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)

Treatment of rats with the vitamin B12 analogue hydroxy-cobalamin[c-lactam] (HCCL) impairs methylmalonyl-CoA mutase function and leads to methylmalonic aciduria due to intracellular accumulation of propionyl and methylmalonyl-CoA. Since accumulation of these acyl-CoAs disrupts normal cellular regulation, the present investigation characterized metabolism in hepatocytes and liver mitochondria from rats treated subcutaneously with HCCL or saline (control) by osmotic minipump. Consistent with decreased methylmalonyl-CoA mutase activity, 14CO2 production from 1-14C-propionate (1 mM) was decreased by 76% and 82% after 2-3 wk and 5-6 wk of HCCL treatment, respectively. In contrast, after 5-6 wk of HCCL treatment, 14CO2 production from 1-14C-pyruvate (10 mM) and 1-14C-palmitate (0.8 mM) were increased by 45% and 49%, respectively. In isolated liver mitochondria, state 3 oxidation rates were unchanged or decreased, and activities of the mitochondrial enzymes, citrate synthetase, succinate dehydrogenase, carnitine palmitoyltransferase, and glutamate dehydrogenase (expressed per milligram mitochondrial protein) were unaffected by HCCL treatment. In contrast, activities of the same enzymes were significantly increased in both liver homogenate (expressed per gram liver) and isolated hepatocytes (expressed per 10(6) cells) from HCCL-treated rats. The mitochondrial protein per gram liver, calculated on the basis of the recovery of the mitochondrial enzymes, increased by 39% in 5-6 wk HCCL-treated rats. Activities of lactate dehydrogenase, catalase, cyanide-insensitive palmitoyl-CoA oxidation, and arylsulfatase A in liver were not affected by HCCL treatment. Hepatic levels of mitochondrial mRNAs were elevated up to 10-fold in HCCL-treated animals as assessed by Northern blot analysis. Thus, HCCL treatment is associated with enhanced mitochondrial oxidative capacity and an increased mitochondrial protein content per gram liver. Increased mitochondrial oxidative capacity may be a compensatory mechanism in response to the metabolic insult induced by HCCL administration.
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PMID:Increased hepatic mitochondrial capacity in rats with hydroxy-cobalamin[c-lactam]-induced methylmalonic aciduria. 170 51

The maximal rate (Vmax) of some mitochondrial enzyme activities related to energy transduction (citrate synthase, alpha-ketoglutarate dehydrogenase, malate dehydrogenase, succinate dehydrogenase, NADH-cytochrome c reductase, cytochrome oxidase) and amino acid metabolism (glutamate dehydrogenase, glutamate-pyruvate transaminase and glutamate-oxaloacetate transaminase) are evaluated in non synaptic ("free") and intrasynaptic mitochondria from brain hippocampus. The different mitochondrial populations were isolated from rat subjected to single i.p. treatment with saline solution, almitrine (30 mg/kg) and delta-yohimbine (10 mg/kg). In control rats, the mitochondrial populations exhibit different enzymatic patterns. Acute treatment with almitrine decreases cytochrome oxidase activity in intra-synaptic mitochondria, while acute treatment with delta-yohimbine decreases succinate dehydrogenase activity in both types of free and intra-synaptic mitochondria. NADH-cytochrome c reductase activity is also decreased by acute treatment with almitrine ("free" and "synaptic" mitochondria) and delta-yohimbine (synaptic mitochondria only).
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PMID:Factors involved in drug interference on enzyme activities of three mitochondrial populations from rat hippocampus. 180 34

The effects of arachidonic acid on the enzyme complexes in the electron transport system were investigated using submitochondrial particles from rat brain. Arachidonic acid irreversibly inhibited NADH-CoQ oxidoreductase (complex I) activity, but had no effect on the activities of succinate-CoQ oxidoreductase (complex II), CoQH2-cytochrome c oxidoreductase (complex III), cytochrome c oxidase (complex IV), ATPase (complex V), glutamate dehydrogenase, and malate dehydrogenase up to 50 microM. The inhibition was dose-dependent with an IC50 value of 110 nmol/mg protein. The Lineweaver-Burk plot revealed that the inhibition by arachidonic acid was noncompetitive against CoQ with a Ki value of 33 microM and uncompetitive against NADH with a Ki value of 22 microM.
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PMID:Selective inhibition of NADH-CoQ oxidoreductase (complex I) of rat brain mitochondria by arachidonic acid. 190 30

Haemonchus contortus, incubated in 10 micrograms/ml and 50 micrograms/ml concentrations of Nilzan and albendazole in Tyrode solution were stained for histoenzymatic demonstration of various phosphatases, oxido-reductases and esterases. The intestine showed major alterations after drug treatments. The alkaline phosphatases (AkPase), adenosine triphosphatase (ATPase), glucose-6-phosphatase, succinic dehydrogenase (SDH), glutamate dehydrogenase (GDH), reduced nicotinamide adenine dinucleotide phosphate diaphorase and reduced nicotinamide adenine dinucleotide diaphorase showed a decreased activity in intestine after Nilzan treatment, whereas lactic dehydrogenase (LDH), glucose-6-phosphate dehydrogenase (G-6-PD) and monoamine oxidase resisted increased reaction. The albendazole treatment resulted in altered distribution pattern of the AkPase, ATPase, SDH, and GDH; while LDH, G-6-PD, and non-specific esterases exhibited slightly enhanced activity in the epithelium. The functional significance of these changes has been fully discussed.
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PMID:Effect of Nilzan and albendazole on the absorptive surfaces of Haemonchus contortus (Nematoda)--a histoenzymic study. 196 79

