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)

NADPH diaphorase histochemistry and NOS-1 immunohistochemistry on 60 microm thick frozen sections of rat extensor digitorum longus muscles led to the detection of prominent rings clearly encompassing the surface of the muscle fibres. These so far unknown costameres were usually found as doublets flanking a space of about 2 microm width. Because these costameric doublets did not appear in regular periods, we designate them irregular costameres to discriminate them from regular ones with a 1 microm periodicity overlying Z-discs and M-lines. Irregular costameres were thicker than the regular ones and free of intercostameres. Immunohistochemistry demonstrated that NOS-1 was co-localized with integral (beta-dystroglycan, alpha-sarcoglycan) and peripheral (caveolin-3, dystrophin) members of the enlarged dystrophin complex in the irregular costameres but not with non-sarcolemmal organized proteins (myosin heavy chain, alpha-actinin, desmin and sarcoplasmic reticulum-located Ca2+-dependent ATPase-1). Invaginations of the sarcolemma to form irregular costameres were observed. In teased myofibres the sarcolemma between two following irregular costameres was ballooned, while the irregular costameres themselves clamped the fibres together. Finally, the number of detectable irregular costameres was significantly increased in maximally contracted extensor digitorum longus muscles generated by electric stimulation but decreased in mechanically stretched ones. Combining these observations, we hypothesize that irregular costameres belong to a reserve zone for the sarcolemma necessary for the contraction/relaxation cycle in myofibres.
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PMID:Irregular costameres represent nitric oxide synthase-1-positive sarcolemma invaginations enriched in contracted skeletal muscle fibres. 1125 90

The effects of an intravenous injection of Interleukin-12 (IL-12) after endotoxin administration and without endotoxin administration on diaphragm muscle were studied using Wistar rats. Three treatment groups, namely a control (Saline+endotoxin) group, an IL-12+endotoxin group and an IL-12 only group were studied. E. coli endotoxin (30 mg/kg) was injected intraperitoneally 5 min after Saline or IL-12 (0.25 microg) injection. In the control group, the force-frequency curves, twitch tension (TT) and slope during contraction time (TT/CT) were significantly lower at 4 h than those at 0 h due to endotoxin (P<0.001, P<0.01 and P<0.01, respectively), and NO production was increased at 4 h as shown by NADPH diaphorase staining. In the IL-12+endotoxin group, the decrement of the force-frequency curves, TT and TT/CT induced by endotoxin at 4 h were significantly prevented compared with those of the control group (P<0.001, P<0.05 and P<0.05, respectively), and NO production was blocked at 4 h. In the IL-12 only group, the force-frequency curves were decreased in the range of high frequency and IL-12 resulted in NO production. Furthermore, the positive muscle fibers detected by NADPH diaphorase staining were classified as type I and IIa muscle fibers by ATPase staining in the control and IL-12 only groups. It is concluded that IL-12 prevents the deterioration of diaphragm muscle contraction induced by endotoxin by reducing NO production in type I and IIa muscle fibers. These results suggest that IL-12 and endotoxin may interfere with each other.
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PMID:Interleukin-12 prevents diaphragm muscle deterioration in a septic animal model. 1169 2

