Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:1.6.99.3 (diaphorase)
 5,903 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Several key enzymes related to carbohydrate metabolism were assayed in Setaria digitata. In the cytosolic fraction pyruvate kinase, phosphoenolpyruvate carboxykinase, malate dehydrogenase, malic enzyme, aspartate transaminase and alanine transaminase were found. Among the TCA cycle enzymes succinate dehydrogenase, fumarate reductase, fumarase (malate dehydration), malate dehydrogenase (malate oxidation and oxaloacetate reduction) and malic enzyme (malate decarboxylation) were detected in the mitochondrial fraction. Only reduced nicotinamide adenine dinucleotide (NADH) dehydrogenase, NADH oxidase and NADH-cytochrome c reductase were found in the mitochondrial fraction. The significance of these results with respect to the metabolic capabilities of the worm are discussed.
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PMID:Intermediary carbohydrate metabolism in the adult filarial worm Setaria digitata. 177 15

Bloodstream forms of Trypanosoma brucei brucei (EATRO 110) were cultured with 100 microM difluoromethylornithine (DFMO). After 48 hr, intracellular putrescine was depleted and cells were positive when histochemically stained for the mitochondrial marker enzyme, NAD diaphorase, and exhibited mitochondrial proliferation and cristae development when examined by electron microscopy. This suggested that the mitochondrion was undergoing the physiological transformation necessary for successful transmission of the bloodstream form to the vector, namely the initiation of development of a TCA cycle and cytochrome system. The short stumpy forms that appeared by day 4 of culture, although physiologically transformed, were not viable in so far as they were not capable of transforming to procyclic trypomastigotes when introduced into SDM-79 medium. When rats infected with T. b. brucei were given 4% (w/v) DFMO in their drinking water, they were cured within 72 hr. Trypanosomes removed from animals and stained for NAD diaphorase showed mitochondrial transformation, as well as an intermediate and short stumpy morphology, at 36 and 60 hr, respectively. Data from this study on the growth and transformation characteristics of the DFMO induced intermediate and short stumpy form trypanosomes supports the observation that the intermediate form, and not the short stumpy form, is able to successfully transform to procyclic trypomastigotes.
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PMID:Physiological activation of the mitochondrion and the transformation capacity of DFMO induced intermediate and short stumpy bloodstream form trypanosomes. 249 2

Histochemical studies have been made of the isocitrate dehydrogenase, succinic dehydrogenase, malate dehydrogenase, glutamate dehydrogenase, DPN diaphorase, TPN diaphorase, delta 5-3 beta-hydroxysteroid dehydrogenase and monoamine oxidase in the caput, corpus and cauda epididymides of normal and alpha chlorohydrin (6.5 mg/kg/9 days) treated rats. Administration of alpha chlorohydrin in a low dose caused a conspicuous decrease in all these enzymes except delta 5-3 beta-HSD, in various cell types of epididymal epithelium and sperms. Biochemical estimations of isocitrate dehydrogenase, succinic dehydrogenase, malate dehydrogenase and delta 5-3 beta-HSD have further supported and confirmed these histochemical observations. These changes in enzyme activities after treatment with low dose of alpha chlorohydrin strongly suggest that TCA cycle and amino acid metabolism of epididymis become defective, much earlier before any histological damage to the epididymis becomes visible.
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PMID:Effects of low doses of alpha chlorohydrin on the dehydrogenases and oxidases of rat epididymal epithelium and sperms: a correlative histochemical and biochemical study. 694 44

The bloodstream forms of the protozoan parasite Trypanosoma brucei lack spectrally detectable cytochromes and satisfy energy requirements mainly by glycolysis. When infected blood is ingested by the tse-tse fly vector, the bloodstream form cells differentiate to procyclic forms that have fully functional mitochondria. Procyclic cells have cyanide-sensitive, cytochrome-mediated electron transport and the full complement of TCA cycle enzymes. The developmental regulation of the cytochrome c reductase complex was examined at the RNA and protein levels. RNase T1 protection studies and Northern blot analyses demonstrated that bloodstream and procyclic form cells constitutively expressed the genes for two nuclear encoded cytochrome c reductase subunits, cytochrome c1 and subunit 4. Polyadenylated transcripts of both genes were present in bloodstream form cells at up to 20% of the procyclic cell levels. These levels were significantly up-regulated sometime after the onset of differentiation to the procyclic form. Despite the presence of subunit mRNAs in bloodstream form cells, subunit proteins were not detected until the cells had been allowed to differentiate in vitro for 6 h. Procyclic cell levels of subunit proteins and holocytochromes were reached by 48 h. Our results suggest that cytochrome c reductase is developmentally regulated at multiple levels, some involving post-transcriptional mechanisms.
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PMID:Developmental regulation of Trypanosoma brucei cytochrome c reductase during bloodstream to procyclic differentiation. 796 70

