NO Concentration (no + concentration)

Distribution by Scientific Domains

Kinds of NO Concentration

  • alveolar no concentration


  • Selected Abstracts


    Oxidative stress in glial cultures: Detection by DAF-2 fluorescence used as a tool to measure peroxynitrite rather than nitric oxide

    GLIA, Issue 2 2002
    Sanjoy Roychowdhury
    Abstract 4,5-diaminofluorescein diacetate (DAF-2DA) is widely used as a fluorescent probe to detect endogenously produced nitric oxide (NO). Recent reports that refer to the high sensitivity of DAF-2 toward NO prompted us to test its efficiency and specificity in a mixed murine primary glial culture model, in which the NO-synthesizing enzyme inducible nitric oxide synthase (iNOS) is expressed by stimulation with lipopolysaccharide (LPS) and interferon-, (IFN-,). Cultures were loaded with DAF-2DA and the fluorescence was measured using confocal microscopy. NO production in the cultures was determined using the ozone/chemiluminescence technique. Due to the extremely high photosensitivity of DAF-2, low laser intensities were used to avoid artifacts. No difference in DAF-2 fluorescence was observed in NO-producing cultures compared to control cultures, whereas the NO/peroxynitrite-sensitive dye 2,7-dihydrodichlorofluorescein (DCF) showed a significant fluorescence increase specifically in microglia cells. A detectable gain in fluorescence was seen when NO-containing buffer was added to the DAF-2DA,loaded cells with a minimum NO concentration at 7.7 ,M. An additional gain of DAF-2 fluorescence was obtained when the cells were depleted of glutathione (GSH) with L-buthionine S,R-sulfoximine (BSO). Hence, we monitored the change in DAF-2 fluorescence intensity in the presence of NO and O in a cell-free solution. The fluorescence due to NO was indeed larger when O was added, implying a higher sensitivity of DAF-2 for peroxynitrite. Nevertheless, our results also indicate that measurement of DCF fluorescence is a better tool for monitoring intracellular changes in the levels of NO and/or peroxynitrite than DAF-2. GLIA 38:103,114, 2002. 2002 Wiley-Liss, Inc. [source]


    Tumoricidal activity of high-dose tumor necrosis factor-, is mediated by macrophage-derived nitric oxide burst and permanent blood flow shutdown

    INTERNATIONAL JOURNAL OF CANCER, Issue 2 2008
    Chandrakala Menon
    Abstract This study investigates the role of tumor nitric oxide (NO) and vascular regulation in tumor ulceration following high-dose tumor necrosis factor-, (TNF) treatment. Using TNF-responsive (MethA) and nonresponsive (LL2) mouse tumors, tumor NO concentration was measured with an electrochemical sensor and tumor blood flow by Doppler ultrasound. Mice were also pretreated with a selective inducible nitric oxide synthase (iNOS) inhibitor, 1400 W. Tumors harvested from TNF-treated mice were cryosectioned and immunostained for murine macrophages, or/and iNOS. MethA tumor-bearing mice were depleted of macrophages. Pre- and post-TNF tumor NO levels were measured continuously, and mice were followed for gross tumor response. In MethA tumors, TNF caused a 96% response rate, and tumor NO concentration doubled. Tumor blood flow decreased to 3% of baseline by 4 hr and was sustained at 24 hr and 10 days post-TNF. Selective NO inhibition with 1400 W blocked NO rise and decreased response rate to 38%. MethA tumors showed tumor infiltration by macrophages post-TNF and the pattern of macrophage immunostaining overlapped with iNOS immunostaining. Depletion of macrophages inhibited tumor NO increase and response to TNF. LL2 tumors had a 0% response rate to TNF and exhibited no change in NO concentration. Blood flow decreased to 2% of baseline by 4 hr, recovered to 56% by 24 hr and increased to 232% by 10 days. LL2 tumors showed no infiltration by macrophages post-TNF. We conclude that TNF causes tumor infiltrating, macrophage-derived iNOS-mediated tumor NO rise and sustained tumor blood flow shutdown, resulting in tumor ulceration in the responsive tumor. 2008 Wiley-Liss, Inc. [source]


