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Nitro

Distribution by Scientific Domains
Medical Sciences46%
Chemistry28%
Life Sciences22%
Distribution within Medical Sciences
Pharmacology & Pharmaceutical Medicine45%
Gastroenterology & Hepatology15%
Anesthesia & Pain Management4%
15 Other Subdomains36%

Terms modified by Nitro

  • nitro compound
  • nitro derivative
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  • nitro group
  • nitro groups
    		•
  • nitro interaction
  • nitro substituent
    		•

    Selected Abstracts

    MODULATORY EFFECT OF NARINGENIN ON N -METHYL- N, -NITRO- N -NITROSOGUANIDINE- AND SATURATED SODIUM CHLORIDE-INDUCED GASTRIC CARCINOGENESIS IN MALE WISTAR RATS

    CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 10 2008
    Ekambaram Ganapathy
    SUMMARY 1Naringenin is a flavanone that is believed to have many biological actions, including as an anti-oxidant, free radical scavenger and an antiproliferative agent. The global incidence of gastric carcinoma is increasing rapidly, more than for any other cancer. Therefore, in the present study, we tested the effects of naringenin on gastric carcinogenesis induced by N -methyl- N,-nitro- N -nitrosoguanidine (MNNG) and saturated sodium chloride (S-NaCl) in rats. 2Male Wistar rats were divided into five groups and treated over a period of 20 weeks as follows: (i) a control group given corn oil (1 mL/rat, p.o.) daily 20 weeks; (ii) 200 mg/kg, p.o., MNNG on Days 0 and 14 with S-NaCl (1 mL/rat) administered twice a week for the first 3 weeks; (iii) 200 mg/kg, p.o., MNNG on Days 0 and 14, with naringenin (200 mg/kg, p.o., daily) treatment for the entire 20 weeks; (iv) 200 mg/kg, p.o., MNNG on Days 0 and 14, with naringenin treatment (200 mg/kg, p.o., daily) initiated from 6 to 20 weeks; (v) 200 mg/kg, p.o., naringenin alone daily for 20 weeks. 3In Group II rats in which gastric cancer was inducted with MNNG and S-NaCl, there was a significant increase in hydrogen peroxide and lipid peroxidation levels, with decreases in reduced glutathione, oxidized glutathione, glutathione peroxidase, glutathione reductase and glucose 6-phosphate dehydrogenase. In addition, in Group II rats with gastric cancer, there were significant increases in the activity of cytochrome P450, cytochrome b5 and NADPH cytochrome c reductase, with concomitant decreases in the activity of the phase II enzymes glutathione S-transferase and UDP-glucuronosyl transferase. Naringenin treatment (Groups III and IV) restored enzyme activity to near control levels. 4These results indicate that naringenin has a chemopreventive action against MNNG-induced gastric carcinoma in experimental rats. [source]

    NG -NITRO- l -ARGININE METHYL ESTER POTENTIATES ANAPHYLACTIC VENOCONSTRICTION IN RAT PERFUSED LIVERS

    CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 11 2006
    Toshishige Shibamoto
    SUMMARY 1The effects of the nitric oxide (NO) synthase inhibitor NG -nitro- l -arginine methyl ester (l -NAME) on anaphylaxis-induced venoconstriction were examined in rat isolated livers perfused with blood-free solutions in order to clarify the role of NO in anaphylactic venoconstriction. 2Rats were sensitized with ovalbumin (1 mg) and, 2 weeks later, livers were excised and perfused portally in a recirculating manner at a constant flow with Krebs',Henseleit solution. The antigen (ovalbumin; 0.1 mg) was injected into the reservoir 10 min after pretreatment with l-NAME (100 mmol/L) or d -NAME (100 mmol/L) and changes in portal vein pressure (Ppv), hepatic vein pressure (Phv) and perfusate flow were monitored. In addition, concentrations of the stable metabolites of NO ( and ) were determined in the perfusate using an HPLC,Griess system. 3The antigen caused hepatic venoconstriction, as evidenced by an increase in Ppv from a mean (SEM) baseline value of 7.7 ± 0.1 cmH2O to a peak of 21.4 ± 1.1 cmH2O at 3 min in d -NAME-pretreated livers. Pretreatment with l-NAME augmented anaphylactic venoconstriction, as reflected by a higher Ppv (27.4 ± 0.8 cmH2O) after antigen than observed following d -NAME pretreatment. The addition of l -arginine, a precursor for the synthesis of NO, reversed the augmentation of anaphylactic venoconstricion by l -NAME. This suggests that hepatic anaphylaxis increased the production of NO, which consequently attenuated anaphylactic venoconstriction. However, perfusate NOx levels did not increase significantly after antigen in livers pretreated with either l -NAME or d -NAME. 4In conclusion, l -NAME potentiates rat anaphylactic hepatic venoconstriction, suggesting that NO contributes to the attenuation of the venoconstriction. However, this functional evidence was not accompanied by corresponding changes in perfusate NOx concentrations. [source]

