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)

Repeated injections of rat with 1-thyroxine (50 microgram/kg daily for 5 five-day weeks) retarded the weight gain of the animals and increased the absolute and relative size of the heart, adrenals and interscapular brown adipose tissue. In the myocardium and thigh muscle, thyroxine treatment resulted in elevated activity of oxidative enzymes, succinate dehydrogenase, malate dehydrogenase and citrate synthase, while the activities of glycolytic enzymes remained unchanged. Glycogen content of the heart was decreased following thyroxine regime. In the brown fat, on the other hand, thyroxine injections resulted in a reduction of the activity of oxidative enzymes. This reduction can be accounted for by the decreased protein (enzyme) content of the tissue due to deposition of fat. Furthermore, thyroxine treatment delayed the body cooling of the rats swimming in water at 25 degrees C and enhanced hyperthermic response to injected noradrenaline. All these changes, which were not observable in rats treated with daily alprenolol (20 mg/kg) injections, were as pronounced in rats injected with alprenolol together with thyroxine as in rats injected with thyroxine only. It is concluded that beta blockers do not antagonize the metabolic changes due to hyperthyroidism.
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PMID:Alprenolol fails to antagonize the metabolic changes following repeated thyroxine injections in the rat. 2 61

Noradrenaline-storing granules, a mitochondrial fraction and a microsomal fraction of bovine splenic nerve trunks were prepared by differential centrifugation. These particulate fractions were characterized by their noradrenaline content, succinate dehydrogenase and glucose-6-phosphatase activity. In the presence of ATP-Mg2+ all three fractions accumulated 45Ca2+ during incubation with 0.1 mM 45 CaCl2, buffered with potassium phosphate or glycylglycine (pH 7.5; 28 degrees C). The accumulated 45 Ca2+ was not removable by EGTA, and the uptake was absent at 0 degrees C or after destruction of the particles by sonication. The behaviour of the 45 Ca2+ -uptake into all three fractions against varying ATP-concentrations, metabolic inhibitors (pentachlorophenol, desaspidine, 2,4-dinitrophenol, N-ethylmaleimide, p-chloromercuribenzoate, sodium azide, amobarbital) and drugs (phenoxybenzamine, verapamil, prenylamine, reserpine, bretylium, phentolamine) was studied. Under nearly all conditions there were differences between the 45 Ca2+ -uptake into mitochondria and that into microsomes, which suggests two distinct uptake processes. The 45 Ca2+ -uptake into the granule fraction behaved intermediate between the two other fractions under many conditions, but not under all. Therefore, it is not possible to explain the 45 Ca2+ -uptake into the granule fraction as being due to contamination with mitochondria and microsomes; an inherent ATP-Mg2+ -dependent 45Ca2+ -uptake into the nerve granules must be postulated, which is not directly coupled with the noradrenaline transport into these particles. A particulate fraction (14000-100000 g), containing noradrenaline granules, was prepared from the vas deferens of the rat. Incubation with 5 X 10(-6) M (-)-noradrenaline and 0.1 mM 45Ca2+ showed that the particles of this fraction take up noradrenaline and 45Ca2+. The uptake of both was dependent on ATP-Mg2+. The ATP-Mg2+ -dependent uptake of both noradrenaline and 45Ca2+ was substantially reduced in the corresponding tissue fraction prepared from denervated vasa deferentia.
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PMID:Ca2+ -uptake into noradrenaline-storing granules of bovine splenic nerves. 18 27

Rats were treated by daily alprenolol (10, 20 and 50 mg/kg) injections for 5 days a week for 4 weeks. At 20--21 degrees C alprenolol treatment retarded the weight gain of the animals and increased the weight of the adrenals. These changes were not seen at 29 degrees C. The reduction in size and fat content of the interscapular brovin adipose tissue in drug-treated rats was independent of experimental temperature. At 20--21 degrees C prolonged beta-blockade did not cause any changes in the enzymes of the energy metabolism. At 29 degrees C, however, alprenolol treatment antagonized the decrease in activity of oxidative enzymes (succinate dehydrogenase, malate dehydrogenase, citrate synthase) and the decrease in protein concentration of the cardiac muscle. In skeletal muscle alprenolol treatment significantly decreased the activities of oxidative enzymes and antagonized the rise in the activity of lactate dehydrogenase resulting from warm acclimation. The increased activities of oxidative enzymes in interscapular brown adipose tissue of aprenolol treated rats were coupled with an increase in protein concentration of the tissue. Although these changes were more marked at 29 degree C they were observable at 20--21 degree C, too. The difference in the drug effects at 20--21 degrees C and 29 degrees C can be accounted for by the compensatory catecholamine release at the lower temperature, due to impaired thermoregulatory capacity after alprenolol. Prolonged beta blockade decreased the exercise tolerance and cold tolerance of the rats. An increased response of the diastolic blood pressure to an alpha-adrenergic drug, noradrenaline, and a decreased response to a beta-adrenergic drug, isoprenaline, in alprenolol-treated rats indicates a shift from beta- to alpha-receptors.
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PMID:Effect of prolonged beta-blockade on energy metabolism and adrenergic responses in the rat. 59 3