    Modulation of the cGMP signaling pathway by melatonin in pancreatic , -cells

    JOURNAL OF PINEAL RESEARCH, Issue 2 2009
    Ina Stumpf
    Abstract:, Melatonin influences the second messenger cyclic guanosine 3,,5,-monophosphate (cGMP) signaling pathway in pancreatic , -cells via a receptor-mediated mechanism. In the present study, it was determined how the regulation of cGMP concentrations by melatonin proceeds. The results provide evidence that melatonin acts via the soluble guanylate cyclase (sGC), as molecular investigations demonstrated that long-term incubation with melatonin significantly reduced the expression levels of the sGC mRNA in rat insulinoma , -cells (INS1) cells, whereas mRNA expression of membrane guanylate cyclases was unaffected. Incubation with melatonin abolished the S-nitrosoacetyl penicillamine-induced increase of cGMP concentrations in INS1 cells. In addition, the cGMP-inhibitory effect of melatonin was reversed by preincubation with the sGC inhibitors 1H-(1,2,4)oxadiazolo(4,3- ,)quinoxalin-1-one and 4H-8-bromo-1,2,4-oxadiazolo(3,4-d)benz(b)(1,4)oxazin-1-one. Nitric oxide (NO) production was not influenced after 1 hr of melatonin application, but was influenced after a 4 hr incubation period. Preincubation of INS1 cells with the NO synthase inhibitor NG -monomethyl- l -arginine did not abolish the cGMP-inhibitory effect of melatonin. Transcripts of cyclic nucleotide-gated (CNG) channels were significantly reduced after melatonin treatment in a dose-dependent manner, indicating the involvement of these channels in mediating the melatonin effect in INS1 cells. The results of this study demonstrate that melatonin mediates its inhibitory effect on cGMP concentrations in pancreatic , -cells by inhibiting the sGC, but does not influence NO concentration or NO synthase activity in short-term incubation experiments. In addition, it was demonstrated that melatonin is involved in modulation of CNG channel mRNA. [source]


    Independent Regulation of Periarteriolar and Perivenular Nitric Oxide Mechanisms in the In Vivo Hamster Cheek Pouch Microvasculature

    MICROCIRCULATION, Issue 4 2009
    DAVID D. KIM
    ABSTRACT Objective: We tested the hypothesis that differential stimulation of nitric oxide (NO) production can be induced in pre- and postcapillary segments of the microcirculation in the hamster cheek pouch. Materials and Methods: We applied acetylcholine (ACh) or platelet-activating factor (PAF) topically and measured perivascular NO concentration ([NO]) with NO-sensitive microelectrodes in arterioles and venules of the hamster cheek pouch. We also measured NO in cultured coronary endothelial cells (CVEC) after ACh or PAF. Results: ACh increased periarteriolar [NO] significantly in a dose-dependent manner. ACh at 1 ,M increased [NO] from 438.143.4 nM at baseline to 647.966.3 nM, while 10 ,M of ACh increased [NO] from baseline to 1,035.059.2 nM (P<0.05). Neither 1 nor 10 ,M of ACh changed perivenular [NO] in the hamster cheek pouch. PAF, at 100 nM, increased perivenular [NO] from 326.650.8 to 622.841.5 nM. Importantly, 100 nM of PAF did not increase periarteriolar [NO]. PAF increased [NO] from 3.62.1 to 455.519.9 in CVEC, while ACh had no effect. Conclusions: We conclude that NO production can be stimulated in a differential manner in pre- and postcapillary segments in the hamster cheek pouch. ACh selectively stimulates the production of NO only in arterioles, while PAF stimulates the production of NO only in venules. [source]


    Alveolar and bronchial nitric oxide output in healthy children

    PEDIATRIC PULMONOLOGY, Issue 12 2008
    Anna Sepponen MD
    Abstract Exhaled nitric oxide (NO) concentration is a marker of pulmonary inflammation. It is usually measured at a single exhalation flow rate. However, measuring exhaled NO at multiple flow rates allows assessment of the flow-independent NO parameters: alveolar NO concentration, bronchial NO flux, bronchial wall NO concentration, and bronchial diffusing capacity of NO. Our aim was to determine the flow-independent NO parameters in healthy schoolchildren and to compare two different mathematical approaches. Exhaled NO was measured at four flow rates (10, 50, 100, and 200 ml/sec) in 253 schoolchildren (7,13 years old). Flow-independent NO parameters were calculated with linear method (flows ,50 ml/sec) and non-linear method (all flows). Sixty-six children (32 boys and 34 girls) with normal spirometry and no history or present symptoms of asthma, allergy, atopy or other diseases were included in the analysis. Median bronchial NO flux was 0.4 nl/sec (mean,,SD: 0.5,,0.3 nl/sec) and median alveolar NO concentration was 1.9 ppb (2.0,,0.8 ppb) with the linear method. Bronchial NO flux correlated positively with height (r,=,0.423; P,<,0.001), FEV1 (r,=,0.358; P,=,0.003), and FVC (r,=,0.359; P,=,0.003). With the non-linear method, median bronchial wall NO concentration was 49.6 ppb (68.0,,53.3 ppb) and bronchial diffusing capacity of NO was 10.0 pl/sec/ppb (11.8,,7.5 pl/sec/ppb). The non-linear method gave lower alveolar NO concentration (1.4 [1.5,,0.7] ppb, P,<,0.001) and higher bronchial NO flux (0.5 [0.6,,0.3] nl/sec, P,<,0.001) than the linear method, but the results were highly correlated between the two methods (r,=,0.854 and r,=,0.971, P,<,0.001). In conclusion, the multiple flow rate method is feasible in children but different mathematical methods give slightly different results. Reference values in healthy children are of value when applying bronchial and alveolar NO parameters in the diagnostics and follow-up of inflammatory lung diseases. Pediatr. Pulmonol. 2008; 43:1242,1248. 2008 Wiley-Liss, Inc. [source]


