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)

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

We have examined the morphology and distribution of neurones that contain nicotinamide adenine dinucleotide phosphate (NADPH) diaphorase in human retinae. NADPH-diaphorase reactivity was observed in three different classes of amacrine cells (ND1, ND2, ND3 cells) and in the cone photoreceptors. ND1 cells had relatively large somata (mean, 12.3 microns) located in the inner nuclear layer (INL) and in the ganglion cell layer (GCL). Their dendrites were often strongly labeled and spread into either the middle or outer strata of the inner plexiform layer (IPL). The somata of ND2 cells were medium-sized (mean, 8.2 microns) and located in the INL and in the GCL; their dendrites were usually beaded and often spread in either the middle or outer strata of the IPL. ND3 cells had small, round somata (mean, 5.2 microns) located in either the INL or GCL, and were without labeled processes. The total number of NADPH-diaphorase cells (all classes) was estimated at 118,000, with a mean density of about 100/mm2. The most striking feature of NADPH-diaphorase cells in humans was that their distribution was relatively uniform across the retina, with no evidence of a peak in density at the foveal rim.
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PMID:NADPH-diaphorase neurones of human retinae have a uniform topographical distribution. 227 37

Age-related changes of reduced nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d)-containing neurons were examined quantitatively in the laterodorsal tegmental nucleus (TLD) and the caudate-putamen of mice. Six 2-month-old and six 25- to 30-month-old DDD mice were studied using computer-assisted image analysis. Although no age-related changes in neuronal counts were found in the TLD, the cell size in this nucleus showed a statistically significant reduction with aging. In addition, the degree of the age-related neuronal shrinkage differed within the TLD; the most significant occurring in the rostral, less in the caudal third and no significant alteration being found in the middle third portion of TLD. In contrast, NADPH-d-positive neurons in the striatum did not show distinct age-related changes. NADPH-d-containing neurons in the TLD correspond to cholinergic cells, which project to the forebrain. Thus, the age-related shrinkage of NADPH-d neurons in the TLD may be related to the cholinergic dysfunctions seen in the forebrain of senescent mice.
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PMID:Effect of aging on NADPH-diaphorase neurons in laterodorsal tegmental nucleus and striatum of mice. 236 51

Calcineurin, a multifunctional Ca2+ (divalent cations)-dependent calmodulin-stimulated phosphoprotein phosphatase, has been reported to be present in the striatal neurons which project to the globus pallidus and the substantia nigra. In the present study, we examined what types of cells in the rat striatum express calcineurin. The calcineurin-positive neurons were of medium size (mean diameter of 16 microns) and constituted about 60-70% of the total neuronal population in the striatum. Under light microscopy, the calcineurin-positive neurons had round, triangular, or polygonal cell bodies with a relatively small amount of cytoplasm. Electron microscopic examination of 20 randomly selected striatal calcineurin-immunoreactive neurons revealed that their nuclei did not show any invaginations or intranuclear inclusions. The calcineurin-positive neurons were characterized by Golgi impregnation as the densely spinous type. On the other hand, it was demonstrated that calcineurin-positive neurons are a separate population from the diisopropylfluorophosphate-acetylcholinesterase-positive cells or nicotinamide adenine dinucleotide phosphate diaphorase-positive cells, by means of the combination of immunocytochemistry and enzyme histochemistry. In addition, simultaneous localization of calcineurin and substance P in a single cell was observed in some striatal neurons using a double immunostaining method. On the basis of these findings, it was considered that most calcineurin-immunoreactive neurons in the rat striatum may be classified as medium-size densely spiny neurons.
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PMID:Morphological characterization of the rat striatal neurons expressing calcineurin immunoreactivity. 244 61

Plexiform areas are functionally important units of the pineal complex. The silver impregnation technique by Matsuyama (1972) reveals in the frog that nerve fibres branch and terminate in these areas and that they are presynaptic to nerve cells which are part of the plexiform areas. Histochemically, the nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-diaphorase) method according to Scherer-Singler et al. (1983) indicates that pinealocytes and nerve cells are both stained, a strong stratification of different cell types can be visualized. Plexiform areas of different size exist at the dorsal and ventral surface of the organ; the biggest are located rostrodorsally. Approximately twenty large multipolar nerve cells are localized at the ventral surface of the pineal organ mainly at the rostral and lateral borders. They send long processes mainly in caudal direction. These processes are post-synaptic to the boutons of the endfeet belonging to photosensitive pinealocytes. Processes of several multipolar nerve cells converge to one plexiform area, branch and obviously terminate there. As in horizontal cells the processes of the multipolar cells seem to be capable of both receiving and transmitting signals. On the postsynaptic side of the processes of the multipolar cells are smaller nerve cells juxtaposed to the plexiform areas. They are known as pseudounipolar, unipolar or bipolar cells (Wake et al., 1974); the latter are free of boutons of the pinealocytes, their axons forming the pineal tract. Three different types of photosensitive pinealocytes can be distinguished: a slender, a spherical and a double-cone type. Also, the number of boutons varies in the endfeet: boutons occur alone, in groups of two or three, and in clusters.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The neural organization of the pineal complex in the frog: stratification and regional differences. 251 Aug 1