Skeletal muscle biopsies were performed on 12 healthy sedentary subjects and on 22 non-dyalized chronic renal failure patients (CRF) on a free diet and after overnight fasting. Parathormone, glucagon and insulin were determined at the same time of biopsies. CRF patients showed significantly low ATP and creatine phosphate levels. Regarding enzyme activities, a high hexokinase Vmax was found, while the pyruvate kinase activity was lower than in the control group. For the tricarboxylic acid cycle, citrate synthase, succinate dehydrogenase and malate dehydrogenase activities were higher; total NADH cytochrome c reductase activity was also high, while cytochrome oxidase activity was slightly lower. Both alanine aminotransferase and aspartate aminotransferase activities were considerably high in comparison with the control group. In conclusion, our study revealed a hypermetabolic TCA cycle, but impaired oxidative phosphorylation, which partly explained the reduced ATP concentration. Excessive protein intake and hormonal derangements may play a role in these metabolic changes.
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PMID:Altered muscle energy metabolism in post-absorptive patients with chronic renal failure. 924 94

The effect of alpha-tocopherol pretreatment (6 mg/100 g body wt/day, orally for a period of 90 days) on mitochondrial electron transport in myocardial infarction induced by isoproterenol (20 mg/100 g body wt, subcutaneously for two days) was studied in rats. A significant decrease was observed in the activities of isocitrate dehydrogenase, alpha-ketoglutarate dehydrogenase, succinate dehydrogenase, malate dehydrogenase, NADH dehydrogenase and cytochrome oxidase in heart mitochondria of isoproterenol administered rats. The cytochrome content and the oxidation of succinate in state 3 and state 4 decreased significantly in the cardiac mitochondria treatment. In alpha-tocopherol pretreated rats, the activities of TCA cycle enzymes, concentration of cytochromes and the oxidation of succinate in state 3 and state 4 were retained at near normal values, following isoproterenol administration.
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PMID:Effect of alpha-tocopherol on mitochondrial electron transport in experimental myocardial infarction in rats. 975 71

Combined transcriptome and proteome analysis was carried out to understand metabolic and physiological changes of Escherichia coli during the high cell density cultivation (HCDC). The expression of genes of TCA cycle enzymes, NADH dehydrogenase and ATPase, was up-regulated during the exponential fed-batch period and was down-regulated afterward. However, expression of most of the genes involved in glycolysis and pentose phosphate pathway was up-regulated at the stationary phase. The expression of most of amino acid biosynthesis genes was down-regulated as cell density increased, which seems to be the major reason for the reduced specific productivity of recombinant proteins during HCDC. The expression of chaperone genes increased with cell density, suggesting that the high cell density condition itself can be stressful to the cells. Severe competition for oxygen at high cell density seemed to make cells use cytochrome bd, which is less efficient but has a high oxygen affinity than cytochrome bo(3). Population cell density itself strongly affected the expression of porin protein genes, especially ompF, and hence the permeability of the outer membrane. Expression of phosphate starvation genes was most strongly up-regulated toward the end of cultivation. It was also found that sigma(E) (rpoE) plays a more important role than sigma(S) (rpoS) at the stationary phase of HCDC. These findings should be invaluable in designing metabolic engineering and fermentation strategies for the production of recombinant proteins and metabolites by HCDC of E. coli.
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PMID:Combined transcriptome and proteome analysis of Escherichia coli during high cell density culture. 1255 8