Endotoxin Salmonella typhimurium (LD50) was administered intraperitoneally to mice. It was shown that triamcinolone acetonide in a dose of 1 mg/kg living weight administered to mice 1 hour before endotoxin administration completely prevents the death of the animals and decreases the level of changes in the activities of enzymes of glutamate dehydrogenase, succinate dehydrogenase, monoaminoxidase, cytochrome oxidase in the liver mitochondria in endotoxemia. The level of lipid peroxidation in mitochondria during endotoxemia against the background of triamcinolone acetonide action is close to control. The use of triamcinolone acetonide in the absence of the effect of endotoxin results in an insignificant damage of mitochondrial membranes.
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PMID:[The effect of triamcinolone acetonide on the liver mitochondria in endotoxemia]. 208 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

To evaluate changes in liver metabolic zonation during development of juvenile cirrhosis, zonal activities of succinate dehydrogenase, glutamate dehydrogenase, glucose-6-phosphatase, and nicotinamide adenine dinucleotide phosphate (NADPH) dehydrogenase were measured by quantitative cytochemistry in the liver of developing rats intoxicated with carbon tetrachloride and phenobarbitone. During treatment, activities were most decreased in perivenular zones and subsequently at the periphery of the cirrhotic nodules for succinate dehydrogenase and glucose-6-phosphatase, whereas glutamate dehydrogenase and NADPH dehydrogenase were less affected. In the periportal zones, enzyme activities decreased less. After stopping intoxication, the rats remained cirrhotic, but enzyme activities returned to control perivenular levels at the periphery of the cirrhotic nodule and to control periportal levels at its center. It is concluded that a metabolic zonation persists in carbontetrachloride/phenobarbitone-induced juvenile cirrhosis and that enzyme activities can recover despite persisting cirrhosis. In this model, afferent vessels seem to be located at the center of the cirrhotic nodules, and efferent vessels, at their periphery. A different metabolic zonation may exist in other human and animal liver cirrhosis that could be related to the site of initial liver damage.
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PMID:Adaptative changes of metabolic zonation during the development of cirrhosis in growing rats. 216 52

The activity of alpha-ketoglutarate dehydrogenase and succinic dehydrogenase in readaptation after 15-day hypokinesia was within normal limits, whereas following 30-day hypokinesia it was enhanced on days 11-15. Pyruvate dehydrogenase exhibited hyperactivity in the end of readaptation week 2 both in 15- and 30-day hypokinesia which resulted in rat liver hyperactivity of glutamate dehydrogenase and transaminases. Normal levels of the latter were recorded on readaptation day 12-19.
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PMID:[Activity of various oxidases and transaminases in the rat liver in the readaptation period after hypokinesia up to 30 days]. 232 62

Hepatocytes differ in their metabolism depending on their position in the liver acinus. To assess how such specialization changes during development, we used quantitative cytochemistry to measure succinate dehydrogenase (SDH), glutamate dehydrogenase (GDH), glucose-6-phosphatase (G6P), and NADPH dehydrogenase (ND) activities specifically in periportal and perivenular hepatocytes in developing rats, aged between 1-114 days. Important and distinct changes were observed in each zone for each enzyme during development. An intra-acinar gradient of distribution was present from day 1 for SDH and G6P and from day 5 for GDH and ND. It was being similar to the adult value for SDH but less pronounced for the remaining enzymes. The SDH and G6P activity was greater in periportal cells, and the GDH and ND activity was greater in perivenular cells. The more pronounced distribution with age was due, for G6P, to an initial specific periportal increase combined with a mild perivenular decrease and for GDH to a greater perivenular than periportal increase. The ND first increased simultaneously in both zones, but from day 20 the perivenular increase became prevalent. The SDH changes were parallel in both zones. All zonal enzyme activities changed distinctly after weaning. To what extent the changes in activities and metabolic zonation observed in our study reflect a response to specific metabolic demands of the liver or can be modified by environmental factors remains to be investigated.
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PMID:Developmental changes in the intra-acinar distribution of succinate dehydrogenase, glutamate dehydrogenase, glucose-6-phosphatase, and NADPH dehydrogenase in the rat liver. 254 10

The effect of Ca2+-homopantothenate (HOPA) treatment (250 mg/kg for 5 d) has been studied by evaluating the specific activity of enzymes related to: glycolytic pathway (hexokinase, phosphofructokinase, pyruvate kinase, lactate dehydrogenase), tricarboxylic acid cycle (citrate synthase, malate dehydrogenase), mitochondrial electron transfer chain (succinate dehydrogenase, cytochrome oxidase), NADH redox state (NADH cytochrome c reductase), acetylcholine metabolism (acetylcholinesterase), and glutamate metabolism (glutamate dehydrogenase). The enzymatic activity assays were performed on homogenate in toto, nonsynaptic mitochondria and synaptosomes isolated from: cerebral cortex, hippocampus, striatum, hypothalamus, medulla oblongata, and cerebellum of normoxic rats and rats submitted to intermittent normobaric hypoxia (90:10, N2:O2). In normoxic rats, HOPA was unable to induce any modification. Hypoxia per se induced a decrease in the activity of synaptosomal cytochrome oxidase in cerebral cortex, hippocampus, and cerebellum.
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PMID:Effect of Ca2+-homopantothenate and mild hypoxia on some enzyme activities evaluated in subcellular fractions from different rat brain regions. 254 16


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