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:1.6.5.2 (NQO1)
6,196 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In cultured normal rat liver epithelial cells, the specific activity and/or isozyme expression of NADH-diaphorase (NADH-D), pyruvate kinase (PK), glucose-6 phosphate dehydrogenase (G6PD), gamma-glutamyl transpeptidase (GGT), and alkaline phosphatase (AP) were markedly dependent on the growth state of the cultures. Proliferating, preconfluent cells had higher specific activities of PK, NADH-D, and G6PD but lower activities of GGT and AP than did the more stationary confluent cells. Addition of epidermal growth factor [EGF] to the media of proliferating cells enhanced the specific activities of PK, NADH-D, G6PD, GGT, and lactate dehydrogenase (LDH) of these cells, but the specific activity of AP was markedly depressed. The increase in activity of PK and GGT by EGF appeared to involve new protein synthesis, whereas the effect of EGF on AP appeared to involve the EGF-directed suppression of the synthesis of a form of AP that is produced exclusively by cells in confluent cultures. Furthermore, the preconfluent cells were more responsive to the action of EGF on AP than were confluent cells, i.e., the EGF-mediated decrease in AP activity was seen at lower concentration in preconfluent than in confluent cells. Paradoxically, confluent cells exhibited a two-to threefold higher capacity to bind [125 I]EGF because of an increase in surface receptor number. The results of this study indicate that enzymatic or other biochemical studies performed on cultured cells must take into account the growth-state of the cultures. EGF can modulate enzyme activity in growing and nongrowing cells; one effect of EGF is to maintain higher activity of glycolytic enzymes, suggesting that EGF or EGF-like factors may contribute to the high rate of glycolysis in certain neoplasms.
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PMID:The effects of epidermal growth factor and the state of confluence on enzymatic activities of cultured rat liver epithelial cells. 286 16

The genetic structure of two Chukot Evens subpopulations (314 individuals) for electrophoretic protein systems and taste sensitivity to PTC was studied. 17 of the 39 loci were polymorphic (43.59%). The following systems were completely monomorphic: diaphorase NAD H (Dia); glucose-6-phosphate dehydrogenase (G-6-PD); glutamatoxalate transaminase (GOT); carbonic anhydrase (Ca-1); catalase (Ct), lactate dehydrogenase (loci LDH-A and LDH-B); leucine aminopeptidase (Lap); malate dehydrogenase (MDH); purine nucleoside phosphorylase (PNP); superoxide phosphorylase (PNP); superoxide dismutase (SOD); phosphoglucomutase-2 (PGM2); cholinesterase (locus E1); red cell esterase (4 loci); albumin (Alb); hemoglobin (Hb A and B); ceruloplasmin (Cp); and blood, gren, using the standard method. The following systems were polymorphic: red cell acid phosphatase (AcP); phosphoglucomutase-1 (PGM1); 6-phosphogluconate dehydrogenase (PGD); glutamatepyruvate transaminase (GPT); glyoxalase-1 (GLO-1); esterase (EsD); adenilatkinase (AK); alkaline phosphatase (Pp); cholinesterase (locus E2); haptoglobin (Hp); transferrin (Tf); group-specific component (Gc) and ABO, MN, Lewis, P blood groups and taste sensitivity to PTC. The following allele frequencies for polymorphic loci have been detected: AKI = 0.994; GLO = 1I = 0.082; GPT1 = 0.653; AcPA = 0.400; AcPB = 0.599; AcPC = 0.001; PGDA = 0.944; PGM1(1) = 0.906; EsD1 = 0.897; E2+ = 0.048; HpI = 0.394; GcI = 0,919; Tfc = 0.987; r(O) = 0.669; p(A) = 0.184; q(B) = 0.146; M = 0.711; Le = 0.411; P1+ = 0.521; t = 0.295. The genetic structure of Chukot Evens population is significantly nearer to that of the other ethnic groups of the North-East, in comparison with the genetic structure of Evenks of the Middle Siberia.
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PMID:[Genetic structure of the populations of native inhabitants in the northeastern USSR. V. The Chukot Evens]. 293 99

