Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.6.99.1 (NADPH-diaphorase)
 3,903 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The ventral lateral geniculate nucleus (vLGN) of the tree shrew (Tupaia belangeri) was differentiated into multiple subdivisions (dorsal cap, intergeniculate leaflet, parvicellular segment, and internal and external magnocellular laminae, the latter being further divisible into a lateral and medial division) on the basis of retinal projections, immunochemistry, and histochemistry. Retinal projections traced with intravitreal injections of wheat germ agglutinin conjugated horseradish peroxidase revealed direct bilateral input to all subregions of the vLGN, except for the internal magnocellular lamina (which received only contralateral input) and the parvicellular segment (which was not retinorecipient). Furthermore, retinal inputs clearly distinguished the relatively heavily retinorecipient intergeniculate leaflet from the less prominently labeled dorsal cap. Immunohistochemical localization of Neuropeptide Y (NPY) perikarya revealed their prominence in the intergeniculate leaflet and the external magnocellular laminae with a concentration along the optic tract. NPY immunoreactive fibers were seen in all but the parvicellular subregion. Gamma amino butyric acid immunoreactivity was seen throughout the vLGN, but was most concentrated in the dorsal cap and the magnocellular laminae, followed by the intergeniculate leaflet. Histochemical studies of cytochrome oxidase and nicotinamide adenosine dinucleotide phosphate (NADPH)-diaphorase localization revealed similar patterns of dense reactivity within the external magnocellular lamina, intergeniculate leaflet and dorsal cap, and somewhat less dense, but substantial reactivity in the internal magnocellular lamina. Within the external magnocellular lamina, cells reactive for cytochrome oxidase were noted in the lateral portion bordering the optic tract, whereas those specific for NADPH-diaphorase were dispersed throughout the lamina. Poor reactivity for both histochemical markers was evident in the parvicellular segment. Overall, the markedly different patterns of retinal input and neurochemical organization between the subdivisions of the tree shrew vLGN suggest their involvement in diverse functions. Furthermore, the basic similarity of the organization of the tree shrew vLGN to that of the taxonomically unrelated ground squirrel may indicate a common mammalian scheme.
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PMID:Immunohistochemical organization of the ventral lateral geniculate nucleus in the tree shrew. 131 86

Methylthioketobutyric acid has been used as an indicator for the production of reactive oxygen species during incubation with xanthine oxidase or NADH diaphorase in the presence of an autooxidizable quinone. The production of OH-radical-type oxidants is enhanced in the presence of crocidolite but not by the asbestos types chrysotile or amosite. This activity of crocidolite in the diaphorase system is further stimulated by bisulfite. Crocidolite-dependent ethylene formation from methylthioketo-butyric acid is inhibited by both superoxide dismutase and catalase. In the presence of both crocidolite and bisulfite, however, the inhibition by superoxide dismutase is preserved, but the inhibition by catalase is lost. Since in some respect the NADH-diaphorase quinone system may reflect the situation in the activated macrophage, crocidolite activation may represent a biochemical model system describing potential asbestos toxicity.
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PMID:Cooperative stimulation by sulfite and crocidolite asbestos fibres of enzyme catalyzed production of reactive oxygen species. 285 63

Both phenylbutazon and mofebutazon inhibit oxidative fragmentation of the methionine derivative, 2-keto-4-methylthio-butyric acid (KMB) by xanthine oxidase--or diaphorase mediated OH radical production. Differentiation of the two non-steroidal antiinflammatory drugs is possible by means of determining oxygen reduction by xanthine oxidase or diaphorase in the presence of the naphthoquinone, juglone, where only mofebutazon shows an inhibitory effect.
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PMID:Antioxidative properties of phenazone derivatives: differentiation between phenylbutazon and mofebutazon. 821 10