    Nitric oxide counteracts angiotensin II induced contraction in efferent arterioles in mice

    ACTA PHYSIOLOGICA, Issue 4 2004
    A. Patzak
    Abstract Aim:, Efferent arterioles (Ef) are one of the final control elements in glomerular haemodynamics. The influence of nitric oxide (NO) on Ef remains ambiguous. Methods:, To test the hypothesis that endothelial NO plays an important role in this context, afferent arterioles (Af) and Ef of wild-type mice (WT), and Ef of mice lacking the endothelial NO synthetase [eNOS(,/,)] were perfused. Perfusion was performed in Ef via Af (orthograde) as well as from the distal end of Ef (retrograde), which provides an estimate for the importance of substances derived from the glomerulus. Angiotensin II (Ang II) was added in doses ranging from 10,12 to 10,6 mol L,1 to the bath solution. Results:, Ang II reduced the luminal diameter of Af to 68 ± 7 and in Ef to 55 ± 8% during orthograde, and to 35 ± 6% during retrograde perfusion (10,6 mol L,1 Ang II) in WT. Pre-treatment with NG -Nitro- l -arginine-methylester (l -NAME) (10,4 mol L,1) increased the Ang II sensitivity in retrograde (17 ± 9%) and orthograde perfused Ef (19 ± 9%). The Ang II sensitivity was enhanced in eNOS(,/,) mice compared with WT, too. Already at a dose of Ang II 10,9 mol L,1, luminal diameters diminished to 8 ± 7 and 7 ± 4%. Conclusion:, The increased Ang II sensitivity during l -NAME pre-treatment and in eNOS(,/,) mice indicates a strong counteraction of endothelial derived NO on Ang II induced contraction in Ef. Moreover, Ef are similarly sensitive to Ang II during either retrograde or orthograde perfusion in the absence of NO effects, suggesting that NO mediates, at least in part, the action of potential vasodilatory substances from the glomerulus. [source]

    L -NAME reverses quinolinic acid-induced toxicity in rat corticostriatal slices: Involvement of src family kinases

    JOURNAL OF NEUROSCIENCE RESEARCH, Issue 12 2007
    Cinzia Mallozzi
    Abstract Quinolinic acid (QA) is an endogenous excitotoxin acting on N -methyl- d -aspartate receptors (NMDARs) that leads to the pathologic and neurochemical features similar to those observed in Huntington's disease (HD). The mechanism of QA toxicity also involves free radicals formation and oxidative stress. NMDARs are particularly vulnerable to the action of reactive oxygen species (ROS) and reactive nitrogen species (RNS) that can act as modulators of the activity of protein tyrosine kinases (PTKs) and phosphotyrosine phosphatases (PTPs). Because QA is able to activate neuronal nitric oxide synthase (nNOS) as well as to stimulate the NMDARs, we evaluated the effect of N,-Nitro- l -arginine-methyl ester (l -NAME), a selective nNOS inhibitor, on QA-induced neurotoxicity in rat corticostriatal slices. In electrophysiologic experiments we observed that slice perfusion with QA induced a strong reduction of field potential (FP) amplitude, followed by a partial recovery at the end of the QA washout. In the presence of l -NAME the recovery of FP amplitude was significantly increased with respect to QA alone. In synaptosomes, prepared from corticostriatal slices after the electrophysiologic recordings, we observed that l -NAME pre-incubation reversed the QA-mediated inhibitory effects on protein tyrosine phosphorylation pattern, c-src, lyn, and fyn kinase activities and tyrosine phosphorylation of NMDAR subunit NR2B, whereas the PTP activity was not recovered in the presence of l -NAME. These findings suggest that NO plays a key role in the molecular mechanisms of QA-mediated excitotoxicity in experimental model of HD. © 2007 Wiley-Liss, Inc. [source]

