Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:1.3.5.1 (succinate dehydrogenase)
8,177 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We investigated the role of thyroid hormone in the postnatal development of Ca2+ transport activity of sarcoplasmic reticulum in skeletal muscle (m. gastrocnemius-plantaris). With a Ca2+-stat method using the fluorescent dye fura 2 as Ca2+ indicator, we determined the oxalate-supported maximal Ca2+ uptake activity of sarcoplasmic reticulum in whole muscle homogenates from neonatal rats. Expressed per g tissue wet wt, the activity increased nearly 10-fold during the first 8 weeks after birth, following which time a plateau was reached. This development was absent in hypothyroid pups, in which the level of Ca2+ uptake activity remained constant at 10% of the normal adult value for at least 8 weeks. When the mothers were given 0.05% propylthiouracil in the drinking water 1 week before parturition, these pups ceased to grow after 4 weeks, had a reduced muscle protein content and a characteristic cretinous appearance. The effects of hypothyroidism could be reversed by T3 treatment (0.5 micrograms/100 g BW, daily) starting 1 or 6 weeks after birth. Treatment with bovine GH (0.1 or 0.5 IU/100 g BW; daily) starting on day 5 stimulated body growth, particularly of muscle, but was without effect on the failing development of Ca2+ uptake activity. The postnatal rise in citrate synthase and succinate dehydrogenase activities was impaired in the hypothyroid group, but lactate dehydrogenase and creatine kinase activities rose continuously, although at a reduced rate. T3 treatment also reversed these effects of propylthiouracil. At the higher dosage used bovine GH appeared to stimulate the accumulation of creatine kinase. We conclude that the failing postnatal development of sarcoplasmic reticulum Ca2+ transport activity in hypothyroidism is not secondary to the absence of GH, nor is it part of a general, indiscriminate effect, but, rather, that it indicates an absolute requirement of thyroid hormone for this particular aspect of muscle differentiation.
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PMID:The postnatal development of sarcoplasmic reticulum Ca2+ transport activity in skeletal muscle of the rat is critically dependent on thyroid hormone. 291 9

Muscle homogenates representing slow-twitch oxidative, fast-twitch oxidative-glycolytic, fast-twitch glycolytic, and mixed fiber types were prepared from normal, diabetic, and insulin-treated diabetic rats. Diabetes was induced by injection of 80 mg . kg-1 of streptozotocin. The activities of citrate synthase, succinate dehydrogenase, and 3-hydroxyacyl-CoA dehydrogenase were employed as markers of oxidative potential, whereas phosphorylase, hexokinase, and phosphofructokinase activities were used as an indication of glycolytic capacity. Diabetes was associated with a general decrement in the activity of oxidative marker enzymes for all fiber types except the fast-twitch glycolytic fiber. In contrast, the fast-twitch glycolytic fibers demonstrated the greatest decline in glycolytic enzymatic activity. Insulin-treated animals, either trained or untrained, exhibited enzyme activities similar to their normal counterparts. Exercise training of diabetic rats mimicked the effect of insulin treatment and caused a near normalization of the activity of the marker enzymes. These findings suggest that the enzymatic potential of all skeletal muscle fiber types of diabetic rats may be normalized by exercise training even in the absence of significant amounts of insulin.
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PMID:Influence of training on skeletal muscle enzymatic adaptations in normal and diabetic rats. 293 94

The evaluation of the specific activity of some enzymes related to energy transduction was performed in 7 fresh samples of malignant gliomas and in 4 samples of normal brain tissue. Compared with normal brain tissue, the hexokinase, phosphofructokinase and citrate synthase activities are lower; the lactate dehydrogenase and succinate dehydrogenase are unchanged, while glucose-6-phosphate dehydrogenase and NADP+-isocitrate dehydrogenase activities are higher in gliomas.
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PMID:Enzymes related to energy metabolism in human gliomas. 294 16

The main purpose of the present study was to test the hypothesis that adrenergic stimulation of muscle fibres during exercise is a major stimulus for the training-induced enhancement of skeletal muscle respiratory capacity. Therefore, Sprague-Dawley rats either underwent bilateral surgical ablation of the adrenal medulla or were sham-operated. Furthermore, unilateral surgical extirpation of the lumbar sympathetic chain was performed. Half of the rats were then trained for 12 weeks by swimming (up to 5.5 h X day-1, 4 days X week-1) and the remaining rats were sedentary controls. In the gastrocnemius muscle, training significantly increased the mitochondrial enzymes citrate synthase, succinate dehydrogenase, cytochrome c oxidase, and 3-hydroxyacyl-CoA dehydrogenase. In sham-operated rats, the increases were 40%, 43%, 66%, and 25%, respectively, in legs with intact sympathetic innervation. The training-induced enzyme adaptation after adrenodemedullation and/or sympathectomy was not significantly lower than these control values. In sham-operated rats, training decreased resting plasma insulin and glucagon levels and increased liver glycogen content. Similar changes were induced by adrenodemedullation, but training did not augment these changes in adrenodemedullated rats. In conclusion, the data suggest that neither adrenomedullary hormones nor local sympathetic nerves are prerequisites for the training-induced increase in muscle mitochondrial enzymes. The training-induced decline in resting plasma insulin and glucagon levels in intact rats may be mediated by adrenomedullary hormones.
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PMID:Skeletal muscle and hormonal adaptation to physical training in the rat: role of the sympatho-adrenal system. 298 95