We investigated the relationship between nitric oxide (NO) and Na(+),K(+)-ATPase (NKA) in the gill of anadromous Atlantic salmon. Cells containing NO-producing enzymes were revealed by means of nitric oxide synthase (NOS) immunocytochemistry and nicotinamide adenine dinucleotide phosphate diaphorase (NADPHd) histochemistry, which can be used as an indicator of NOS activity, i.e. NO production. Antibodies against the two constitutive NOS isoforms, neuronal and endothelial NOS, both produced immunoreactivity restricted to large cells at the base and along the secondary lamellae. NADPHd-positive cells showed a corresponding distribution. Antibodies against the inducible NOS isoform only labeled small cells located deep in the filament. Using in situ hybridization and NKA immunoreactivity, cells expressing Na(+),K(+)-ATPase alpha-subunit mRNA were found to have a similar distribution to the NOS cells. Double labeling for NOS immunoreactivity and NKA alpha-subunit mRNA revealed cellular colocalization of NKA alpha-subunit mRNA and nNOS protein in putative chloride cells at the base of the lamellae and interlamellar space. Along the lamellae, some NOS- or NKA-immunoreactive cells possessed a relatively lower expression of NKA alpha-subunit mRNA in smolts. A clear increase in NADPHd staining in the gill was demonstrated from parr to smolt. The regulatory role of NO on gill NKA activity was studied in vitro using sodium nitroprusside (SNP; 1 mmol l(-1)) and PAPA-NONOate (NOC-15; 0.5 mmol l(-1)) as NO donors. Both SNP and NOC-15 inhibited gill NKA activity by 30% when compared to controls. The study shows that NO systems are abundant in the gill of Atlantic salmon, that NO may be produced preferentially by a constitutive NOS isoform, and suggests that NO influence on gill functions is mediated via intracellular, possibly both auto/paracrine, inhibition of Na(+),K(+)-ATPase activity in chloride cells. Furthermore, the increase in NADPHd in the gill during smoltification suggests a regulatory role of NO in the attenuation of the smoltification-related increase in Na(+),K(+)-ATPase activity prior to entering seawater.
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PMID:Nitric oxide synthase in the gill of Atlantic salmon: colocalization with and inhibition of Na+,K+-ATPase. 1576 2

The mechanisms of human mutant superoxide dismutase-1 (mSOD1) toxicity to motor neurons (MNs) are unresolved. We show that MNs in G93A-mSOD1 transgenic mice undergo slow degeneration lacking similarity to apoptosis structurally and biochemically. It is characterized by somal and mitochondrial swelling and formation of DNA single-strand breaks prior to double-strand breaks occurring in nuclear and mitochondrial DNA. p53 and p73 are activated in degenerating MNs, but without nuclear import. The MN death is independent of activation of caspases-1, -3, and -8 or apoptosis-inducing factor within MNs, with a blockade of apoptosis possibly mediated by Aven up-regulation. MN swelling is associated with compromised Na,K-ATPase activity and aggregation. mSOD1 mouse MNs accumulate mitochondria from the axon terminals and generate higher levels of superoxide, nitric oxide, and peroxynitrite than MNs in control mice. Nitrated and aggregated cytochrome c oxidase subunit-I and alpha-synuclein as well as nitrated SOD2 accumulate in mSOD1 mouse spinal cord. Mitochondria in mSOD1 mouse MNs accumulate NADPH diaphorase and inducible nitric oxide synthase (iNOS)-like immunoreactivity, and iNOS gene deletion extends significantly the life span of G93A-mSOD1 mice. Prior to MN loss, spinal interneurons degenerate. These results identify novel mechanisms for mitochondriopathy and MN degeneration in amyotrophic lateral sclerosis (ALS) mice involving blockade of apoptosis, accumulation of MN mitochondria with enhanced toxic potential from distal terminals, NOS localization in MN mitochondria and peroxynitrite damage, and early degeneration of alpha-synuclein(+) interneurons. The data support roles for oxidative stress, protein nitration and aggregation, and excitotoxicity as participants in the process of MN degeneration caused by mSOD1.
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PMID:Motor neuron degeneration in amyotrophic lateral sclerosis mutant superoxide dismutase-1 transgenic mice: mechanisms of mitochondriopathy and cell death. 1709 94

Subfractionation of preparations of rat liver microsomes with a suitable concentration of sodium deoxycholate has resulted in the isolation of a membrane fraction consisting of smooth surfaced vesicles virtually free of ribonucleoprotein particles. The membrane fraction is rich in phospholipids, and contains the microsomal NADH-cytochrome c reductase, NADH diaphorase, glucose-6-phosphatase, and ATPase in a concentrated form. The NADPH-cytochrome c reductase, a NADPH (or pyridine nucleotide unspecific) diaphorase, and cytochrome b(5) are recovered in the clear supernatant fraction. The ribonucleoprotein particles are devoid of, or relatively poor in, the enzyme activities mentioned. Those enzymes which are bound to the membranes vary in activity according to the structural state of the microsomes, whereas those which appear in the soluble fraction are stable. From these findings the conclusion is reached that certain enzymes of the endoplasmic reticulum are tightly bound to the membranes, whereas others either are loosely bound or are present in a soluble form within the lumina of the system. Some implications of these results as to the enzymic organization of the endoplasmic reticulum are discussed.
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PMID:ENZYME-STRUCTURE RELATIONSHIPS IN THE ENDOPLASMIC RETICULUM OF RAT LIVER : A Morphological and Biochemical Study. 1986 14

