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:1.6.99.1 (NADPH-diaphorase)
3,903 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Neuronal degeneration that occurs in both ischemia and degenerative neurologic illnesses may involve excitotoxic mechanisms. In the present study, we examined whether cortical lesions with agonists acting at subtypes of glutamate receptors result in selective patterns of neuronal death. Injections of quinolinic acid, NMDA, homocysteic acid, kainic acid (KA), and alpha-amino-3-hydroxy-5-methylisoxazole-4-proprionic acid (AMPA) were made at 2 sites in the dorsolateral frontoparietal cortex in rats. After 1 week, the cerebral cortex was either dissected for neurochemical studies, or animals were perfused for histologic evaluation. Concentrations of somatostatin (SS), neuropeptide Y (NPY), substance P (SP), cholecystokinin (CCK), and vasoactive intestinal polypeptide (VIP) were measured by radioimmunoassay, while amino acids and catecholamines were measured by high-performance liquid chromatography (HPLC) with electrochemical detection. NMDA agonists (quinolinic acid, homocysteic acid, and NMDA itself) resulted in dose-dependent reductions in glutamate and GABA, while SS, NPY, SP, CCK, and VIP were either unchanged or significantly increased in concentration. KA and AMPA at doses that resulted in comparable GABA depletions caused significant reductions in SS concentrations. Markers of cortical afferents were spared. All excitotoxins resulted in dose-dependent marked increases in uric acid concentrations. Histologic examination verified that lesions with NMDA agonists produced relative sparing of NADPH-diaphorase, SS, VIP, and CCK neurons. These results show that NMDA excitotoxin lesions result in a pattern of selective neuronal damage in the cerebral cortex that is similar to that which occurs in both ischemia and Huntington's disease.
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PMID:Neurochemical characterization of excitotoxin lesions in the cerebral cortex. 167 Jul 82

It is generally thought that the oxidative modification of hemoproteins leads to their inactivation. In the current study, however, a transiently activated form of myoglobin was shown to be formed when the prosthetic heme group became covalently bound to the polypeptide during the reaction of myoglobin with low levels of HOOH. In the presence of an enzymatic metmyoglobin reducing system containing diaphorase and methylene blue with excess NADH, this HOOH-altered myoglobin catalyzed NADH oxidation and oxygen consumption; the overall stoichiometry indicated a two-electron reduction of oxygen to HOOH. This reaction was not catalyzed by iron released from heme, as desferrioxamine had no effect on the activity. Stoichiometric amounts of HOOH were sufficient to produce the activated oxidase state of myoglobin, whereas larger amounts of HOOH lead to heme destruction, iron release, and inactivation of the oxidase activity. The alteration of myoglobin to an enzyme that can form toxic oxygen metabolites may have pathological importance, especially in myocardial injury caused by ischemia and reperfusion, where myoglobin is present in large amounts and HOOH is formed. Furthermore, the oxidase form may be involved in the mechanism of destruction of the heme seen with oxidative treatment of myoglobin.
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PMID:Oxidative modification by low levels of HOOH can transform myoglobin to an oxidase. 187 Nov 23

In the present study we investigated the relative vulnerability of neuronal subsets in the striatum to ischemia that was induced by bilateral transient ligation of the common carotid arteries in gerbils. After 4 days of survival, brains were evaluated using histochemical methods (NADPH-diaphorase and silver degeneration procedures) and neurochemical methods with radioimmunoassays for somatostatin-, neuropeptide Y-, and substance P-like immunoreactivity and measurements of amino acids using high-pressure liquid chromatography with electrochemical detection. NADPH-diaphorase-positive neurons were strikingly preserved in the ischemic dorsolateral portion of the striatum, in which there was severe neuronal loss. There was no significant depletion of NADPH-diaphorase-positive neurons in the striatum or cerebral cortex. Concentrations of neuropeptide Y-like and somatostatin-like immunoreactivity were unchanged despite a significant 25% depletion of substance P-like immunoreactivity and gamma-aminobutyric acid. Ischemic brain damage may be mediated by a neurotoxic effect of glutamate acting at the N-methyl-D-aspartate (NMDA) receptor. Previous studies of NMDA excitotoxin lesions in rat striatum have shown a sparing of neurons containing NADPH-diaphorase, somatostatin, and neuropeptide Y. The similar sparing of these neurons following ischemic lesions in gerbil striatum provides further evidence that NMDA receptor activation may play a role in ischemic injury.
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PMID:Selective sparing of NADPH-diaphorase-somatostatin-neuropeptide Y neurons in ischemic gerbil striatum. 197 76

