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 case of a 35 years-old man, with chronic proximal muscle atrophy in which at the muscle biopsy tubular aggregates were found by histochemistry procedures is reported. The tubular aggregates stained positive with the modified Gomori trichrome, haematoxylin-eosin, DPNH-diaphorase, non specific esterases, phosphorylase, P.A.S., oil red O and lactate dehydrogenase. They did not show in the routine and acid pre-incubated ATPase, acid and alkaline phosphatases and succinate dehydrogenase. Only found in type II fibers. A brief discussion about the pathogenesis and function of the tubular aggregates is made. The authors believe that the tubular aggregates in this case are secondary to prolonged use of phenobarbital and diphenylhydantoin, associated with the basic denervation process and alcohol abuse.
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PMID:[Tubular aggregates in a case of chronic proximal spinal atrophy]. 8 34

Nitric oxide synthase (NOS), the enzyme with reduced nicotinamide-adenine dinucleotide phosphate (NADPH)-diaphorase activity, generates nitric oxide (NO) which is an important bioregulatory molecule in the nervous, immune, and cardiovascular systems. NOS is linked to non-adrenergic non-cholinergic (NANC) neuronal pathways and modulation of the N-methyl-D-aspartate receptors, yet its modification by ethanol has been little explored. A possible modification by chronic ethanol administration of activity and/or localization of NADPH-diaphorase (NO-synthase) in rat brain may thus provide the pathogenic basis of alcohol-induced brain injury. When female Wistar rats were treated chronically with ethanol for 50 days, the NADPH-diaphorase staining of granular neurons and neurons located in the molecular layer of the cerebral cortex was significantly reduced. Chronic ethanol consumption led to a significant reduction in NADPH-diaphorase staining in the superficial layers of the superior colliculus. The number of NADPH-diaphorase-positive neurons was significantly reduced (P < 0.001) in the stratum zonale and stratum griseum superficiale (by 42.3-65.6% of control values). This could alter synaptic processes in the highly organized structures involved in oculomotor and somatic motor coordination and thus contribute to the motor disturbances which are associated with alcohol abuse.
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PMID:The influence of chronic moderate ethanol administration on NADPH-diaphorase (nitric oxide synthase) activity in rat brain. 971 91

Alcohol-induced oxidative stress is linked to the metabolism of ethanol. Three metabolic pathways of ethanol have been described in the human body so far. They involve the following enzymes: alcohol dehydrogenase, microsomal ethanol oxidation system (MEOS) and catalase. Each of these pathways could produce free radicals which affect the antioxidant system. Ethanol per se, hyperlactacidemia and elevated NADH increase xanthine oxidase activity, which results in the production of superoxide. Lipid peroxidation and superoxide production correlate with the amount of cytochrome P450 2E1. MEOS aggravates the oxidative stress directly as well as indirectly by impairing the defense systems. Hydroxyethyl radicals are probably involved in the alkylation of hepatic proteins. Nitric oxide (NO) is one of the key factors contributing to the vessel wall homeostasis, an important mediator of the vascular tone and neuronal transduction, and has cytotoxic effects. Stable metabolites--nitrites and nitrates--were increased in alcoholics (34.3 +/- 2.6 vs. 22.7 +/- 1.2 micromol/l, p < 0.001). High NO concentration could be discussed for its excitotoxicity and may be linked to cytotoxicity in neurons, glia and myelin. Formation of NO has been linked to an increased preference for and tolerance to alcohol in recent studies. Increased NO biosynthesis also via inducible NO synthase (NOS, chronic stimulation) may contribute to platelet and endothelial dysfunctions. Comparison of chronically ethanol-fed rats and controls demonstrates that exposure to ethanol causes a decrease in NADPH diaphorase activity (neuronal NOS) in neurons and fibers of the cerebellar cortex and superior colliculus (stratum griseum superficiale and intermedium) in rats. These changes in the highly organized structure contribute to the motor disturbances, which are associated with alcohol abuse. Antiphospholipid antibodies (APA) in alcoholic patients seem to reflect membrane lesions, impairment of immunological reactivity, liver disease progression, and they correlate significantly with the disease severity. The low-density lipoprotein (LDL) oxidation is supposed to be one of the most important pathogenic mechanisms of atherogenesis, and antibodies against oxidized LDL (oxLDL) are some kind of epiphenomenon of this process. We studied IgG oxLDL and four APA (anticardiolipin, antiphosphatidylserine, antiphosphatidylethanolamine and antiphosphatidylcholine antibodies). The IgG oxLDL (406.4 +/- 52.5 vs. 499.9 +/- 52.5 mU/ml) was not affected in alcoholic patients, but oxLDL was higher (71.6 +/- 4.1 vs. 44.2 +/- 2.7 micromol/l, p < 0.001). The prevalence of studied APA in alcoholics with mildly affected liver function was higher than in controls, but not significantly. On the contrary, changes of autoantibodies to IgG oxLDL revealed a wide range of IgG oxLDL titers in a healthy population. These parameters do not appear to be very promising for the evaluation of the risk of atherosclerosis. Free radicals increase the oxidative modification of LDL. This is one of the most important mechanisms, which increases cardiovascular risk in chronic alcoholic patients. Important enzymatic antioxidant systems - superoxide dismutase and glutathione peroxidase - are decreased in alcoholics. We did not find any changes of serum retinol and tocopherol concentrations in alcoholics, and blood and plasma selenium and copper levels were unchanged as well. Only the zinc concentration was decreased in plasma. It could be related to the impairment of the immune system in alcoholics. Measurement of these parameters in blood compartments does not seem to indicate a possible organ, e.g. liver deficiency.
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PMID:Oxidative stress, metabolism of ethanol and alcohol-related diseases. 1117 77