    Flooding induced emissions of volatile signalling compounds in three tree species with differing waterlogging tolerance

    PLANT CELL & ENVIRONMENT, Issue 9 2010
    LUCIAN COPOLOVICI
    ABSTRACT To gain insight into variations in waterlogging responsiveness, net assimilation rate, stomatal conductance, emissions of isoprene and marker compounds of anoxic metabolism ethanol and acetaldehyde, and stress marker compounds nitric oxide (NO), volatile products of lipoxygenase (LOX) pathway and methanol were studied in seedlings of temperate deciduous tree species Alnus glutinosa, Populus tremula and Quercus rubra (from highest to lowest waterlogging tolerance) throughout sustained root zone waterlogging of up to three weeks. In all species, waterlogging initially resulted in reductions in net assimilation and stomatal conductance and enhanced emissions of ethanol, acetaldehyde, NO, LOX products and methanol, followed by full or partial recovery depending on process and species. Strong negative correlations between gs and internal NO concentration and NO flux, valid within and across species, were observed throughout the experiment. Isoprene emission capacity was not related to waterlogging tolerance. Less waterlogging tolerant species had greater reduction and smaller acclimation capacity in foliage physiological potentials, and larger emission bursts of volatile stress marker compounds. These data collectively provide encouraging evidence that emissions of volatile organics and NO can be used as quantitative measures of stress tolerance and acclimation kinetics in temperate trees. [source]


    Elevated alveolar nitric oxide concentration after environmental challenge in hypersensitivity pneumonitis

    RESPIROLOGY, Issue 4 2010
    Toshihiro SHIRAI
    ABSTRACT We describe a 57-year-old male patient admitted to hospital with hypersensitivity pneumonitis (HP) that resolved without treatment. The total and alveolar nitric oxide (NO) concentrations were measured on initial admission and after re-exposure to his home environment. Following environmental exposure he became ill again, alveolar NO concentration was increased to the same level as on initial admission and impaired pulmonary function and radiologic abnormalities were found. It suggested a diagnosis of environmentally induced HP. The clinical value of measuring alveolar NO as an acute-phase reactant in HP is demonstrated in this patient. [source]


    Chronologic Changes of Nitric Oxide Concentration in the Cochlear Lateral Wall and Its Role in Noise-Induced Permanent Threshold Shift

    THE LARYNGOSCOPE, Issue 5 2008
    Yuh-Shyang Chen MD
    Abstract Objective: The objective of this study was to investigate the chronologic changes of nitric oxide (NO) concentration in the cochlear lateral wall and to explore its possible role in permanent threshold shift (PTS) after intense noise exposure. Materials and Methods: Seventeen guinea pigs were subjected to a single continuous exposure to broadband white noise at 105 2 dB sound pressure level (SPL) for 40 hours and were divided into four groups according to various postnoise recovery periods. Another 12 guinea pigs were not exposed to noise and served as controls. The hearing status of all animals was evaluated with auditory brainstem responses (ABR) evoked by condensation "click" sounds. ABR were recorded both prior to noise exposure and immediately before killing the animal. After death, NO concentration in the cochlear lateral wall was directly measured with an NO/ozone chemiluminescence technique. Results: An approximately 1.7-fold increase in NO concentration was observed immediately postnoise exposure, which persisted for up to 28 days. The threshold of ABR elevation (mean, 30 dB SPL) peaked immediately after cessation of noise exposure and gradually resolved to a PTS (mean, 14.5 dB SPL) 56 days after noise exposure when NO concentration had returned to its prenoise exposure level. Conclusion: Noise-induced threshold shift, which resolved to a mild PTS, can be partially attributed to NO elevation in the cochlear lateral wall. Our results revealed a nonlinear correlation between ABR recovery and depletion of NO, indicating that the mechanisms of NO changes in the cochlear lateral wall may be more complicated than previously conceived and that other pathophysiologic mechanisms may also play important roles in noise-induced PTS. [source]


    Selective neuronal nitric oxide synthase inhibitors and the prevention of cerebral palsy,

    ANNALS OF NEUROLOGY, Issue 2 2009
    Haitao Ji PhD
    Objective To design a new class of selective neuronal nitric oxide synthase (NOS) inhibitors, and demonstrate that administration in a rabbit model for cerebral palsy (CP) prevents hypoxia-ischemia,induced deaths and reduces the number of newborn kits exhibiting signs of CP. Methods We used a novel computer-based drug design method called fragment hopping to identify new chemical entities, synthesized them, and conducted in vitro enzyme inhibition studies with the three isozymes of NOS and in vivo experiments to monitor cardiovascular effects on pregnant rabbit dams, NOS activity, and NOx (NO and NO2) concentration in fetal brain, and assess neurobehavioral effects on kits born to saline- and compound treated dams. Results The computer-based design led to the development of powerful and highly selective compounds for inhibition of neuronal NOS over the other isozymes. After maternal administration in a rabbit model of CP, these compounds were found to distribute to fetal brain, to be nontoxic, without cardiovascular effects, inhibit fetal brain NOS activity in vivo, reduce NO concentration in fetal brain, and dramatically ameliorate deaths and number of newborn kits exhibiting signs of CP. Interpretation This approach may lead to new preventive strategies for CP. Ann Neurol 2008 [source]