On the material of early autopsies of the above patients the activity of the following myocardial enzymes was undergone the quantitative histochemical study: succinate, lactate, (beta-oxybutyrate, d-glycerophosphate, glucose 6-phosphate and alcohol dehydrogenase, NAD-diaphorase, catalase, phosphorylase. The increase of the activity of practically all enzymes studied was observed in the myocardial areas with no circulation disturbances. This increase was due to the moderate myocardial hypertrophy. On the contrary, in the areas with a non-even blood supply (ischemia) the decrease of the activity of all oxidative-reductive enzymes was observed. The presence of such foci in the myocardium which occur in 70% cases studied facilitates the development of the ventricular fibrillation with a fatal outcome. The enzyme depression is particularly pronounced against the background of a high alcoholic content.
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PMID:[A histochemical study of enzyme activity in the myocardium of victims of sudden death with small-focal cardiosclerosis]. 259 77

Excitatory amino acids have been implicated in ischemic neuronal injury. To test this hypothesis in neonatal hypoxia-ischemia, lesions of the cortex and striatum were induced in 7-day-old rats by unilaterally ligating their carotid arteries and subjecting them to hypoxic conditions for 2 hours. Brains examined 1 week later demonstrated, within the regions of ischemic damage, a striking preservation of neurons that stained histochemically for nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d) activity. Concentrations of the neuropeptides somatostatin and neuropeptide Y, which colocalize in neurons containing NADPH-d, were unaffected in the areas of ischemic damage. The same pattern of injury with sparing of NADPH-d-reactive neurons was reproduced by focal microinfusion of the excitotoxin quinolinic acid, an endogenous N-methyl-d-aspartate (NMDA) agonist, into the striatum. These results support the hypothesis that neonatal hypoxic-ischemic injury is mediated through excitatory transmitters acting at the NMDA receptor and that the NADPH-d-reactive neurons in the neonate are resistant to excitotoxic damage. This pattern of cell vulnerability is unique to the developing striatum and may relate to the distinct pathological appearance of the basal ganglia that follows neonatal asphyxia.
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PMID:Selective sparing of NADPH-diaphorase neurons in neonatal hypoxia-ischemia. 290 92

After ischemia (3, 6, 9 and 12 h) of the hind extremities in dogs with a subsequent revascularization for 2 h, enzymatic activity of hepatocytes changes. After ischemia for 3 h the enzymatic activity increases. Restoration of the blood flow at later stages of the experiment results in a progressive decrease of dehydrogenase and diaphorase activities. To a greater extend the changes of the enzymatic activity are observed in perivenular hepatocytes (in the 3d zone of the hepatic acinus).
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PMID:[Changes in hepatocyte dehydrogenase activity in different zones of liver acini during the revascularization of ischemic extremities]. 341 96

To evaluate the diagnostic role of histochemically demonstrated aerobic dehydrogenases in ischemic myocardial injury NADH-diaphorase, succinate dehydrogenase (SDH), beta-hydroxybutyrate dehydrogenase (HBDH) and malate dehydrogenase (MDH) were demonstrated histochemically and the corresponding enzyme activities were measured biochemically in isolated perfused rats hearts after global ischemia from 0 to 12 h. The present data show that the enzyme-histochemical methods when used properly are more sensitive indicators of early ischemic injury than classical histological staining procedures. From the enzymes tested here the histochemical demonstration of HBDH turned out to be best suited for use when suspecting ischemic myocardial injury at autopsy.
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PMID:Oxidative enzyme activities and respective histochemical reactions in ischemic rat myocardium. 342 4

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

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

The effect of transient forebrain ischemia on NADPH-diaphorase-containing neurons was examined in the dentate gyrus of the gerbil. NADPH-diaphorase histochemistry was performed in animals subjected to temporary occlusion of the common carotid arteries and sham-operated animals. Seven days following transient ischemia, the number of NADPH-diaphorase-positive neurons in the infragranular zone of the dentate gyrus was reduced by approximately 50% compared with control animals. Since neighboring granule cells are known to be resistant to this level of ischemic challenge, the present observations indicate that NADPH-diaphorase-containing neurons in the dentate gyrus are selectively vulnerable to brief ischemia.
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PMID:Selective loss of NADPH-diaphorase-containing neurons in the dentate gyrus following transient ischemia. 750 92


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