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 evaluation of NADPH-diaphorase in the post-mitochondrial fraction of rat liver has been shown a sensitive method to estimate alterations of microsomal oxidase systems in acute and chronic intoxications. It is also useful to demonstrate the interaction of drugs with barbiturates, which normally induce this enzyme. To study the biochemical liver damage which may occur in the toxic rapeseed oil syndrome, we measured NADPH-diaphorase in the post-mitochondrial fraction of rats given oral doses of toxic rapeseed oil (1 ml/day for 6 days), or oleil or linoleil anilide (10 mg/kg for 6 days). One-half the rats were sacrificed at the end of the dosing period and the other half were killed 4 weeks later. In both circumstances one-half the rats were treated with 2 doses of 80 mg phenobarbital/kg. NADPH-diaphorase was strongly inhibited by toxic oil and fatty acid anilides (72-93%). Phenobarbital induction was completely depressed. Enzyme activity remained depressed after a 4-week latency period.
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PMID:NADPH-diaphorase used to estimate alterations in the toxic rapeseed oil syndrome. 665 3

In a search for airway epithelial mechanisms that may affect the subepithelial microcirculation, we examined plasma exudation responses to NG-nitro-L-arginine-methyl ester (L-NAME), a nitric oxide synthase (NOS) inhibitor. L-NAME was applied topically on the tracheal mucosa of guinea pigs that had previously received 125I-albumin and/or colloidal gold particles (5 nm) intravenously. Luminal entry of plasma was determined by the levels of 125I-albumin in tracheal lavage fluid. Topical L-NAME (2.2, 9, and 22 mumol), but not intravenous L-NAME (375 mumol/kg), produced plasma exudation into the airway lumen (p < 0.01 to p < 0.001). The L-NAME enantiomer NG-nitro-D-arginine-methyl ester (D-NAME, 9 mumol) produced no exudative response. Coadministration of L-arginine (27 mumol) abolished the L-NAME-induced exudation. The extravasated plasma was distributed in the lamina propria and between epithelial cells (colloidal gold). The epithelial surface structure (scanning electron microscopy) appeared intact. Staining with nicotinamide adenine dinucleotide phosphate (NADPH)-diaphorase suggested that epithelial basal may contain nitric oxide synthases. We suggest that endogenously released nitric oxide from epithelial or other superficial cells tonically suppresses the macromolecular permeability of the subepithelial microcirculation.
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PMID:Mucosal nitric oxide may tonically suppress airways plasma exudation. 802 53