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)

Histochemical and histoenzymatic features of the adrenal medulla were studied 60 days after the end of an exposure to detergents. The findings obtained, point to an increase in the quantity of nucleic acids, and an intensified activity of nonspecific esterases as well as the cytochrome oxidase in rats maintained in a detergent manufacturing plant. The activity of isocitrate dehydrogenase was reduced in the control animals, as well as the activity of lactate dehydrogenase and isoenzyme "S" lactate dehydrogenase. The activity of isoenzyme "F" lactate dehydrogenase, glucose-6-phosphate dehydrogenase and succinate dehydrogenase is greater in the group which had been exposed to detergent influence. An active engagement of medullocytes is emphasized at this term of the experiment. The agent applied elicits a disturbance in the metabolism of glucose and a number of other substances. The author is of the opinion that an altered and stimulated synthesis and secretion of catecholamines takes place in the adrenal medullocytes under the experimental conditions which were investigated. The neuroendocrine system has been engaged in a series of processes which had been studied.
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PMID:[Histoenzymatic characteristics of the adrenal medulla 60 days after ending exposure to detergents]. 207 70

Two carbon catabolite repression mutants of S. cerevisiae were isolated and characterized. In spite of the selection procedure (red colonies after tetrazolium overlay at high glucose concentration) the mutants exhibited a respiration which was as repressed as that of the parental strain or even more repressed. When grown at high glucose concentration the mutants display hyper-repression of cytochrome aa3 and of certain mitochondrial enzymes (L- and D-lactate dehydrogenases) but not of others (malate dehydrogenase, succinate dehydrogenase), indicating the existence of separate control sites for the different genes involved in the mitochondrial biogenesis. The data obtained pointed out that the same mutation affects both repression and derepression. In addition, the mutation(s) give rise to the complete derepression of the cytoplasmic enzyme NAD-glutamate dehydrogenase at 10% glucose whereas the enzyme is normally repressed at 3% glucose. The results of the genetic analysis indicate the mitochondrial nature of the mutation(s).
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PMID:Isolation and characterization of carbon catabolite repression mutants in Saccharomyces cerevisiae. 208 99

The neurochemical changes induced by malathion, an organophosphate compound, were determined in rats. Maximal changes were found in the brain 2 h after the administration of malathion in a dose of 500 mg/kg ip. The activities of cholinesterase and succinic dehydrogenase were reduced whereas those of glycogen phosphorylase, phosphoglucomutase, and hexokinase were increased; the lactate content of brain was also increase. In malathion treated adrenalectomized animals, changes in the activities of cerebral cholinesterase and succinic dehydrogenase were still present; other changes were, however, abolished by adrenalectomy. Activities of certain enzymes, glucose-6-phosphatase, glucose-6-phosphate dehydrogenase, and lactate dehydrogenase were not significantly altered by malathion in normal or adrenalectomized animals. The results indicate that cerebral cholinergic mechanism in malathion treated animals was not modified by adrenalectomy which, however, abolished or reduced changes in the activities of certain glycolytic and glycogenolytic enzymes that are involved in the utilization or metabolism of glucose. The brain lactate content in malathion treated adrenalectomized animals was, also, not significantly different from the control values, suggesting that modification of induced changes by adrenalectomy.
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PMID:Modification of malathion induced neurochemical changes by adrenalectomy in rats. 209 80

To evaluate the relationship between enhanced insulin action and level of exercise training, in vivo glucose uptake was assessed in the absence of added insulin and during insulin-stimulated conditions for three activity levels of voluntarily trained rats (low 2-5 km/day, medium 6-9 km/day, high 11-16 km/day). After rats rested for 24 h and fasted overnight, glucose uptake was estimated by comparing steady-state serum glucose (SSSG) levels at low insulin (SSSI) concentrations achieved during an insulin suppression test. In the absence of added insulin, SSSI averaged approximately 20 microU/ml and glucose uptake was similar for high runners and younger weight-matched controls. However, with insulin added to sustain SSSI at approximately 35 microU/ml, SSSG was significantly reduced in all runners (P less than 0.02), with the lowest value attained in high runners. Fasting serum triglycerides were also reduced in all runners (P less than 0.05), with the lowest values seen in medium and high runners. The concentration of glycogen in liver and select skeletal muscles at the start of the study was not different between trained and control rats, suggesting that enhanced insulin-stimulated glucose uptake was not the result of lower glycogen levels. In addition, glycogen synthase and succinate dehydrogenase activities in biceps femoris muscle were only elevated for high runners, but glycogen synthase activity was not enhanced in plantaris muscle and was decreased in soleus muscle. These findings indicate that enhanced insulin-stimulated glucose uptake and reduced serum triglyceride concentrations induced in exercise-trained rats at varying activity levels are dissociated from changes in glycogen synthase and oxidative enzyme activity for skeletal muscle.
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PMID:Differences in insulin-induced glucose uptake and enzyme activity in running rats. 210 19

