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)

A procedure for preparing highly purified brush border membranes from rabbit kidney cortex using differential and density gradient centrifugation is described. Brush border membranes prepared by this procedure were substantially free of basal-lateral membranes, mitochondria, endoplasmic reticulum and nuclear material as evidenced by an enrichment factor of less than 0.3 for (Na+ + K+)-ATPase, succinate dehydrogenase, NADPH-cytochrome c reductase and DNA. Alkaline phosphatase was enriched ten fold indicating that the membranes were enriched at least 30 fold with respect to other cellular organelles. The yield of brush border membranes was 20%. Transport of D-glucose by the membranes was identical to that previously reported except that the Arrhenius plot for temperature dependence of transport was curvilinear (EA = 11.3--37.6 kcal/mol) rather than biphasic. Transport of p-aminohippuric acid and uric acid were increased by the presence of NaCl, either gradient or preequilibrated. However, no overshoot was obtained in the presence of a NaCl gradient, and KCl and LiCl also produced equivalent stimulation of transport suggesting a nonspecific ionic strength effect. Uptakes of p-aminohippuric acid and uric acid were not saturable, and were increased markedly by reducing the pH from 7.5 to 5.6. Probenecid (1 mM) reduced p-aminohippuric acid and uric acid (50 muM) uptake by 49% and 21%, respectively. We conclude that the uptake of uric acid and p-aminohippuric acid by renal brush border membranes of the rabbit occurs primarily by a simple solubility-diffusion mechanism.
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PMID:Transport of p-aminohippuric acid, uric acid and glucose in highly purified rabbit renal brush border membranes. 3 45

Three glycerol-nonutilizing mutants deficient in the mitochondrial glycerol-3-phosphate (G3P) dehydrogenase (EC 1.1.99.5) were isolated from inl(ts) derivatives of Neurospora crassa following inositolless death at elevated temperatures on minimal glycerol medium. These mutants failed to grow on glycerol as a sole carbon source, but could grow on acetate, glucose, or mannitol media and were female fertile in genetic crosses, thereby distinguishing them from the previously reported polyol-protoperithecial defective Neurospora mutants. In addition, these glp mutants exhibited a distinct morphological alteration during vegetative growth on sucrose slants and colonial growth on sorbose-containing semicomplete medium. The glp-2 locus was assigned a location between arg-5 and nuc-2 on chromosome IIR on the basis of two-factor crosses and by duplication coverage by insertional translocation ALS176, but not NM177. All mutations were allelic as judged from the absence of both complementation in forced heterokaryons and genetic recombination among glp-2 mutations. The reversion frequency of all three mutations was less than 10(10), indicating probable deletions in these strains. No G3P dehydrogenase activity could be detected in either cytosolic or mitochondrial extracts from mutant strains grown on glycerol, glucose, or galactose media. These results suggest that the glp-2 locus may be the structural gene for both the cytosolic and mitochondrial forms of G3P dehydrogenase or for a cytosolic precursor of the mitochondrial G3P dehydrogenase. The defect is specific for the G3P dehydrogenase since normal activities of the mitochondrial cytochrome oxidase and succinate dehydrogenase and the cytosolic glycerol dehydrogenase and dihydroxyacetone phosphate reductase are detected in mutant extracts. During attempted growth of glp-2 mutants on glycerol media, there was an accumulation of G3P in culture filtrates, a reduction in the mycelial growth rate, and a decreased level of glycerokinase induction.
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PMID:Isolation and characterization of glycerol-3-phosphate dehydrogenase-defective mutants of Neurospora crassa. 15 57

Folate nephropathy was selected as a model to study renal mitochondrial response after tubular injury. 20 h after injection, 14C-leucine incorporation was suppressed to 20--30% of control, 14C-mannose incorporation was 63--78% greater than control while the activities of succinic dehydrogenase and monoamine oxidase were unaltered. By 40 h, 14C-leucine incorporation had been restored to control values. Also, at 20 h, ATPase activity sensitive to oligomycin inhibition had increased by 45--73%, whereas K+-stimulated ATPase activity was reduced in the experimental mitochondrial fractions. The results are discussed along with other studies of mitochondria in experimental renal disease.
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PMID:Alterations of mitochondrial properties in folate nephropathy. 16 16