Disease caused by viruses, especially white spot syndrome virus (WSSV), present the greatest challenge to shrimp aquaculture worldwide. Massive tissue disintegration occurs in WSSV-infected ectodermal and mesodermal tissues of penaeid shrimp. The activities of membrane bound phosphatases (Na(+)K(+)ATPase, Ca(2+)ATPase, Mg(2+)ATPase and Total ATPase), transaminases (alanine transaminase (ALT) and aspartate transaminase (AST)) and mitochondrial enzymes (isocitrate dehydrogenase (ICDH), succinate dehydrogenase (SDH), malate dehydrogenase (MDH), alpha-ketoglutarate dehydrogenase (KGDH), NADH dehydrogenase, cytochrome C oxidase) in WSSV-infected tissues (hemolymph, hepatopancreas, gills and muscle) of Fenneropenaeus indicus were determined at intervals after WSSV infection (0, 24, 48, 72 and after 72 h (moribund)). The activities of phosphatases, transaminases and mitochondrial enzymes in healthy as compared with WSSV-infected hemolymph, hepatopancreas, gills and muscle showed marked divergence throughout the course of infection. WSSV infected hemolymph, hepatopancreas, gills and muscle exhibited significantly reduced activity of membrane bound phosphatases compared with the uninfected animals. Inactivation of these enzymes may occur due to increased production of free radicals, that cause conformational change by oxidation of 'SH' groups present at the active site. Significantly marked elevation in the activities of transaminases (ALT and AST) was observed in WSSV-infected hemolymph, hepatopancreas, gills and muscle compared to the uninfected tissues. This may be due to leakage of these enzymes from the damaged tissues. The activities of mitochondrial enzymes in WSSV-infected tissues were significantly decreased compared to the activities in uninfected animals. WSSV-infected animals showed reduced feeding that may have led to decreased oxidation of glucose via the TCA cycle. Excessive production of free radicals in WSSV-infected animals may have affected aerobic oxidation leading to lower production of ATP. It is concluded that membrane dynamics play a major role in the pathogenesis of WSSV infection.
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PMID:Activities of membrane bound phosphatases, transaminases and mitochondrial enzymes in white spot syndrome virus infected tissues of Fenneropenaeus indicus. 1641 26

The efficacy of ifosfamide (IFO), an antineoplastic drug, is severely limited by a high incidence of nephrotoxicity of unknown etiology. We hypothesized that inhibition of complex I (C-I) by chloroacetaldehyde (CAA), a metabolite of IFO, is the chief cause of nephrotoxicity, and that agmatine (AGM), which we found to augment mitochondrial oxidative phosphorylation and beta-oxidation, would prevent nephrotoxicity. Our model system was isolated mitochondria obtained from the kidney cortex of rats treated with IFO or IFO + AGM. Oxidative phosphorylation was determined with electron donors specific to complexes I, II, III, or IV (C-I, C-II, C-III, or C-IV, respectively). A parallel study was done with (13)C-labeled pyruvate to assess metabolic dysfunction. Ifosfamide treatment significantly inhibited oxidative phosphorylation with only C-I substrates. Inhibition of C-I was associated with a significant elevation of [NADH], depletion of [NAD], and decreased flux through pyruvate dehydrogenase and the TCA cycle. However, administration of AGM with IFO increased [cyclic AMP (cAMP)] and prevented IFO-induced inhibition of C-I. In vitro studies with various metabolites of IFO showed that only CAA inhibited C-I, even with supplementation with 2-mercaptoethane sulfonic acid. Following IFO treatment daily for 5 days with 50 mg/kg, the level of CAA in the renal cortex was approximately 15 micromol/L. Taken together, these observations support the hypothesis that CAA is accumulated in renal cortex and is responsible for nephrotoxicity. AGM may be protective by increasing tissue [cAMP], which phosphorylates NADH:oxidoreductase. The current findings may have an important implication for the prevention of IFO-induced nephrotoxicity and/or mitochondrial diseases secondary to defective C-I.
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PMID:Ifosfamide-induced nephrotoxicity: mechanism and prevention. 1688 87

Mitochondria are an important intracellular source and target of reactive oxygen species. The life span of a species is thought to be determined, in part, by the rate of mitochondrial damage inflicted by oxygen free radicals during the course of normal cellular metabolism. In the present study, we have investigated the protective effect of squalene supplementation for 15 days and 30 days on energy status and antioxidant defense system in liver mitochondria of 18 young and 18 aged rats. The dietary supplementation of 2% squalene significantly minimized aging associated alterations in mitochondrial energy status by maintaining the activities of TCA cycle enzymes (isocitrate dehydrogenase, alpha-ketoglutarate dehydrogenase, succinate dehydrogenase and malate dehydrogenase) and respiratory marker enzymes (NADH dehydrogenase and cytochrome-c-oxidase) at higher level in the liver mitochondria of aged rats compared with unsupplemented controls. It exerted an antioxidant effect by inhibiting mitochondrial lipid peroxidation (malondialdehyde) in liver of young and aged rats. Supplementation with squalene also maintained the mitochondrial antioxidant defense system at higher rate by increasing the level of reduced glutathione and the activities of glutathione-dependent antioxidant enzymes (glutathione peroxidase and glutathione-S-transferase) and antiperoxidative enzymes (superoxide dismutase and catalase) in the liver of young and aged rats. The results of this study provide evidence that dietary supplementation with squalene can improve liver mitochondrial function during aging and minimize the age-associated disorders in which reactive oxygen species are a major cause.
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PMID:Protective effect of dietary squalene supplementation on mitochondrial function in liver of aged rats. 1757 27


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