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)

Nitric oxide (NO) plays an important physiological role in regulating gastrointestinal motility. Involvement of endogenous NO was evaluated in the response to non-adrenergic, non-cholinergic (NANC) nerve stimulation of the dog sphincter muscle of Oddi. Transmural electrical stimulation (TES), nicotine (10(-5) M) and K+ (10 mM) produced only a relaxation in the sphincter muscle strips contracted with substance P, which was not potentiated by atropine. The TES-induced relaxation was abolished by tetrodotoxin (3 x 10(-7) M) and oxyhaemoglobin (1.6 x 10(-5) M), but not affected by atropine (10(-7) M), propranolol (10(-7) M), phentolamine (10(-7) M), indomethacin (10(-6) M), cholecystokinin (CCK, 10(-8) M) and vasoactive intestinal polypeptide (VIP, 10(-8) M). The relaxation was also abolished by treatment with NG-nitro-L-arginine (L-NA, 10(-5) M), an NO synthase inhibitor. Nicotine produced a transient relaxation, which was abolished by tetrodotoxin, hexamethonium (10(-5) M) and L-NA, but not affected by atropine and NG-nitro-D-arginine (D-NA, 10(-5) M). The addition of K+ elicited a transient relaxation, which was abolished by tetrodotoxin and L-NA. The inhibitory effects of L-NA were antagonized by L-arginine (10(-3) M). The presence of neurons containing nicotinamide adenine dinucleotide phosphate (NADPH)-diaphorase was histochemically demonstrated in the sphincter of Oddi. These findings may indicate that TES, nicotine and K+ liberate NO from NANC inhibitory nerve which is involved in the relaxation of the dog sphincter of Oddi. The muscular tone does not seem to be regulated by cholinergic nerves under the experimental conditions used.
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PMID:Functional role and histological demonstration of nitric-oxide-mediated inhibitory nerves in dog sphincter of Oddi. 857 10

Nicotine adenine dinucleotide phosphate-diaphorase staining was used to study nitric oxide synthase activity and distribution in the midbrain visual structures of white leghorn chick embryos and post-hatched chickens. Enzyme staining first appeared in the isthmic region at the tenth embryonic day (E10) in the neuropil of the nucleus isthmi, pars parvocellularis. At E11 faint enzyme positivity appeared also in the nucl. isthmi pars magnocellularis, the nucl. semilunaris and the nucl. isthmo-opticus. The staining intensity of the isthmic nuclei dramatically increased between the 12.5th and the 13th days of incubation. The nucl. isthmi, pars parvocellularis showed the strongest enzyme reaction throughout embryonic life. A day before hatching all the isthmic nuclei were heavily stained, however, nicotine adenine dinucleotide phosphate-diaphorase-positive cells occurred exclusively in the nucleus isthmo-opticus. In the tectum opticum, intensely stained cells occupied the stratum fibrosum et griseum superficiale. The layer containing the projection neurons to the isthmo-optic nucleus was unstained. In the isthmic region, the intensity of staining surpassed that of the tectum and reached its maximum at E17 and then slowly decreased till the end of the experimental period (120 days post-hatched). The tractus isthmo-opticus showed nicotine adenine dinucleotide phosphate-diaphorase activity throughout the investigated period of life of the chicken, but the tractus tectoisthmo-opticus was unstained. Our results suggest that in the isthmic nuclei, nicotine adenine dinucleotide phosphate-diaphorase-positive neurons occur only in the isthmo-optic nucleus and optic tectum. The other positively stained structures are the fibers and terminals of tectal cells. In most brain areas nicotine adenine dinucleotide phosphate-diaphorase indicates nitric oxide synthase that produces nitric oxide. The transient appearance of this molecule is probably necessary for neuronal differentiation or the establishment of synaptic connections in the isthmic nuclei, and these developmental changes are under the control of the optic tectum.
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PMID:Developmental changes of NADPH-diaphorase positive structures in the isthmic nuclei of the chick. 1090 5