We describe the cloning and characterization of the complete gene for the iron-sulfur protein subunit of succinate dehydrogenase (EC 1.3.99.1) from Saccharomyces cerevisiae. The promoter and coding sequence have been cloned into an Escherichia coli-yeast shuttle vector. The cloned gene complements the defect in a succinate dehydrogenase-deficient yeast mutant isolated by us, and gene expression is fully responsive to induction by glucose deprivation, indicating that the promoter is intact.
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PMID:Cloning and characterization of the iron-sulfur subunit gene of succinate dehydrogenase from Saccharomyces cerevisiae. 219 48

The effects of endurance training (running 1 h/day at 35 m/min, 10% grade) on glucose homeostasis during exercise (running 20 m/min) was studied in 30-h fasted rats. Primed-continuous infusion of [6-3H]- and [U-14C]glucose were employed to assess rates of appearance (Ra), disappearance (Rd), and apparent recycling. Training resulted in a 65% increase in skeletal muscle succinate dehydrogenase (SDH) activity but did not significantly influence body weight. Resting blood glucose concentrations were not significantly different between controls, 5.01 +/- 0.19 mM, and trained animals, 4.86 +/- 0.16 mM. Exercise resulted in a more rapid decline in blood glucose levels for control animals, reaching a value of 2.35 +/- 0.39 mM at 60 min, compared with 3.69 +/- 0.47 mM for trained animals. Glucose Ra was not significantly different between groups at rest, and rose for both groups during exercise. However, for controls Ra plateaued between 15 and 60 min of exercise at 11.03 +/- 0.73 mumol.100 g-1.min-1, whereas trained animals demonstrated a continuous rise to 17.13 +/- 1.18 mumol.100 g-1.min-1. Glucose Rd values were not significantly different between groups during the first 30 min of exercise but were significantly higher for trained animals during the final 30 min. As a result of the higher glucose Ra, trained animals demonstrated a smaller mean difference between Ra and Rd during exercise when compared with controls, -0.27 +/- 0.14 vs. -0.96 +/- 0.17 mumol.100 g-1.min-1. Trained animals further demonstrated significantly higher rates of glucose carbon recycling during the final 30 min of exercise.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Training improves glucose homeostasis in rats during exercise via glucose production. 231 21

Continuous exposure of Chinese hamster ovary (CHO) cells to an atmosphere of 98% O2, 2% CO2 (normobaric hyperoxia) leads within a period of several days to cytostasis and clonogenic cell death. Here we report respiratory failure as an important early symptom of oxygen intoxication in CHO cells, resulting in a more than 80% inhibition of oxygen consumption within 3 days of hyperoxic exposure. This inhibition appeared to be correlated with selective inactivation of three mitochondrial key enzymes, NADH dehydrogenase, succinate dehydrogenase, and alpha-ketoglutarate dehydrogenase. The latter enzyme controls the influx of glutamate into the Krebs cycle and is particularly critical for oxidative ATP generation in most cultured cells, which depends on exogenous glutamine rather than glucose as a carbon source. As expected, the inactivation of alpha-ketoglutarate dehydrogenase was correlated with a fall in cellular glutamine utilization, which became apparent from the first day of hyperoxic exposure. Thereafter, glucose utilization and lactate excretion started to increase, up to 3-fold, indicating a cellular response to respiratory failure aimed at increased ATP generation from glycolysis. However, in spite of this response, the cellular ATP level progressively decreased, up to 2.5-fold. Thus, killing of CHO cells by normobaric hyperoxia seems to be due to a severe disturbance of mitochondrial metabolism eventually leading to a depletion of cellular ATP pools.
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PMID:Respiratory failure and stimulation of glycolysis in Chinese hamster ovary cells exposed to normobaric hyperoxia. 235 58