The primary structure of the succinyl-CoA synthetase of Escherichia coli has been deduced from the nucleotide sequence of a 2451-base-pair segment of DNA containing the corresponding sucC (beta subunit) and sucD (alpha subunit) genes. The genes are located at one end of a gene cluster that encodes several citric acid cycle enzymes: gltA-sdhCDAB-sucABCD; gltA, citrate synthase; sdh, succinate dehydrogenase; sucA and sucB, the dehydrogenase (E1) and succinyltransferase (E2) components of the 2-oxoglutarate dehydrogenase complex. The sucC and sucD genes are separated from the sucA and sucB genes by a 273-base-pair segment containing four palindromic units, but they appear to be expressed from a sucABCD read-through transcript that extends from the suc promoter to a potential rho-independent terminator at the distal end of sucD. The stop codon of the sucC gene overlaps the sucD initiation codon by a single nucleotide, indicating close translational coupling of the sucC and sucD genes. The sucC gene comprises 1161 base pairs (388 codons, excluding the stop codon), and it encodes a polypeptide of Mr 41 390 corresponding to the beta subunit of succinyl-CoA synthetase. The sucD gene comprises 864 base pairs (288 codons, excluding the start and stop codons), and it encodes a product of Mr 29 644, corresponding to the alpha subunit of succinyl-CoA synthetase. The alpha subunit contains a 12-residue amino acid sequence that is identical with the histidine peptide previously isolated from the phosphoenzyme. This sequence forms part of one of the two potential nucleotide binding sites detected in the alpha subunit.
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PMID:Primary structure of the succinyl-CoA synthetase of Escherichia coli. 300 35

It has been reported that the mitochondrial cytochromes and citrate cycle enzymes occur in constant proportions to each other and increase or decrease roughly in parallel in response to various stimuli. The purpose of this study was to determine whether this proportionality is an obligatory consequence of the way in which mitochondria are assembled. Severe iron deficiency was used to bring about decreases of the iron-containing constituents of the mitochondrial respiratory chain in skeletal muscle. Cytochrome c concentration and cytochrome oxidase activity were decreased approximately 50%, while succinate dehydrogenase and NADH dehydrogenase activities were decreased by 78% in iron-deficient muscle. On electron microscopic examination, mitochondria in iron-deficient muscles had relatively sparse numbers of cristae. The iron deficiency had little or no effect on the levels of a range of mitochondrial matrix enzymes, including citrate synthase, isocitrate dehydrogenase, fumarase, aspartate aminotransferase, 3-hydroxyacyl-CoA dehydrogenase, 3-ketoacid-CoA transferase, and acetoacetyl-CoA thiolase. These results show that the usual constant proportions between the constituents of the mitochondrial respiratory chain and matrix enzymes are not obligatory; they provide evidence that mitochondrial matrix enzymes and respiratory chain constituents can be incorporated into mitochondria independently and that the ratios between them can vary within wide limits.
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PMID:Perturbation of mitochondrial composition in muscle by iron deficiency. Implications regarding regulation of mitochondrial assembly. 302 53

The contribution of the liver to the increased metabolic efficiency of the obese rat (fa/fa) was examined. Oxygen consumption of isolated hepatocytes and isolated mitochondria, and hepatic activities of mitochondrial enzymes were measured. Hepatocyte oxygen consumption was similar in the obese and nonobese rats for all substrates tested. Mitochondrial respiration also was similar in both phenotypes for all substrates tested. Activities of citrate synthase, succinate dehydrogenase, and cytochrome oxidase were similar for obese and nonobese rats. Taken together, these data show that in vitro hepatic oxygen consumption and oxidative capacity are similar in obese and nonobese rats. Rates of mitochondrial respiration with palmitoylcarnitine further show that the capacity for hepatic lipid oxidation is similar in obese and nonobese rats. Therefore, the increased metabolic efficiency of the obese rat probably cannot be attributed to an intrinsic decreased hepatic oxidative capacity. Further, there is no defect in hepatic lipid oxidative capacity in the young obese rat.
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PMID:Oxygen consumption and oxidative capacity of hepatocytes from young male obese and nonobese Zucker rats. 302 May 65

