in loss of most of the succinate-dichlorophenolindophenol reductase activity and almost complete hydrolysis of phospholipid. Succinate dehydrogenase maintains its capability to participate in mitochondrial electron transport for several hours if the phospholipase treated complex is reconstituted with lysolecithin at the time of assay. Phospholipids are therefore not required for the stabilization process, but rather for formation of an active reductase complex. A lipophilic environment, if required for stabilization, can be provided by diglycerides. Diglycerides also can provide an environment conducive to electron transfer from succinate to ubiquinone but do so less efficiently than intact phospholipids.
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PMID:The role of protein and lipids in stabilizing the activity of bovine heart succinate dehydrogenase. 112 75

It was observed that either propranolol or iproveratril could increase the succinate oxidation activity by rat heart mitochondria to 444% and to 371% respectively. Both drugs decreased the respiratory control coefficient and ADP/O ratio. No effect on mitochondrial succinic dehydrogenase, succinic dehydrogenase-Co Q-reductase and malic dehydrogenase was observed. It was pointed out that these drugs would act preventing the reoxidation of NADH+ + H+ through the respiratory chain.
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PMID:Regulation of succinic dehydrogenase activity of heart mitochondria by anti-arrhythmic drugs. 115 65

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

The pharmacology and toxicity in animals of synthetic analogs of essential metabolites, which show in vitro antagonism of the metabolite, may point out pathology associated with a deficiency of the metabolite. On this basis, 2-hydroxy-3-n-dodecylmercapto-1,4-naphthoquinone, a potent in vitro inhibitor of a mitochondrial coenzyme Q10-enzyme, was administered to rats. The specific activities and the percent deficiencies of the succinate dehydrogenase-coenzyme Q10 reductase in cardiac mitochondria were significantly increased (0.001 less than P less than 0.01). These enzyme activities were unchanged in leucocytes and in the dorsal aorta. This biochemical cardiotoxicity of an antimetabolite of coenzyme Q10 adds to the advancing knowledge on coenzyme Q10 in cardiac metabolism and disease, and could correlate with the cardiotoxicity of the clinical antitumor drug, adriamycin.
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PMID:Models for clinical disease. I. Biochemical cardiotoxicity of a coenzyme Q10-inhibitor in rats. 125 16

The experiments carried out for the study aimed at determining the prenatal sensitivity to cadmium in the aspect of beth morphological and functional condition of placenta. The experiments were carried out on 80 pregnant female rats divided into three experimental groups and a control one. The experimental animals were daily administered, intragastrically, aqueous solution of cadmium chloride, from the 7th to the 19th day of pregnancy, in doses differing between the experimental groups: 2, 10 and 22 mg of CdCl2 per kilogram of body weight, respectively. The animals were decapitated on the 21st day of pregnancy. Placenta sections, besides hematoxylin and eosin staining, were examined for the activity of the following enzymes: succinic dehydrogenase (SDH) E.C.1.3.99.1., lactate dehydrogenase (LDH) E.C.1.1.1.27., NADH-tetrazole reductase (NADH-t.r.), without a catalog number, and their glycogen reaction was checked. The results of the experiments proved cadmium chloride to cause considerable damage to the enzymatic apparatus of placenta, leading to energy deficit in the cells of both the fetal and the maternal part of this organ. The multienzymatic changes observed preceded the morphologic ones by far.
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PMID:[Dynamics of morphological and cytochemical changes in the placenta following cadmium chloride intoxication]. 130 26

In mitochondria, electrons derived from the oxidation of succinate by the tricarboxylic acid cycle enzyme succinate-ubiquinone oxido-reductase are transferred directly to the quinone pool. Here we provide evidence that the soluble form of this enzyme (succinate dehydrogenase) behaves as a diode that essentially allows electron flow in one direction only. The gating effect is observed when electrons are exchanged rapidly and directly between fully active succinate dehydrogenase and a graphite electrode. Turnover is therefore measured under conditions of continuously variable electrochemical potential. The otherwise rapid and efficient reduction of fumarate (the reverse reaction) is severely retarded as the driving force (overpotential) is increased. Such behaviour can arise if a rate-limiting chemical step like substrate binding or product release depends on the oxidation state of a redox group on the enzyme. The observation provides, for a biological electron-transport system, a simple demonstration of directionality that is enforced by kinetics as opposed to that which is assumed from thermodynamics.
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PMID:Diode-like behaviour of a mitochondrial electron-transport enzyme. 154 73

The etiology of idiopathic dilated cardiomyopathy (DCM) is yet unknown; this study aimed at further differentiation of the disease by means of enzyme histochemistry. Endomyocardial biopsies from the left ventricle of 40 DCM patients and 5 control specimens had enzymes examined histochemically and semiquantitatively and analyzed according to staining intensities of nicotinamide adenine dinucleotide tetrazolium reductase (NADH-TR), succinate dehydrogenase, cytochrome c oxidase, lactate dehydrogenase and acid phosphatase (aPh). In DCM, the NADH-TR activity was elevated as compared to controls, indicating impaired mitochondrial oxidative phosphorylation. However, a concrete relation of enzyme histochemical intensity to anamnestic, hemodynamic or histomorphometric data could not be determined, except for the fact that the intensity of the lysosomal enzyme aPh was elevated in DCM patients with a relatively high left ventricular ejection fraction. The results demonstrate an interindependence of structural, hemodynamic and historical parameters as well as enzyme concentrations in DCM. Thus, a pathological change in the enzyme concentrations tested here cannot be responsible for the functional myocardial impairment in DCM.
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PMID:Enzyme histochemistry of endomyocardial biopsies in idiopathic dilated cardiomyopathy. 165 Nov 62


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