The effects of chronic hypoxia (CH) on respiratory muscle are poorly understood. The aim of the present study was to examine the effects of CH on respiratory muscle structure and function, and to determine whether nitric oxide is implicated in respiratory muscle adaptation to CH. Male Wistar rats were exposed to CH for 1-6 weeks. Sternohyoid and diaphragm muscle contractile properties, muscle fibre type and size, the density of fibres expressing sarco/endoplasmic reticulum calcium-ATPase (SERCA) 2 and sodium-potassium ATPase (Na+,K+-ATPase) pump content were determined. Muscle succinate dehydrogenase (SDH) and reduced nicotinamide adenine dinucleotide phosphate (NADPH) dehydrogenase activities were also assessed. Acute and chronic blockade of nitric oxide synthase (NOS) was employed to determine whether or not NO is critically involved in functional remodelling in CH muscles. CH improved diaphragm, but not sternohyoid, fatigue tolerance in a time-dependent fashion. This adaptation was not attributable to increased SDH or NADPH dehydrogenase activities. The areal density of muscle fibres and relative area of fibres expressing SERCA2 were unchanged. Na+,K+-ATPase pump content was significantly increased in CH diaphragm. Chronic NOS inhibition decreased diaphragm Na+,K+-ATPase pump content and prevented CH-induced increase in muscle endurance. This study provides novel insight into the mechanisms involved in CH-induced muscle plasticity. The results may be of relevance to respiratory disorders characterised by CH, such as chronic obstructive pulmonary disease.
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PMID:Chronic hypoxia increases rat diaphragm muscle endurance and sodium-potassium ATPase pump content. 2114 31

Cyanobacteria possess an environmental adaptation known as a CO(2) concentrating mechanism (CCM) that evolved to improve photosynthetic performance, particularly under CO(2)-limiting conditions. The CCM functions to actively transport dissolved inorganic carbon species (Ci; HCO(3)(-) and CO(2)) resulting in accumulation of a pool of HCO(3)(-) within the cell that is then utilised to provide an elevated CO(2) concentration around the primary CO(2) fixing enzyme, ribulose bisphosphate carboxylase-oxygenase (Rubisco). Rubisco is encapsulated in unique micro-compartments known as carboxysomes and also provides the location for elevated CO(2) levels in the cell. Five distinct transport systems for active Ci uptake are known, including two types of Na(+)-dependent HCO(3)(-) transporters (BicA and SbtA), one traffic ATPase (BCT1) for HCO(3)(-) uptake and two CO(2) uptake systems based on modified NADPH dehydrogenase complexes (NDH-I(3) and NDH-I(4)). The genes for a number of these transporters are genetically induced under Ci limitation via transcriptional regulatory processes. The in-membrane topology structures of the BicA and SbtA HCO(3)(-) transporters are now known and this may aid in determining processes related to transporter activation during dark to light transitions or under severe Ci limitation.
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PMID:Inorganic carbon transporters of the cyanobacterial CO2 concentrating mechanism. 2135 51

Calf and human thyroids have been disrupted by nitrogen microcavitation, and the thyroid membranes prepared by repeated centrifugation in low ionic strength buffers. Two classes of membranes were prepared by centrifugation on a discontinuous gradient of ficoll. A lighter fraction was comprised of somewhat larger vesicles; they were higher in Na(+)-K(+)-activated ATPase, phosphodiesterase, and 5'-nucleotidase than was the heavier fraction. The heavier fraction had a higher nicotinamide adenine nucleotide dehydrogenase-diaphorase activity. Thus the lighter fraction appears to have been enriched in fragments derived from the plasma membrane.
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PMID:Preparation and properties of thyroid cell membranes. 2417 60


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