A character originating from Saccharomyces cerevisiae 1403-7A is described which interferes with maltose growth in the respiratory-deficient state. This character is inherited in an apparently non-Mendelian way, but at present no statement can be made concerning the localization of this character on a plasmid or the involvement of multiple genes. As a revertant of this character, a flaky mutant was isolated, showing a heavy flocculation during growth on liquid medium and resistance to catabolite repression for maltase, alpha-methyl-glucosidase, invertase, and succinate dehydrogenase. In wild-type cells, repression (caused by growth on 2% glucose) and derepression (caused by growth on 2% galactose) can be correlated with a lower and a higher level of cyclic 3',5'-adenosine monophosphate (cAMP), respectively. In cells of flaky mutant, growth on these carbon sources results in the same levels of cAMP as observed for the wild type. Consequently, in this mutant derepression in the presence of 2% glucose is not reflected in a higher level of cAMP.
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PMID:Isolation of a catabolite repression mutant of yeast as a revertant of a strain that is maltose negative in the respiratory-deficient state. 16 13

beta-penta-O-acetyl-D-galactopyranose stimulated succinate oxidation in intact liver mitochondria (100%), in broken mitochondria (50%) and in EP1 particles (20%), no effect was observed on purified succinic dehydrogenase. This compound enhances the oxidation of succinate in the presence of Ca2+ and ATP; no effect appeared in the absence of calcium. beta penta-O-acetyl-D-galactopyranose prevents the reversal of Ca2+-induced swelling by EGTA. It seems that this sugar derivative would act, in some way, in the efflux of calcium from mitochondria leading to an accumulation of this bivalent ion in the mitochondria.
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PMID:Sugar derivatives and liver mitochondria. II. Effect of beta-penta-O-acetyl-D-galactopyranose. 45 46

The cell envelope of Neisseria gonorrhoeae, colony type 4, was studied. Outer membrane was isolated by lysozyme and ethylenediaminetetraacetic acid treatment of plasmolyzed cells according to Wolf-Watz et al. (1973). The degree of purity of the membrane preparations was checked by electron microscopy. The membrane fraction obtained had a density of 1.25 g/cm(3), was rich in phospholipase A and lysophospholipase, and contained only 10% of the total membrane activity of succinate dehydrogenase and d-lactate dehydrogenase. The outer membrane protein profile after sodium dodecyl sulfate-polyacrylamide gel electrophoresis revealed at least six major proteins. The predominating protein showed a molecular weight of 35,000. The lipopolysaccharide component was characterized by gas chromatography. The carbohydrates found were galactose, glucose, and glucosamine. d-Glycero-l-manno-heptose was present in very low amounts. Lipid A contained lauric acid, stearic acid, and beta-hydroxy-myristic acid. About 20% of the fatty acids in the outer membrane was derived from lipid A. The phospholipids were characterized as phosphatidylethanolamine, phosphatidylglycerol, and diphosphatidylglycerol. There was no evidence for a lipoprotein anchored to the peptidoglycan. The peptidoglycan of N. gonorrhoeae was of the chemotype I. The cell envelope of N. gonorrhoeae was found to be highly permeable to gentian violet. Cell envelopes of one penicillin-resistant and two penicillin-sensitive strains were compared. Only moderate differences in fatty acid composition were found.
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PMID:Cell envelope of Neisseria gonorrhoeae: outer membrane and peptidoglycan composition of penicillin-sensitive and-resistant strains. 80 26

Subcellular localization of renin in the rabbit kidney cortex was investigated using two centrifugation techniques. Renin was indirectly assayed on the basis of pressor activity and the reference enzymes such as succinic dehydrogenase, acid phosphatase and D-glucose-6-phosphatase for the other subcellular particulates were biochemically determined. Renin activity was found mainly in the mitochondrial fraction with very little in the microsomal fraction by a differential centrifugation. By a discontinuous sucrose density gradient centrifugation, renin granules were mainly recovered in the fraction corresponding to 1.5 M sucrose, while most of mitochondria, lysosomes and microsome equilibrated in the upper fractions. This renin granular fraction contained approximately 50% of total granular renin activity having a specific activity about six times that seen in the homogenate. After recentrifugation of the renin granular fraction, most of renin activity was recovered in the sediment. Repeated freezing and thawing of this fraction resulted in an increase of renin activity. On the basis of these experimental data it is assumed that renin located in the different subcellular particulates from mitochondria, lysosomes and microsomes in the rabbit kidney cortex.
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PMID:Distribution of renin in subcellular fractions from the rabbit kidney. 118 2