    Amino-acid hydroselenites: synthesis and cytotoxicity,

    APPLIED ORGANOMETALLIC CHEMISTRY, Issue 4 2002
    E. Lukevics
    Abstract Amino acids, di- and tri-peptides readily react with selenic acid (H2SeO3, formed during solution of selenium(IV) oxide in water) to give the corresponding ammonium hydroselenites. Most selenites synthesized are very active (0.4,11,g,ml,1) against mouse hepatoma MG-22A and readily increase NO concentration in the cultural medium on the HT-1080 line (up to TG100,=,1500%). The amino-acid hydroselenites studied influenced the cell phenotype. Copyright 2002 John Wiley & Sons, Ltd. [source]


    Apoptosis-Inducing High .

    CHEMMEDCHEM, Issue 10 2008
    NO Concentrations Are Not Sustained Either in Nascent or in Developed Cancers
    Abstract Nitric oxide (.NO) induces apoptosis at high concentrations by S-nitrosating proteins such as glyceraldehyde-3-phosphate dehydrogenase. This literature analysis revealed that failure to sustain high . NO concentrations is common to all cancers. In cervical, gastric, colorectal, breast, and lung cancer, the cause of this failure is the inadequate expression of inducible nitric oxide synthase (iNOS), resulting from the inhibition of iNOS expression by TGF-,1 at the mRNA level. In bladder, renal, and prostate cancer, the reason for the insufficient . NO levels is the depletion of arginine, resulting from arginase overexpression. Arginase competes with iNOS for arginine, catalyzing its hydrolysis to ornithine and urea. In gliomas and ovarian sarcomas, low . NO levels are caused by inhibition of iNOS by N -chlorotaurine, produced by infiltrating neutrophils. Stimulated neutrophils express myeloperoxidase, catalyzing H2O2 oxidation of Cl, to HOCl, which N-chlorinates taurine at its concentration of 19,mM in neutrophils. In squamous cell carcinomas of the skin, ovarian cancers, lymphomas, Hodgkin's disease, and breast cancers, low . NO concentrations arise from the inhibition of iNOS by N -bromotaurine, produced by eosinophil-peroxidase-expressing infiltrating eosinophils. Eosinophil peroxidase catalyzes the H2O2 oxidation of Br, to HOBr, which N-brominates taurine to N -bromotaurine at its concentration of 15,mM in eosinophils. In microvascularized tumors, the . NO concentration is further depleted; . NO is rapidly consumed by red blood cells (RBCs) through S-nitrosation of RBC glutathione and hemoglobin, and by oxidation to nitrate by RBC oxyhemoglobin. Angiogenesis-inhibiting antibodies are currently used to treat cancers; their mode of action is not, as previously thought, reduction of the tumor O2 or nutrient supply. They actually decrease the loss of . NO to RBCs. [source]


    Comparison of cysteinyl leukotriene concentrations between exhaled breath condensate and bronchoalveolar lavage fluid

    CLINICAL & EXPERIMENTAL ALLERGY, Issue 12 2008
    E. Ono
    Summary Background Collection of exhaled breath condensate (EBC) is a simple, non-invasive method of obtaining samples from the airways and it can be repeated in short intervals without side effects; therefore, it provides an opportunity to monitor the changes in concentration of inflammatory mediators in the airways. However, EBC analysis still has several unresolved issues. Objective To better understand the characteristics of EBC, we compared cysteinyl leukotriene (CysLT) concentrations between bronchoalveolar lavage fluid (BALF) and EBC. We also attempted to correct CysLT concentrations in BALF and EBC diluted with saline and water vapour using biological markers. Methods EBC was collected from 14 patients with idiopathic pulmonary fibrosis before bronchoscopy. We measured CysLT concentrations and also quantified tyrosine, urea and total protein as possible biomarkers for correcting dilution. Results (1) We have validated the quantification of CysLTs in EBC. (2) Although a significant correlation was observed among tyrosine and urea concentrations in BALF, urea and total protein concentrations were below the detection limit in EBC. (3) CysLT concentrations were higher in BALF than in EBC (median, 15.96 pg/mL vs. 5.5 pg/mL; P=0.001) and there was no correlation of CysLT concentrations in BALF with those in EBC. A significant correlation of the ratio of total CysLT concentration to tyrosine concentration (CysLT/Y) in EBC with that in BALF was observed (r=0.547, P=0.043). (4) CysLT/Y in EBC correlated with serum KL-6 concentration and total cell count in BALF, and CysLT/Y in BALF also correlated with exhaled NO concentration and %VC. Conclusions CysLT/Y in EBC significantly correlated with that in BALF and some clinical parameters correlated with CysLT/Y. Tyrosine concentration may be used to correct the dilution error for CysLT concentrations, and CysLT/Y in EBC can be a surrogate marker for CysLT concentrations in BALF. [source]