Osteogenesis of the body of the mandible in embryonic and neonatal rats was studied histologically and by histochemistry to determine the role of Meckel's cartilage in bone formation. Meckel's cartilage showed intense activity of lactate dehydrogenase and NADH2-diaphorase and weak activity of acid phosphatase, indicating a functioning citric acid cycle, pentose phosphate shunt and a capacity for anaerobic metabolism. The activity of these enzymes declined after hypertrophy of Meckel's cartilage. Alkaline phosphatase was the major enzyme of mineralising mandibular osteoid and was present in the osteoblasts and osteoprogenitor cells but not in Meckel's cartilage. After the differentiation of Meckel's cartilage and intramembranous bone, Meckel's cartilage supported mandibular bone formation by endochondral ossification in the anterior part of the mandible.
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PMID:Enzyme histochemical analysis of Meckel's cartilage. 325 49

Recent studies have suggested that large amounts of free zinc may be coreleased during excitatory synaptic transmission at glutamatergic synapses, and may act postsynaptically to decrease actions mediated by N-methyl-D-aspartate (NMDA) receptors, while often increasing neuroexcitation mediated by quisqualate receptors. The present study examined the ability of zinc to alter excitatory amino acid (EAA) neurotoxicity. Murine cortical cell cultures were exposed to EAAs for 5 min in defined solutions, and neuronal cell injury was examined the following day both morphologically and by lactate dehydrogenase assay. Inclusion of 30-500 microM zinc in the exposure solution produced a zinc concentration-dependent, noncompetitive attenuation of NMDA-induced neuronal injury, with an ED50 of about 80 microM. In contrast, zinc produced the same concentration-dependent potentiation of quisqualate neurotoxicity; and with 500 microM zinc, a small potentiation of kainate neurotoxicity was suggested. The effect of zinc on the neurotoxicity of the broad-spectrum agonist glutamate was consistent with these effects on specific agonists, as well as with a previous study showing that glutamate neurotoxicity normally depends predominantly on NMDA-receptor activation. Zinc produced a concentration-dependent reduction in glutamate-induced neuronal injury in a fashion similar to that seen with NMDA, but less effectively. In addition, despite this overall protective effect, zinc paradoxically increased the glutamate-induced destruction of nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d)-containing neurons, a subpopulation that was shown in the preceding paper (Koh and Choi, 1988) to exhibit resistance to NMDA receptor-mediated neurotoxicity, and vulnerability to non-NMDA receptor-mediated neurotoxicity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Zinc alters excitatory amino acid neurotoxicity on cortical neurons. 338 93

The results of quantitative histoenzymologic investigations of succinate dehydrogenase, lactate dehydrogenase and NAD-diaphorase in cardiomyocytes of dogs with acute experimental arterial occlusion in ischemic and postischemic periods are reviewed. An increased activity of dehydrogenases in the early periods (3,6 h) of ischemia and during recirculation was established, with its noticeable reduction at later terms (9,12 h). Medical correction of postischemic disorders was shown to improve cardiomyocyte metabolism.
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PMID:[Changes in the dehydrogenase activity of cardiomyocytes during acute experimental arterial occlusion of extremities]. 373 May 53

The clonal study of L cell culture has shown that the clone-forming cells are heterogeneous both in form and in the activities of enzymes (succinate dehydrogenase, lactate dehydrogenase, NAD- and NADP-diaphorase) which were determined by histochemical methods. The morphological heterogeneity is characteristic for clones with not less than 10 cells manifesting itself earlier and heterogeneity as to the activity of the studied enzymes--later, in clones with more than 15-20 cells.
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PMID:[Heterogeneity of L-line cells in the early stages of clone development]. 384 12

Various aspects of the cardiotoxicity of the anthracycline derivative and antineoplastic drug daunorubicin were investigated using isolated and cultured cells from neonatal rat hearts as a model system. Treatment of the cells with concentrations of daunorubicin of the same order of magnitude as those used in chemotherapy was accompanied by marked toxic effects, e.g. a decreased or abolished contraction, and release of lactate dehydrogenase, pyruvate and oxidized glutathione to the medium. A decreased frequency of contraction appeared to be the most sensitive probe of daunorubicin toxicity, followed by release of pyruvate and oxidized glutathione/lactate dehydrogenase. Daunorubicin and/or its metabolites also bound to cellular protein and DNA. Exposure to daunorubicin was shown to be accompanied by a rapid induction of primarily DT-diaphorase and a slower induction of glutathione transferase. The latter observations are interpreted to indicate a protective role of quinone- and peroxide-metabolizing enzymes, respectively, and support the hypothesis that daunorubicin toxicity involves generation of free radical derivatives, which initiate lipid peroxidation. This conclusion is further substantiated by the demonstration that addition of daunorubicin leads to an increased oxygen consumption.
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PMID:Toxic effects of daunorubicin on isolated and cultured heart cells from neonatal rats. 398 1