A single oral dose of di-n-butyl phthalate (DBP) to male rats caused histologically a sloughing of the germ cells at 6 h. On Days 1 and 2 more severe sloughing was seen, followed by atrophy and the dissociation of the germ cells from the Sertoli cells and the spermatogonia. Biochemically, there was elevation of gamma-glutamyl transferase, a decrease in sorbitol levels at 3 h and a decrease in the activity of aldose reductase at 6 h, in the testes of treated rats. This was followed by decreases in fructose levels and increases in the activity of lactate dehydrogenase (LDH) and in lactate levels at 12 h, and decreases in the activities of sorbitol dehydrogenase and succinate dehydrogenase on Day 2. LDH isoenzymes 4 and 5 increased at 6 h prior to the increase in lactate levels. Increases in the levels of inositol and the activities of alkaline phosphatase and lactate dehydrogenase were also observed. Thus, these data suggest that DBP-induced testicular toxicity is caused by a shortage of energy fuels from glucose metabolism or by an anoxia.
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PMID:Mechanism of testicular atrophy induced by di-n-butyl phthalate in rats. Part 2. The effects on some testicular enzymes. 239 8

Administration of carbon tetrachloride to normal rats increased activities of hepatic 5(1)-nucleotidase, acid phosphatase, acid ribonuclease while the activities of succinate dehydrogenase, glucose 6-phosphatase, superoxide dismutase and cytochrome P450 were decreased. Levels of lipid peroxides, total lipids and cholesterol of liver were also increased. The activities of serum glutamate oxaloacetate transaminase, glutamate pyruvate transaminase and alkaline phosphatase were increased. Other serum parameters showing changes after carbon tetrachloride were: bilirubin, proteins, cholesterol, triglycerides and lipoprotein-X. Picroliv (from the plant Picrorhiza kurroa) in doses of 6 and 12 mg/kg provided a significant protection against most of the biochemical alterations produced by carbon tetrachloride. The degree of protection afforded by picroliv, when administered simultaneously or as a pretreatment was almost equal.
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PMID:Hepatoprotective activity of picroliv against carbon tetrachloride-induced liver damage in rats. 240 41

Chronic administration of the estrogen 17 beta-estradiol induces kidney tumors in male Syrian hamsters within 6 months of initial exposure. Although these tumors have previously been studied histologically and histochemically and have been postulated to be derived from proximal tubular and/or interstitial cells, there exists no unambiguous evidence for an epithelial or mesenchymal origin. To elucidate the histogenesis of these neoplasms, kidney sections of hamsters treated with estradiol for 4, 5, and 6 months and age-matched untreated controls were investigated histologically and histochemically. Proliferating foci were observed in kidneys exposed to estradiol for 5 and 6 months. They consisted of clusters of spindle-shaped cells forming solid blocks, cords, or branches located between tubules. These foci were judged to be precursors of larger tumors identified in the latter treatment group. The histological and histochemical profile of foci and tumors matched closely. These lesions were marked by very high activities of alkaline phosphatase, adenyl cyclase, and glucose 6-phosphate dehydrogenase. In contrast, glycogen content and activities of glucose 6-phosphatase, succinate dehydrogenase, and gamma-glutamyl transpeptidase were low or absent. Immunofluorescence of the intermediate filaments revealed that foci and tumors solely expressed vimentin and desmin but not cytokeratin. The morphology, enzyme histochemical pattern, and immunofluorescence strongly support a mesenchymal origin of the estradiol-induced hamster kidney tumors studied. The neoplasms were probably derived from vascular smooth muscle cells of a cell subtype particularly sensitive to hormonal stimulation and transformation.
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PMID:Histochemical analysis of the development of estradiol-induced kidney tumors in male Syrian hamsters. 244 29


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