    Nitric oxide evaluation in upper and lower respiratory tracts in nasal polyposis

    CLINICAL & EXPERIMENTAL ALLERGY, Issue 7 2008
    C. Delclaux
    Summary Background A decrease in nasal nitric oxide (NO) and an increase in exhaled NO have been demonstrated in patients with nasal polyposis (NP). Objectives The aims were to evaluate the flux of NO from the three compartments of the respiratory tract, namely, upper nasal, lower conducting and distal airways, and to search for relationships between NO parameters and indexes of upper and lower disease activity (bronchial reactivity and obstruction). The effect of medical treatment of polyposis was also evaluated. Methods Seventy patients with polyposis were recruited. At baseline, pulmonary function tests (spirometry, plethysmography, bronchomotor response to deep inspiration using forced oscillation measurement of resistance of respiratory system, methacholine challenge, multiple flow rates of exhaled NO and nasal NO measurements) were performed together with an assessment of polyposis [clinical, endoscopic and computed tomography (CT) scores]. Results Statistical relationships were demonstrated between nasal NO flux and severity scores (clinical: ,=,0.31, P=0.015; endoscopic: ,=,0.57, P<0.0001; CT: ,=,0.46, P=0.0005), and between alveolar NO concentration and distal airflow limitation (FEF25,75, ,=,0.32, P=0.011). Thirty-six patients were assessed after 11 [7,13] (median [interquartile]) months of medical treatment, demonstrating an improvement in clinical and endoscopic scores, an increase in nasal NO flux, a decrease in NO flux from conducting airways, an improvement in the mild airflow limitation (forced expiratory volume in 1 s, FEF25,75, even in non-asthmatic patients) and a decrease in the bronchoconstrictor effect of deep inspiration. Conclusions The medical treatment of NP improves both airway reactivity and obstruction, whatever the presence of asthma, suggesting a functional link between upper and lower airway functions. [source]


    Exhaled and nasal nitric oxide in mechanically ventilated preterm and term newborns

    ACTA PAEDIATRICA, Issue 10 2002
    O Aikio
    Aim: Nitric oxide (NO) is an important mediator required for neonatal pulmonary circulatory adaptation and for pulmonary defence. Both deficient and excessive NO production have been proposed to play a role in neonatal lung disease. This study aimed to establish a method that allows direct measurement of exhaled and nasal NO concentrations in newborn infants who require intubation and ventilation. Methods: A rapid-response chemiluminescence NO analyser was used. Gas was sampled from the endotracheal intubation tube, and tidal volumes and flow rates were measured. The nasal NO was sampled from the non-intubated nostril. The accuracy of the method was validated using a lung model. NO levels from six preterm and six term/near-term newborns were studied. Measurements were performed on a daily basis during the first week. Results: An expiration >0.2 s in duration with a flow rate >1.7mls,1 could be accurately analysed for the presence of >1 parts per billion of NO. The very preterm infants with neonatal lung disease had a different postnatal NO output pattern from the lower and upper airways compared with the ventilated term/near-term infants. Conclusion: A novel method for measurement of exhaled NO of an intubated newborn is presented. The possible association of exhaled NO concentration with the development of chronic lung disease remains to be studied. [source]


    A Comparison of Membrane Inlet Mass Spectrometry and Nitric Oxide (NO) Electrode Techniques to Detect NO in Aqueous Solution

    ELECTROANALYSIS, Issue 4 2010
    Chingkuang Tu
    Abstract The NO electrode and membrane inlet mass spectrometry (MIMS) have the advantage of being sensitive, direct, and real time detectors of NO in aqueous solution. They do not require reacting NO with labels or purging of NO with an inert gas. We show that the NO electrode and MIMS are comparable in sensitivity detecting NO concentrations to 0.5,nM in aqueous solution, and both give identical results in a biological measurement, the reactions of deoxyhemoglobin with nitrite. [source]


    Enhanced exoenzyme activities in sediments in the presence of deposit-feeding Chironomus riparius larvae