Histochemical study of enzymatic activity in the myocardium was performed in sudden cardiac death. Human hearts in which there were no macroscopic and histological focal or diffuse changes served as material. The following enzymes were studied in the anterior or posterior walls of the left ventricle or in the interventricular septum: succinate dehydrogenase, lactate dehydrogenase (LDH), beta-hydroxybutyrate dehydrogenase (OHBDH), alpha-glycerophosphate- and glucose-6-phosphate dehydrogenase, NAD-diaphorase and phosphorylase. Increased activity of OHBDH and LDH was found: 36,0 and 22,6% higher than in trauma and brain hemorrhage that served as control. These alterations seem to be connected with the increase of blood content of fatty acids, and lactate as a response to the catecholamine excess. Foci of an acute ischemia were found in the interventricular septum in 80% of cases in which phosphorylase was revealed. The appearance of the ischemic foci was obviously due to the coronary arteries contraction.
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PMID:[Histoenzymological characteristics of the myocardium in sudden cardiac death]. 405 12

By means of the light and electron microscopy, histochemical and cytophotometrical methods the anterior subarea of the cerebral limbic cortex has been studied in 30 experimental and 30 control rabbits. The experimental animals have been given 3, 15 and 30 sessions (1 h per day) of electric irritation (0.05 mA, 50 Hz, 1 msec) on the posterior hypothalamic field (PHF). Twelve rabbits from 30 control animals make an intact group and 18--a group with inactive electrodes inserted into the PHF. After 3 and especially after 15 sessions it has been revealed: in neurons--an acute swelling, edematous alterations, hyperchromatosis and shrinkage, changes in lactate dehydrogenase, succinic dehydrogenase, nicotinamide-adenine-dinucleotide-diaphorase and nicotinamide-adenine-dinucleotide-phosphate-diaphorase activities, in neuroglia--hypertrophy and weakly manifested hyperplasia. After 30 sessions synapses degenerated after the dark type are revealed. More intensive structural and metabolic changes are noted in the middle cytoarchitectonical complex. The changes of the enzymatic activity are considered as certain signs of weakening mitochondrial processes, connected with energy production, increasing glycolysis, decreasing level of the energetic provision of the cytoplasmic synthesis, arising under conditions of a disturbed transneuronal influence on the cortex by the hypothalamus.
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PMID:[Structural and metabolic changes in the limbic cortex of the rabbit in response to experimentation with the hypothalamus]. 408 71

A histochemical study of the metabolism of rat renal arteries and arterioles. Rat renal arteries and arterioles were examined histochemically to determine their metabolic profiles. Succinate, malate and NAD-isocitrate dehydrogenase, cytochrome oxidase and ubiquinone were assessed to determine aerobic metabolism. Glucose-6-phosphate dehydrogenase and DPN diaphorase were evaluated to determine hexose-monophosphate-shunt activity. Anaerobic metabolism was evaluated via lactate dehydrogenase, and the substrate, glycogen. Gomori's lipase, beta-hydroxybutyrate dehydrogenase and amounts of neutral fat and free fatty acids were assessed as indicators of lipid utilization. Myosin ATPase activity was evaluated as an index of ATP utilization for contraction. Deoxyribonucleic and ribonucleic acids were appraised as indicators of protein synthesis. In general, the oxidative enzymes and myosin ATPase demonstrate considerable activity in renal arteries and arterioles which suggests aerobic metabolism and ATP usage. Renal arteries and arterioles also appear capable of anaerobic metabolism as indicated by strong lactate dehydrogenase reactivity and by the presence of slight to moderate quantities of glycogen, while high levels of glucose-6-phosphate dehydrogenase and moderate amounts of deoxyribonucleic acid suggest a potential for beta-hydroxybutyrate dehydrogenase, minimal lipase activity, and the absence of fatty acids with substantial amounts of neutral fat, indicate limited lipid catabolism.
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PMID:A histochemical study of the metabolism of rat renal arteries and arterioles. 620 11


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