1. Adult male rats were treated with propranolol (2.0 mg kg-1 day-1 i.p.), pindolol (0.2 mg kg-1 day-1 i.p.) or 0.9% NaCl day-1 i.p. and exposed to +4 degrees C for 42 days, or treated with 0.9% NaCl day-1 i.p. and kept at +23 degrees C for 42 days. They were weighed once a week, when a 24 h urine sample was also collected and colon temperature measured. 2. Urinary noradrenaline (NA), adrenaline (Ad) and dopamine were analysed by high-performance liquid chromatography with an electrochemical detector. After the acclimatization period the interscapular brown adipose tissue was excised and weighed and the activity of the oxidative enzymes succinate dehydrogenase and cytochrome oxidase measured. 3. The pindolol-treated and propranolol-treated rats gained weight during the cold-acclimatization period. The amount of interscapular brown adipose tissue increased in the cold, but the increase was lowest in the pindolol-treated group. No changes were seen in the other brown adipose tissue parameters in cold-exposed animals. The excretion of catecholamines followed the same pattern in all three cold-exposed groups, with an initial rise in noradrenaline and adrenaline excretion and a slight rise in dopamine excretion. 4. The results suggest possible connections between beta-adrenoceptor antagonists, weight gain and cold acclimatization. Pindolol had a slight inhibitory effect on cold-induced brown adipose tissue hypertrophy in rats.
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PMID:Influence of two beta-adrenoceptor antagonists, propranolol and pindolol, on cold adaptation in the rat. 197 90

Heart transplantation involves chronic effects due to denervation, rejection, and treatment of rejection. The chronically denervated dog heart provides a model for the effects of denervation alone. These hearts have been shown to contain intrinsic neurons with VIP and NPY as possible neurotransmitters. Myocardial tissue noradrenaline concentration falls to very low levels after degeneration of postganglionic sympathetic neurons, but dopamine remains in near-normal concentration and is probably synthesized extraneuronally. ANP is present and released normally; however, the natriuretic response to atrial distension is blunted, suggesting that this response is mainly due to a reflex mechanism. Chronically denervated myocardial tissue exhibits increased oxygen consumption in vitro and increased Na-K, ATPase activity but has normal tissue levels of ATP and creatine phosphate. Glucose oxidation is inhibited in vivo, associated with increased levels of fructose-6-phosphate but normal glucose-6-phosphate, suggesting inhibition of phosphofructokinase activity. However, the enzyme protein concentration of phosphofructokinase, as judged by maximal in vitro activity, is normal. Maximal in vitro activities of succinate dehydrogenase, cytochrome oxidase, monoamine oxidase, calcium-dependent ATPase, and glyceraldehyde-3-dehydrogenase are also normal. From these findings, we would predict that patients with transplanted hearts are likely to show myocardial metabolic inefficiency.
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PMID:Cellular abnormalities in chronically denervated myocardium. Implications for the transplanted heart. 253 6

An experimental model of myocardiopathy was induced in rhesus monkeys following noradrenaline (NA) infusion (20 ug/kg body wt/minute), for a period of 2 hours daily for three consecutive days. The animals were sacrificed after two hours (acute phase), forty-eight hours (sub-acute phase) and twenty-one days (chronic phase). Focal depletion of succinic dehydrogenase, increase in adenosine triphosphatase, acid phosphatase and appearance of large fat droplets in myocardial muscle was noted in the acute phase. Histopathological examination revealed focal edema, opacity and fuchsinorrhagia of the muscle fibres distributed in both the ventricles. Myofibrillar degeneration, myocytolysis and vacuolization with aggregation of lymphomononuclear cells were the significant features in the acute phase. During sub-acute and chronic phases, these features became less prominent and reparative changes with proliferation of fibroblasts became more marked. By the twenty-first day, irregular, focal scars replaced the necrosed myocardium. Ultrastructurally, heart muscle showed myofibrillar disorganisation, distortion of Z and A bands, dilatation of sarcoplasmic reticulum and swelling and rupture of mitochondria. Altered membrane permeability was evidenced by the presence of reaction products of horseradish peroxidase within the cardiac cells. In the reparative phase, however, myocytolytic changes regressed and collagen deposition was the prominent feature. This experimental study has several histological features simulating human cases of myocardial infarction without coronary occlusion.
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PMID:Catecholamine-induced experimental cardiomyopathy--a histopathological, histochemical and ultrastructural study. 259 40