    FRESHWATER BIOLOGY, Issue 9 2007
    PETER STIEFArticle first published online: 10 JUN 200
    Summary 1. The combined effects of deposit-feeding, bioturbation and bioirrigation by benthic macrofauna on the enzymatic hydrolysis of organic matter were studied in microcosms. Chironomus riparius larvae (Insecta, Diptera) served as model macrofauna and stinging nettle leaves (Urtica dioica) were used as a detrital food source. 2. In the upper 10 mm of the sediment (the habitat of C. riparius larvae), the activities of several exoenzymes, the contents of several fractions of particulate organic matter (POM), and the concentrations of dissolved oxidants (O2, NO) were measured on a small scale. Fluorescent particles (luminophores) were used to quantify the vertical redistribution of particles within the same layer. 3. In control sediment, the addition of detrital food enhanced exoenzyme activities in the 0,2 mm layer only. In the presence of C. riparius larvae, exoenzyme activities increased to 10 mm depth. Further, the content of POM in the 0,2 mm layer was lower in the presence than in the absence of larvae, suggesting ingestion and subduction of the added detritus. After prolonged incubation without further food addition, exoenzyme activities returned close to background values in both treatments, whereas the vertical distribution of POM remained unchanged. 4. The overall penetration depth of O2 and NO into the sediment was greater in the presence than the absence of C. riparius, the differences being more pronounced after prolonged incubation. Locally high O2 and NO concentrations due to bioirrigation by C. riparius were measured deep in the sediment. Net downward transport of particles was observed only in the presence of C. riparius larvae and only at the beginning of the incubation. 5. I conclude that deposit-feeding and bioturbation by macrofauna can quickly remove freshly deposited POM from the sediment surface and transfer it to less oxygenated sites (i.e. animal guts and deep sediment layers). Bioirrigation also increases the availability of oxidants deep in the sediment. The oscillation of oxidant supply to POM particles by ingestion,egestion, burial and re-burial, and the intermittent bioirrigation of subsurface sediment, is probably the cause of the increased rate of organic matter hydrolysis, the rate-limiting step in mineralization. [source]


    AUF-1 mediates inhibition by nitric oxide of lipopolysaccharide-induced matrix metalloproteinase-9 expression in cultured astrocytes

    JOURNAL OF NEUROSCIENCE RESEARCH, Issue 2 2006
    Wenlan Liu
    Abstract Neuroinflammatory diseases are associated with increased production of matrix metalloproteinase-9 (MMP-9) and excessive generation of nitric oxide (NO). NO hasbeen reported to have variable effects on MMP-9 gene expression and activation in various cell types. Inthe present study, we investigated the effect of NOon MMP-9 expression in primary cortical astrocytes. Zymography and real-time PCR showed that lipopolysaccharide (LPS) dramatically increased latent MMP-9 gelatinolytic activity and MMP-9 mRNA expression. By using the NO donor DETA NONOate, we observed a dose-dependent inhibition of MMP-9 induction by LPS. Active forms of MMP-9 were not found by zymography after NO treatment. The MEK1/2 inhibitor U0126 completely inhibited LPS-induced MMP-9, which was partially inhibited by the p38 MAPK inhibitor SB203580. NO had no effect on LPS-stimulated ERK1/2 and p38 MAPK activation, suggesting that the inhibitory action of NO occurs downstream of MAPK cascades. Real-time PCR analysis showed that NO accelerated the degradation of MMP-9 mRNA after LPS induction. Western blotting and pull-down assay demonstrated that NO increased AUF-1 expression as well as its specific binding to the MMP-9 gene 3,-untranslated region. Knockdown of AUF-1 with siRNA partially reversed the inhibitory action of NO on LPS-stimulated MMP-9 induction. We conclude that NO does not activate MMP-9 in astrocyte cultures but reduces LPS-induced MMP-9 expression via accelerating MMP-9 mRNA degradation, which is partially mediated by AUF-1. Our results suggest that elevated NO concentrations may suppress MMP-9 and restrict the inflammatory response in neurodegenerative diseases. 2006 Wiley-Liss, Inc. [source]


    Pharmacodynamic interactions between recombinant mouse interleukin-10 and prednisolone using a mouse endotoxemia model

    JOURNAL OF PHARMACEUTICAL SCIENCES, Issue 3 2005
    Abhijit Chakraborty
    Abstract The pharmacodynamic interactions between recombinant mouse interleukin-10 (IL-10) and prednisolone were examined in lipopolysaccharide (LPS)-induced experimental endotoxemia in Balb/c mice. Treatment phases consists of single doses of IL-10 (10 ,g/kg i.p.), prednisolone (25 (mg/kg i.p.), IL-10 (2.5 ,g/kg i.p.) with prednisolone (6.25 mg/kg i.p.), or placebo (saline). Measurements included plasma steroid kinetics and IL-10 concentrations and responses to LPS including proinflammatory cytokines (TNF-,, IFN-,) and circulatory NO measured as plasma nitrate/nitrite concentrations. The intraperitoneal dosing of LPS produced large and transient elevations of plasma TNF-,, IFN-,, and NO concentrations. Noncompartmental and model fitting using extended indirect response models based on drug inhibition of multiphase stimulation of biomarkers by LPS were used to describe the in vivo pharmacodynamics and drug interactions. Dosing with prednisolone, IL-10, or their combinations produced strong inhibition of cytokine and NO production. The IC50 values of prednisolone ranged from 54 to 171 ng/mL, and IC50 values for IL-10 ranged from 0.06 to 0.69 ng/mL. The production of NO was described as a cascading consequence of the TNF-, and IFN-, plasma concentrations. The joint dosing of IL-10 with prednisolone produces moderately synergistic immunosuppressive effects in this system. Both drugs were sufficiently protective in suppressing the inflammatory mediators when administered prior to the LPS trigger, while such effects were modest when administered after the inflammatory stimulus was provoked. The integrated and complex pharmacokinetic/pharmacodynamic models well capture the in vivo processes, drug potencies, and interactions of IL-10 and prednisolone. 2005 Wiley-Liss, Inc. and the American Pharmacists Association J Pharm Sci 94:590,603, 2005 [source]