The sensory projections from the whiskers of mice and other rodents synapse somatotopically in 3 subnuclei in the brainstem trigeminal complex, in the ventrobasal complex of the thalamus and in the somatosensory cortex. Deafferentation of the whiskers in adult animals results in qualitative and quantitative changes in activities of the metabolic enzymes in the somatosensory cortex (e.g. J. Neuro-sci., 1 (1981) 929-935). We determined the time course and extent of changes in the subcortical trigeminal centers of adult mice after deafferentation. The right infraorbital nerve was sectioned in mice under surgical anesthesia; the animals survived for periods up to 26 weeks. The optic nerve was also cut to evaluate the effects of central tract section. Some brains were prepared histochemically for the mitochondrial enzymes cytochrome oxidase (CO) and succinic dehydrogenase (SDH), and some were prepared for microchemical analysis of the enzymes citrate synthase (CS), malate dehydrogenase (MDH) and phosphorylase. All deafferented and intact nuclei were examined in each animal quantitatively. The oxidative enzymes (CO, SDH, CS and MDH) that were analyzed by histochemical and microchemical approaches showed a decrease in activities as early as 3 weeks postdeafferentation, a trend that continued up to 12 weeks in all the subcortical trigeminal stations and lateral geniculate nucleus (LGN) when compared with the intact side. By 25 weeks postlesion, the levels were comparable to the intact side except that in the LGN, the levels remained depressed. The phosphorylase levels increased at around 3 weeks postoperation and remained elevated 25 weeks postlesion. Each case provided results on the effects of deafferentation at a given time point throughout the trigeminal pathway. Direct quantitative correlation of histochemical and microchemical approaches for glycolytic enzymes is consistent with a coordinate regulation of these molecules. The changes in enzyme levels in all nuclei occur simultaneously and to a similar degree. This strongly suggests that neuronal activity plays an important role in regulating metabolic machinery throughout this pathway in adults.
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PMID:Quantitative histochemical and microchemical changes in the adult mouse central nervous system after section of the infraorbital and optic nerves. 303 55

In the present study the effects of chronic administration of dextroamphetamine on energy metabolism in the brain of the rat were examined. The enzymes studied were: hexokinase (soluble and particulate forms), phosphofructokinase, pyruvate kinase, lactate dehydrogenase, citrate synthase, NAD+ and NADP+-dependent isocitrate dehydrogenases, succinate dehydrogenase and malate dehydrogenase. All the activities of the enzymes were assayed in four regions of the brain of the rat (cerebellum, medulla oblongata and pons, cererbral cortex and diencephalon). Rats were injected intaperitoneally once daily with dextroamphetamine for 20 consecutive days. The initial dose was 5 mg/kg/day and the dose was then increased by 1 mg/kg/every 5 days up to a total of 8 mg/kg/day on days 16-20. In the glycolytic enzymes a reduction of the activity of phosphofructokinase was found in the diencephalon and an increase of the activity of pyruvate kinase and lactate dehydrogenase in the diencephalon and medulla oblongata and pons, respectively. Citrate synthase was the only enzyme in the Krebs' cycle affected by chronic administration of dextroamphetamine. The results presented here show that chronic administration of dextroamphetamine produced important changes in some enzymes of glycolysis and the Krebs' cycle in the brain of the rat.
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PMID:Effects of chronic administration of dextroamphetamine on enzymes of energy metabolism in regions of the rat brain. 303 25

The activities of the mitochondrial enzymes citrate synthase (citrate oxaloacetatelyase, EC 4.1.3.7), NADP-linked isocitrate dehydrogenase (threo-Ds-isocitrate:NADP+ oxidoreductase (decarboxylating), EC 1.1.1.42), and succinate dehydrogenase (succinate: FAD oxidoreductase, EC 1.3.99.1) as well as their kinetic behavior in the two developmental forms of Trypanosoma cruzi at insect vector stage, epimastigotes and infective metacyclic trypomastigotes, were studied. The results presented in this work clearly demonstrate a higher mitochondrial metabolism in the metacyclic forms as is shown by the extraordinary enhanced activities of metacyclic citrate synthase, isocitrate dehydrogenase, and succinate dehydrogenase. In epimastigotes, the specific activities of citrate synthase at variable concentrations of oxalacetate and acetyl-CoA were 24.6 and 26.6 mU/mg of protein, respectively, and the Michaelis constants were 7.88 and 6.84 microM for both substrates. The metacyclic enzyme exhibited the following kinetic parameters: a specific activity of 228.4 mU/mg and Km of 3.18 microM for oxalacetate and 248.5 mU/mg and 2.75 microM, respectively, for acetyl-CoA. NADP-linked isocitrate dehydrogenase specific activities for epimastigotes and metacyclics were 110.2 and 210.3 mU/mg, whereas the apparent Km's were 47.9 and 12.5 microM, respectively. No activity for the NAD-dependent isozyme was found in any form of T. cruzi differentiation. The particulated succinate dehydrogenase showed specific activities of 8.2 and 39.1 mU/mg for epimastigotes and metacyclic trypomastigotes, respectively, although no significant changes in the Km (0.46 and 0.48 mM) were found. The cellular role and the molecular mechanism that probably take place during this significant shift in the mitochondrial metabolism during the T. cruzi differentiation have been discussed.
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PMID:Differential energetic metabolism during Trypanosoma cruzi differentiation. I. Citrate synthase, NADP-isocitrate dehydrogenase, and succinate dehydrogenase. 305 38


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