The effect was studied of chronic alcohol intake in the rat during pregnancy and lactation on the brown adipose tissue (BAT) in pups. The idea was to find a possible relationship to cot death since in some cot death victims increased amounts of BAT have been observed. Exposure to ethanol increased the relative weight of the brown adipose tissue in pups and enhanced both its total protein content and the activities of the oxidative enzymes, succinate dehydrogenase and cytochrome oxidase. In the BAT of pups sympathetic activity, as demonstrated by noradrenaline, was also increased by long-term exposure to alcohol. In theory, an increased thermogenic capacity of the BAT in the newborn together with other factors such as emotional stress and infections could lead to death from hyperthermia, in which case only non-specific morphological signs would be found in the cadaver.
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PMID:Foetal and lactational exposure to alcohol increases oxidative capacity of brown adipose tissue in the rat. A possible relationship to cot death. 260 16

Copper (Cu) deficiency, induced in rats by suckling from Cu-deficient dams and by offering a semisynthetic low-Cu diet from weaning, resulted in cardiac enlargement. This enlargement was not due to accumulation of excess fluid in the heart but was characterized by mitochondrial hypertrophy as demonstrated by electron microscopy and biochemical studies. Administration of reserpine limited the extent of cardiac enlargement; however, heart total noradrenaline (NA), unchanged by Cu deficiency, was significantly reduced by reserpine. It was concluded that cardiac enlargement in Cu deficiency was not directly related to NA concentration. An alteration in cardiac energy status, however, was suggested by reduction in activity of the nonheme iron-dependent enzyme, succinic dehydrogenase.
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PMID:The effects of reserpine upon the cardiac enlargement of copper deficiency. 284 63

Acute cooling of rats led to stimulation of NAD+-dependent isocitrate dehydrogenase (ICDH), succinate dehydrogenase (SDH) and NAD(P)+-transhydrogenase (TH) but did not affect the NADP+-ICDH activity in liver, heart and skeletal muscle mitochondria. After pretreatment of the animals with propranolol the stimulating effect was decreased, thus suggesting that endogenous catecholamines and beta-adrenoreceptors are of importance in activation of NAD+-ICDH, SDH and TH. The effects of cooling, noradrenaline and cAMP did not summarize. Role of catecholamines in stimulation of mitochondrial oxidative enzymes under conditions of cooling is discussed.
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PMID:[Stimulation of mitochondrial oxidative enzymes in acute cooling and its catecholamine mechanisms]. 302 85

Mice fasted for 24 h showed reductions in carcass fat and gonadal fat depots and atrophy of brown adipose tissue (BAT) that was characterized by loss of protein and succinate dehydrogenase. These changes were reversed on 24 h of refeeding. Cycling mice experienced 14 cycles of 1 day of fast followed by 2 days of refeeding, whereas control mice were fed ad libitum. Weight loss during each fast remained constant, and the animals lost and regained in excess of twice their initial weights within 6 wk. However, final weight and carcass and gonadal fat weights were similar to those of animals fed ad libitum. Total food intake was similar between cycling mice and those fed ad libitum suggesting an increase in feeding efficiency. There was no development of resistance to food deprivation since the preceding fasting experience of the animal had no effect on weight and carcass fat loss during a 24- or 48-h fast. Norepinephrine-stimulated oxygen consumption that was reduced in cycling mice was probably the result of a reduction of BAT thermogenic capacity. BAT succinate dehydrogenase content and the concentration of uncoupling protein in isolated mitochondria were significantly reduced. These changes in BAT composition were not observed when the refeeding period of each cycle was increased to 6 days. These results suggest that reduced energy expenditure in BAT may play a role in the conservation of energy during intermittent and frequent bouts of food deprivation.
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PMID:Effects of repeated cycles of fasting-refeeding on brown adipose tissue composition in mice. 340 68


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