    Effects of nitrate nitrogen pollution on Central European unionid bivalves revealed by distributional data and acute toxicity testing

    AQUATIC CONSERVATION: MARINE AND FRESHWATER ECOSYSTEMS, Issue 2 2010
    Karel Douda
    Abstract 1.Studies from Central Europe have shown a relationship between the impaired population status of threatened freshwater mussel species and elevated nitrate nitrogen (N,NO) concentrations in running waters. 2.Causal mechanisms, however, remain unknown, and no experimental data or comprehensive studies involving more species are available, which causes uncertainty in prioritizing conservation actions. 3.This study uses both descriptive and experimental approaches to identify the effects of nitrates on freshwater mussels and demonstrates the need for integrating different research methods for development of conservation strategies for threatened species. 4.Spatial co-occurrence of five native freshwater mussel species (Anodonta anatina, Pseudanodonta complanata, Unio pictorum, Unio tumidus, Unio crassus) and N,NO concentrations were examined in a 7th-order river catchment (Lu,nice River, Czech Republic) with anthropogenically-induced increasing N,NO levels and declining populations of these species during the 20th century. 5.Acute toxicity of N,NO was then estimated for artificially reared juveniles of A. anatina and U. crassus using both lethal and sublethal test endpoints. 6.Results showed that the probability of occurrence of all species was significantly reduced in reaches with elevated N,NO levels. 7.In contrast, the results of toxicity testing revealed that the juvenile stages of the two tested species were less sensitive to N,NO than most previously tested freshwater macroinvertebrates. The detected 96-h median lethal N,NO concentrations were two orders of magnitude higher than the limits derived from distributional data. 8.Despite the probable absence of a direct negative effect of N,NO on freshwater mussel populations, N,NO has potential to be used as an effective indicator of biotope conditions. Identification of causal mechanisms responsible for the observed relationship between unionids and N,NO will require further research. Copyright 2009 John Wiley & Sons, Ltd. [source]


    Production, localisation and possible roles of nitric oxide in drought-stressed grapevines

    AUSTRALIAN JOURNAL OF GRAPE AND WINE RESEARCH, Issue 1 2010
    A.A. PATAKAS
    Abstract Background and Aims:, The aim of this study was to monitor nitric oxide (NO) production in response to progressive soil drying as well as to evaluate its possible role as an intermolecular signalling molecule mediating drought-stress responses in grapevines. Methods and Results:, NO production in response to water stress was examined in potted grapevine plants (Vitis vinifera L. cv. Mavrodafni). The cellular sites of NO production and localisation in stressed plants were monitored by fluorometric techniques. Results indicated that both abscisic acid and NO concentrations increased significantly in leaves of stressed plants. The stomatal guard cells seemed to be the sites of earlier NO accumulation. The changes in stomatal conductance seemed to be closely related to both abscisic acid and NO increase, while there was no significant correlation between stomatal conductance and hydrogen peroxide concentration. Conclusions:, The close relationships between stomatal conductance and NO concentrations indicate a potential role of this molecule in drought-signalling pathway in grapevines. Significance of the Study:, Results suggest a contribution of hydrogen peroxide to triggering NO production as well as a possible role of NO on both stomatal closure and antioxidant defence in drought-stressed grapevines. [source]


    Apoptosis-Inducing High .