The effects of up to 4 months dietary supplementation with 40% galactose on muscle and nerve function were examined in rats. Galactitol, a polyol pathway metabolite, accumulated to high levels in both tissues. This led to changes similar to those found in experimental diabetes, which were largely prevented by treatment with an inhibitor of the first enzyme in the pathway, aldose reductase. For fast twitch extensor digitorum longus muscle there was weight loss, fibre damage, slowing of twitch time to peak, increased twitch tension, and reduced tetanic tension. There were no relaxation deficits. For slow twitch soleus there were no changes in tension production. However, contraction and relaxation for both twitch and tetanus were prolonged. Fatigue resistance was reduced after 1 week. Damage in soleus led to a reduction in mean fibre area after 2 months, which largely recovered by 4 months. There was a selective loss of fast oxidative glycolytic fibres. Histochemical staining for succinic dehydrogenase was normal in galactosaemic soleus, in contrast to the marked reduction seen in diabetes. Sciatic nerve conduction velocity was reduced after 2 months, particularly in normally fast conducting motor and sensory fibres. Resistance to hypoxic conduction block was increased in galactosaemic nerves to diabetic levels. It was concluded that polyol pathway hyperactivity is likely to contribute to the aetiology of diabetic myopathy and neuropathy, and that experimental galactosaemia provides a good model in which to study pathway effects without the complicated hormonal changes found in diabetes.
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PMID:Muscle and nerve dysfunction in rats with experimental galactosaemia. 153 21

Na-coupled D-glucose transport in rabbits with cis-diamminedichloride platinum (CDDP; cisplatin) induced acute renal failure (ARF) has been studied. ARF occurred at 3 days after injection of CDDP (3 mg/kg i.v.). Na-coupled D-glucose transport into brush-border membrane vesicles (BBMV) from both outer cortex (OC) and outer medulla (OM) of ARF rabbits under zero-trans condition was decreased. Increased Km (i.e., decreased affinity of transport carrier for D-glucose) in OC and decreased Vmax (i.e., decreased number of glucose carrier) in OM were observed in CDDP-induced ARF rabbits. Decrease glucose transport was also observed under equilibrium exchange condition. Intravesicular volume of BBMV from OC and OM of ARF rabbits was decreased. In homogenate and BBMV from OC and OM of ARF rabbits, activities of gamma-glutamyl transpeptidase and alkaline phosphatase (marker enzymes of brush-border membrane) were decreased. Activities of succinate dehydrogenase, glucose-6-phosphatase, and Na-K ATPase (marker enzymes of mitochondria, endoplasmic reticulum, and basal lateral membrane, respectively) were not affected by CDDP administration. These results suggested that one of the main target sites of CDDP in kidney is brush-border membrane (BBM) along the proximal tubule, that is, not only Na-coupled D-glucose transport carrier protein but also other proteins in BBM.
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PMID:Decreased sodium dependent D-glucose transport across renal brush-border membranes in cis-diamminedichloride platinum induced acute renal failure. 156 86

To establish the difference of mechanism between irritative and paralytic nystagmus, alterations of Na-K-ATPase and succinic dehydrogenase activity in the vestibular sensorineural elements were investigated for 20 guinea pigs, and glucose uptake of the vestibular nuclei for 13 guinea pigs were measured by the [14C]-2-deoxy-D-glucose method. Irritative and paralytic nystagmus were experimentally provoked by introducing K+ into the perilymphatic space. From the results it was concluded that irritative nystagmus is provoked by increased excitability of vestibular sensory cells, while paralytic nystagmus is provoked by decreased excitability. However, the direction of nystagmus was eventually decided by the tonus imbalance between the bilateral vestibular nuclei. The ipsilateral vestibular nucleus was predominant during irritative nystagmus, while the contralateral vestibular nucleus was predominant during paralytic nystagmus.
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PMID:The mechanism of irritative nystagmus and paralytic nystagmus. A histochemical study of the guinea pig's vestibular organ and an autoradiographic study of the vestibular nuclei. 192 91


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