Neocortical neurons that utilise nitric oxide (NO) differ in morphology in different mammalian species. In the present study we examine these differences in the neocortex of mouse, rat, guinea-pig, rabbit, cat and monkey using histochemistry for nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) and immunocytochemistry for nitric oxide synthase (NOS), gamma amino-butyric acid (GABA), calbindin (CB), parvalbumin (PV) and calretinin (CR). NO neurons are non-pyramidal and can be divided into two distinct types, both of which react for NOS and NADPH-d. Type I neurons have a relatively large soma with heavy reaction product filling even the fine processes. They occur in all species, mainly near the border between the cortex and white matter, with fewer in the cortex, mostly in the superficial layers (II-IV). Type II cells are more numerous, smaller, and lighter in reactivity. They are in all species examined here except rodents, and in all cortical layers, but mainly layers II-IV. Most intracortical and some subcortical Type I neurons express GABA. A few intracortical Type I cells contain CB. All Type II cells express GABA and most also CB. Neither Type I nor Type II cells stain for PV or CR. We conclude that there is a tendency for a reduction of Type I cells, and increase of Type II, in mammalian neocortex with phylogeny.
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PMID:Morphological diversity of nitric oxide synthesising neurons in mammalian cerebral cortex. 917 29

NADPH diaphorase activity in the rabbit retina is modulated by the state of visual adaptation. In this study, we tested possible glutamatergic control of this phenomenon. Rabbits were injected intravitreally with agonists and antagonists of glutamate. After adaptation (3 hours) to either room light or darkness, the rabbits were killed and the retinae were prepared for NADPH diaphorase histochemistry. Kainic acid significantly reduced the number of NADPH diaphorase amacrine cells but augmented NADPH diaphorase activity in horizontal cells in both light- and dark-adapted animals. 6,7-Dinitroquinoxaline-2,3(1H,4H)-dione exerted no effect on amacrine cells but eliminated NADPH diaphorase activity in horizontal cells. 2-Amino-4-phosphono butyric acid did not affect NADPH diaphorase activity in horizontal cells but reduced the degree of staining in the neuronal processes of amacrine cells. MK-801 and N-methyl-D-aspartic acid (NMDA) had no effect on NADPH diaphorase activity in horizontal cells. However, MK-801 reduced staining in the neuronal processes of amacrine cells but not in their cell bodies. NMDA effects were expressed in a significant reduction in the number and size of amacrine cells that were NADPH diaphorase positive. These results indicate that activation of NADPH diaphorase in horizontal cells by darkness is mediated by the activation of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)/kainic acid (KA)-type glutamate receptors. The ON pathway in the retina is probably involved in modulation of NADPH diaphorase in the neuronal processes of amacrine cells. Amacrine cells that are NADPH diaphorase positive contain NMDA-type and AMPA/KA-type receptors and are highly susceptible to NMDA and kainic acid toxicity.
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PMID:NADPH diaphorase activity in the rabbit retina is modulated by glutamatergic pathways. 1116 88

Primary dystonia is a common movement disorder with an unknown pathophysiology, but basal ganglia dysfunctions seem to play a critical role. Previous studies in the dtsz mutant hamster, an animal model of primary paroxysmal dystonia, demonstrated a deficit of striatal gamma-amino-butyric acid (GABA) containing interneurons, which normalized at the age of the spontaneous remission of the symptoms. Whereas the reduction of striatal parvalbumin-reactive interneurons is thought to be critically involved in the pathogenesis of dystonia in the hamster mutant, the impact of a reduced density of nitric oxide synthase (NOS) reactive interneurons within the striatum is still unclear. Beside GABA, these interneurons contain somatostatin, neuropeptide Y, nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) and neuronal NOS, an enzyme which produces NO after the activation of the interneurons. In order to clarify if the reduced density of NOS-reactive interneurons contributes by an altered striatal production of nitric oxide (NO) to the occurrence of dystonic attacks in the hamster mutant, we performed microinjections of the NOS inhibitors 7-nitroindazole (7-NI) and Nomega-propyl-L-arginine (NPLA) and of the precursor of NO, L-arginine, into the striata of dtsz hamsters. Neither 7-NI (0.1 and 0.4 microg per hemisphere) and NPLA (2.5, 5 and 7.5 microg per hemisphere) nor L-arginine (9 and 18 microg per hemisphere) exerted any effects on the severity of dystonic movements in the dtsz mutant. Therefore, a critical involvement of striatal changes of NO in the pathophysiology of dystonic attacks in the dtsz hamster cannot be confirmed by the results of these pharmacological examinations. In view of the ontogenetic reduction of the other types of GABAergic interneurons, the deficit of NOS-reactive interneurons is possibly due to the same underlying unknown mechanism, but is less important for the pathophysiology of primary paroxysmal dystonia in the dtsz hamster mutant.
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PMID:Striatal microinjections of nitric oxide synthase inhibitors and L-arginine fail to exert effects on paroxysmal dystonia in the dtsz mutant. 1642 62