Enzymes in the human myocardium following sudden death were examined for activity in a quantitative histoenzymological study, these were NAD-dependent dehadrogenases of succinate (SDG), lactate (LDG), beta-hydroxybutyrate (beta-HOBDG), alpha-glycerophosphate (alpha-GPDG), alcohol (ADG), glucoso-6-phosphate (G-6-PDG), and NAD-diaphorase (NADse), and catalase. Autopsies were performed within 3 h after death. beta-HOBDG and LDG were found to show an increase in activity in the cardiomyocytes of sudden death subjects with coronary heart disease without apparent changes. In the myocardium from death subjects with coronary heart disease and large postinfarct cardiosclerosis, the activity of the enzymes was directly related to the severity of myocardial hypertrophy and signs of chronic heart failure. As myocardial hypertrophy developed, the enzyme activity increased; when there appeared signs of chronic heart failure it decreased. The myocardium from sudden death subjects with alcoholic cardiomyopathy showed diminished redox enzyme activity and higher activity of the enzyme utilizing alcohol (ADG and catalase). The findings suggest that changes in the enzyme activity in the myocardium are of various type and depend on previous cardiac abnormalities.
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PMID:Quantitative histoenzymological characteristics of the myocardium in sudden cardiac death. 252 98

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

Retrograde transport of fluorescent tracers and nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) histochemical techniques were combined in a study of septohippocampal projections in the rat. The dorsal (DH) and ventral (VH) hippocampus were simultaneously injected with different tracers (Fast Blue or Fluoro-Gold). Histochemical procedures revealed many NADPH-d positive cells located in the medial septum and the horizontal limb of the diagonal band. In the medial septum, NADPH-d positive neurons were mostly located lateral to the midline region and some of these were double-labeled by the tracer injected into the VH. Also, NADPH-d positive cells were found in the horizontal diagonal band and some of these were double-labeled following injections into the DH. No fluorescence/NADPH-d double-labeled neurons were observed in other structures known to project to the hippocampus.
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PMID:A study of NADPH-diaphorase positive septohippocampal neurons in rat. 261 69

The metabolism of chemical carcinogens was investigated in liver preparations from 28 captive woodchucks (Marmota monax). Of these, 23 were naturally infected with the woodchuck hepatitis virus (WHV), and eight also had primary hepatocellular carcinoma (PHC). Twenty-nine parameters were investigated in liver subcellular fractions, including cross-reactivity with HBsAg, and biochemical parameters, such as gamma-glutamyl transpeptidase, cytochrome P-450 and microsomal monooxygenases (aryl hydrocarbon hydroxylase, ethoxycoumarin and ethoxyresorufin deethylases, aminopyrine and dimethylnitrosamine demethylases, and testosterone 7 alpha-, 16 alpha- and 6 beta-hydroxylases), uridine 5'-diphosphoglucuronosyl transferase, GSH and related enzymes (peroxidase, reductase and S-transferase), as well as other cytosolic enzyme activities (glucose 6-phosphate and 6-phosphogluconate dehydrogenases, NADPH- and NADH-dependent diaphorases, and DT diaphorase). In addition, liver preparations were used in order to quantify the metabolic activation into bacterial mutagens of five procarcinogens (aflatoxin B1, the pyrolysis products Trp-P-2 and MeIQ, 2-aminofluorene and dimethylnitrosamine) and the decrease of potency of three direct-acting mutagens (sodium dichromate, ICR 191 and 4-nitroquinoline 1-oxide). WHV infection produced a significant stimulation of carcinogen metabolism, as shown by the simultaneous change in detoxification parameters (GSH depletion) and activation indices (enhancement of microsomal monooxygenases and of procarcinogen activation into mutagenic metabolites). There were no significant differences between WHV-positive samples from animals without PHC and the noncancerous tissue of PHC-bearing animals, whereas a decrease of both activation and detoxification indices was recorded in the tumorous tissue. There was a considerable interindividual variability among WHV carriers, which was tentatively ascribed to genetic factors. Pregnancy was the only known factor influencing the results in WHV carriers. However, even by excluding pregnant animals, the effects on carcinogen metabolism produced by WHV infection were still statistically significant. These results, together with previous data obtained in humans, revealed that metabolic factors may play a role in the synergism between viral hepatitis and chemical hepatocarcinogens in the etiopathogenesis of PHC.
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PMID:Enhanced metabolic activation of chemical hepatocarcinogens in woodchucks infected with hepatitis B virus. 272 Sep 3

Neurofibrillary tangles in Alzheimer's disease show a predilection for cortical pyramidal and subcortical projection neurons. The antigenic composition, neuronal specificity and distribution of aluminum-induced neurofibrillary degeneration were examined in regions of rabbit brain analogous to those that develop neurofibrillary tangles in Alzheimer's disease. Neurofibrillary degeneration was induced by intraventricular instillation of aluminum chloride. In aluminum-treated rabbits, intensely immunoreactive filamentous aggregates were seen in affected neuronal perikarya after staining with an antiphosphorylated neurofilament antibody (SMI 31), while in controls immunoreactivity was confined to axon-like elements. Monoclonal antibodies against Microtubule-associated protein 2 and tau, which stain human neurofibrillary tangles, did not stain aluminum-induced neurofibrillary degeneration. Pyramidal neurons exhibiting neurofibrillary degeneration formed a discrete linear pattern in layers III and V of cortex. Cortical somatostatin and nicotinamide adenine dinucleotide phosphate diaphorase-reactive neurons identified in double-stained sections were unaffected. Large perikarya in the vicinity of the globus pallidus, some of which contained acetylcholinesterase, were frequently SMI 31-immunoreactive. Among the cell groups affected in the upper brainstem were the nucleus raphe dorsalis and locus coeruleus. These findings show that aluminum-induced neurofibrillary degeneration differs antigenically from neurofibrillary tangles in Alzheimer's disease. Nevertheless, many neuronal subsets that are particularly susceptible to Alzheimer's disease, including cortical pyramidal neurons, basal forebrain cholinergic neurons and upper brainstem catecholaminergic neurons, are also affected by aluminum-induced neurofibrillary degeneration.
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PMID:Aluminum-induced neurofibrillary degeneration affects a subset of neurons in rabbit cerebral cortex, basal forebrain and upper brainstem. 272 61


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