    CHEMMEDCHEM, Issue 10 2008
    NO Concentrations Are Not Sustained Either in Nascent or in Developed Cancers
    Abstract Nitric oxide (.NO) induces apoptosis at high concentrations by S-nitrosating proteins such as glyceraldehyde-3-phosphate dehydrogenase. This literature analysis revealed that failure to sustain high . NO concentrations is common to all cancers. In cervical, gastric, colorectal, breast, and lung cancer, the cause of this failure is the inadequate expression of inducible nitric oxide synthase (iNOS), resulting from the inhibition of iNOS expression by TGF-,1 at the mRNA level. In bladder, renal, and prostate cancer, the reason for the insufficient . NO levels is the depletion of arginine, resulting from arginase overexpression. Arginase competes with iNOS for arginine, catalyzing its hydrolysis to ornithine and urea. In gliomas and ovarian sarcomas, low . NO levels are caused by inhibition of iNOS by N -chlorotaurine, produced by infiltrating neutrophils. Stimulated neutrophils express myeloperoxidase, catalyzing H2O2 oxidation of Cl, to HOCl, which N-chlorinates taurine at its concentration of 19,mM in neutrophils. In squamous cell carcinomas of the skin, ovarian cancers, lymphomas, Hodgkin's disease, and breast cancers, low . NO concentrations arise from the inhibition of iNOS by N -bromotaurine, produced by eosinophil-peroxidase-expressing infiltrating eosinophils. Eosinophil peroxidase catalyzes the H2O2 oxidation of Br, to HOBr, which N-brominates taurine to N -bromotaurine at its concentration of 15,mM in eosinophils. In microvascularized tumors, the . NO concentration is further depleted; . NO is rapidly consumed by red blood cells (RBCs) through S-nitrosation of RBC glutathione and hemoglobin, and by oxidation to nitrate by RBC oxyhemoglobin. Angiogenesis-inhibiting antibodies are currently used to treat cancers; their mode of action is not, as previously thought, reduction of the tumor O2 or nutrient supply. They actually decrease the loss of . NO to RBCs. [source]


    DOES NITRIC OXIDE MODULATE TRANSMITTER RELEASE AT THE MAMMALIAN NEUROMUSCULAR JUNCTION?

    CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 4 2007
    Travis J Nickels
    SUMMARY 1Application of the nitric oxide (NO) donor, sodium nitrite and the NO synthase substrate l -arginine had no effect on nerve-evoked transmitter release in the rat isolated phrenic nerve/hemidiaphragm preparation; however, when adenosine A1 receptors were blocked with the adenosine A1 receptor antagonist 1,3-dipropyl-8-cyclopentylxanthine (DPCPX) prior to application of sodium nitrate or l -arginine, a significant increase in transmitter release was observed. In addition, the NO donor s -nitroso- N -acetylpenicillamine (SNAP) significantly increased transmitter release in the presence of DPCPX. In the present study, we have made the assumption that these NO donors elevate the level of NO in the tissue. Future studies should test other NO-donating compounds and also monitor the NO concentrations in the tissue to ensure that these effects are, in fact, NO induced. 2Elevation of cGMP in this preparation with the guanylyl cyclase activator 3-(5,-hydroxymethyl-2,-furyl)-1-benzyl indazole (YC-1) significantly enhanced transmitter release. In the presence of DPCPX and the selective guanylyl cyclase inhibitor 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ), which blocks the production of cGMP, the excitatory effects of sodium nitrite and l -arginine were abolished. 3These results suggest that NO serves to enhance transmitter release at the rat neuromuscular junction (NMJ) via a cGMP pathway and this facilitation of transmitter release can be blocked with adenosine. Previously, we demonstrated that adenosine inhibits N-type calcium channels. Because NO only affects transmitter release when adenosine A1 receptors are blocked, we suggest that NO enhances transmitter release by enhancing calcium influx via N-type calcium channels. Further studies are needed to confirm that NO alters transmitter release via cGMP and that this action involves the N-type calcium channel. 4The results of the present study are consistent with a model of NO neuromodulation that has been proposed for the mammalian vagal,atrial junction. This model suggests that NO acts on NO-sensitive guanylyl cyclase to increase the intracellular levels of cGMP. In turn, cGMP inhibits phosphodiesterase-3, increasing levels of cAMP, which then acts on the N-type calcium channels to enhance calcium influx, leading to an increase in transmitter release. Our only modification to this model for the NMJ is that adenosine serves to block the modulation of transmitter release by NO. [source]


    Exhaled and nasal nitric oxide in mechanically ventilated preterm and term newborns

    ACTA PAEDIATRICA, Issue 10 2002
    O Aikio
    Aim: Nitric oxide (NO) is an important mediator required for neonatal pulmonary circulatory adaptation and for pulmonary defence. Both deficient and excessive NO production have been proposed to play a role in neonatal lung disease. This study aimed to establish a method that allows direct measurement of exhaled and nasal NO concentrations in newborn infants who require intubation and ventilation. Methods: A rapid-response chemiluminescence NO analyser was used. Gas was sampled from the endotracheal intubation tube, and tidal volumes and flow rates were measured. The nasal NO was sampled from the non-intubated nostril. The accuracy of the method was validated using a lung model. NO levels from six preterm and six term/near-term newborns were studied. Measurements were performed on a daily basis during the first week. Results: An expiration >0.2 s in duration with a flow rate >1.7mls,1 could be accurately analysed for the presence of >1 parts per billion of NO. The very preterm infants with neonatal lung disease had a different postnatal NO output pattern from the lower and upper airways compared with the ventilated term/near-term infants. Conclusion: A novel method for measurement of exhaled NO of an intubated newborn is presented. The possible association of exhaled NO concentration with the development of chronic lung disease remains to be studied. [source]