Effect of nicotine on nitric oxide synthase (NOS) expression in various hypothalamic regions was investigated in rats via nicotineamide adenine dinucleotide phosphate-diaphorase (NADPH-d) histochemistry. Sprague-Dawley rats were divided into the fed group, the fed and nicotine-treated group, the food-deprived group, and the food-deprived and nicotine-treated group. The fed groups received abundant food and water, while food was withheld from the food-deprived groups for 48 h. The nicotine-treated groups were injected with nicotine. Following food deprivation, enhanced NAPDH-d expression was detected in the paraventricular nucleus, ventromedial hypothalamic nucleus, and lateral hypothalamic area of the hypothalamus. Nicotine administration to the food-deprived rats resulted in decreased NADPH-d positivity. The present results indicate that nicotine administration is effective in limiting the enhancement in NOS expression following food restriction.
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PMID:Nicotine administration decreases nitric oxide synthase expression in the hypothalamus of food-deprived rats. 1195 36

Nitric oxide (NO) has been implicated in neurotoxicity and cerebral blood flow changes in chronic neurodegeneration, but its activity in the mammalian prion diseases has not been studied in detail. Nicotine adenine dinucleotide phosphate (NADPH)-diaphorase (NADPH-d) histochemistry is a simple and robust histochemical procedure that allows localization of the tissue distribution of NO synthases. The aim of the present study is to assess whether NADPH-d histochemical activity is altered in the hippocampus in the ME7 model of prion disease in C57BL/6J mice. At early and late stages after the initiation of the disease we assessed features of the NADPH-d positive cells and the neuropil histochemical activity in CA1 and dentate gyrus using densitometric analysis. In C57BL/6J mice 13 weeks postinjection of the prion agent ME7, when behavioural changes first become apparent, neuropil NADPH-d histochemical staining increases, whereas at late stages it decreases dramatically. Both type I and type II NADPH-d positive cells were found to survive throughout the hippocampal formation into the late stages of the disease, but diaphorase activity was reduced in dendritic branches and abnormal varicosities were present in both dendritic and axonal processes of NADPH-d positive type I cells. The pathophysiological implications of the results remain to be investigated but both blood flow alteration and NO neurotoxicity may be features of the disease.
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PMID:Neuropil and neuronal changes in hippocampal NADPH-diaphorase histochemistry in the ME7 model of murine prion disease. 1517 82

Nicotine was shown to be associated with mature vacuoles isolated from protoplasts of Nicotiana rustica. The vacuolar preparations also contained high levels of acid phosphatase, ATPase, and approximately 30% of the soluble protoplastic protein. The contamination of the vacuolar isolate by chlorophyll, succinate dehydrogenase, and NADPH cytochrome c reductase (markers for chloroplasts, mitochondria, and endoplasmic reticulum) was low. The enzymic activity associated with the vacuoles was not due to the exogenously supplied digestive enzymes used in the preparation of the protoplast. The relatively easy isolation of tobacco vacuoles makes this an excellent system for biochemical investigations of the vacuole.
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PMID:Investigations of vacuoles isolated from tobacco: I. Quantitation of nicotine. 1666 Sep 18

The dorsal raphe nucleus (DRN), a major source of forebrain serotonin, mediates various neural functions including anxiety. The nucleus locus coeruleus (LC) is likewise involved in mediating central components of the stress response and anxiety. An anxiety-reducing effect is widely believed to underlie many cases of nicotine dependence. While much is known about nicotine-serotonin interactions, little is known about how nicotine engages the DRN non-serotonergic domain in specific physiological functions that influence organismal behavior. The aim of this study was to determine how chronic nicotine withdrawal influences neuronal nitric oxide (NO) synthase (nNOS) and galanin immunoreactivity in the DRN and LC of adult rats. Compared with saline, nicotine increased nicotinamide adenine dinucleotide phosphate diaphorase profiles within distinct DRN subregions and also enhanced intensity in nNOS and galanin cell bodies in the rostral DRN as well as galanin in the LC. Nicotine-induced nNOS/galanin staining of somata was abundant in the rostral ventromedial DRN. Galanin-positive terminals surrounded nNOS-containing cell bodies in the DRN lateral wing subregions. These observations suggest that the DRN NOS-galanin domain and galanin in the LC are engaged in the organism's neural adaptation to chronic nicotine exposure. Hence NO and galanin synthesized or released within the DRN and LC or at the respective target sites might regulate the whole animal behavioral response to nicotine exposure.
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PMID:Nicotine withdrawal upregulates nitrergic and galaninergic activity in the rat dorsal raphe nucleus and locus coeruleus. 2330 19