    Alcohol Up-Regulates TLR2 Through a NO/cGMP Dependent Pathway

    ALCOHOLISM, Issue 1 2010
    Kristina L Bailey
    Background:, Heavy alcohol consumption is associated with severe bronchitis. This is likely related to increased inflammation in the airways of alcohol abusers. Toll-like receptor 2 (TLR2) is an important mediator of inflammation in the airway epithelium. TLR2 initiates an inflammatory cascade in response to gram-positive bacteria. We have previously shown that alcohol up-regulates TLR2 in the airway epithelium. However, the mechanism of alcohol-mediated up-regulation of TLR2 has not been identified. Methods:, A human airway epithelial cell line, 16HBE14o,, was exposed to biologically relevant concentrations of alcohol (100 mM) in the presence and absence of N, -Nitro- l -arginine methyl ester hydrochloride, a nitric oxide (NO) synthase inhibitor; and Rp-8-Br-cGMP-S, an antagonist analogue of cGMP. TLR2 was measured using real-time PCR and Western blots. In addition, 16HBE14o, cells were incubated with sodium nitroprusside (SNP), an NO donor, and 8-Br-cGMP, a cGMP analogue. TLR2 was measured using real-time PCR. Results:,N, -Nitro- l -arginine methyl ester hydrochloride blocked the alcohol-mediated up-regulation of TLR2. This indicates that NO plays a key role in alcohol's up-regulation of TLR2. SNP, a NO donor, up-regulated TLR2. Rp-8-Br-CGMP-S attenuated alcohol's up-regulation of TLR2, suggesting that NO was working through cGMP/PKG. 8-Br-cGMP up-regulated TLR2, also demonstrating the importance of cGMP/PKG. Conclusions:, Alcohol up-regulates TLR2 through a NO/cGMP/PKG dependent pathway in the airway epithelium. This is an important observation in the understanding how alcohol modulates airway inflammation. In addition, this is the first time that cyclic nucleotides have been shown to play a role in the regulation of TLR2. [source]

    Characterization of agonist-induced endothelium-dependent vasodilatory responses in the vascular bed of the equine digit

    JOURNAL OF VETERINARY PHARMACOLOGY & THERAPEUTICS, Issue 1 2008
    Y. BERHANE
    The role of endothelium-derived relaxing factors was studied in the regulation of vascular responses in the Krebs perfused equine isolated digit. Perfusion pressure was recorded in response to bolus doses of 5-hydroxytryptamine (6 nmol) alone or co-administered with carbachol (CCh; 0.2 ,mol), bradykinin (BK; 0.2 nmol), substance P (SP; 0.2 nmol) or sodium nitroprusside (SNP; 0.2 ,mol). N, -Nitro- l -Arginine methyl ester hydrochloride (l -NAME; 300 ,m) caused partial but significant inhibition of CCh-induced vasodilatory response, whereas BK and SP-induced responses were resistant to l -NAME. High potassium (K+, 30 mm) and the cytochrome P - 450 (CYP) epoxygenase inhibitor, clotrimazole (10 ,m) plus l -NAME (100 ,m), completely abolished the CCh, BK and SP-induced vasodilatory responses, whereas the response to SNP was unaffected. In contrast, the l -NAME-resistant proportion of CCh, BK and SP-induced vasodilatory response was not inhibited by the highly selective CYP2C9 inhibitor, sulphaphenazole (10 ,m). The cyclo-oxygenase inhibitor, ibuprofen (10 ,m) did not affect the CCh, BK and SP-induced responses. These data demonstrate that CCh, BK and SP-induced relaxation in the equine digit involve a combination of the NO and endothelium-derived hyperpolarizing factor (EDHF) pathways. These results do not support the evidence for the involvement of CYP-derived epoxyeicosatrienoic acids and the exact nature of EDHF in the equine digit remains to be established. [source]

    Catalytic Asymmetric Conjugate Addition of Nitroalkanes to 4-Nitro-5-styrylisoxazoles,

    ANGEWANDTE CHEMIE, Issue 49 2009
    Andrea Baschieri
    Zweimal Nitro: 4-Nitro-5-styrylisoxazole dienten als maskierte ,,,-ungesättigte Carbonsäuren in der katalytischen asymmetrischen Titelreaktion. Der 4-Nitroisoxazolkern aktiviert das konjugierte Alken und eine latente Carboxylatfunktion. Die Reaktion läuft mit 5,Mol-% eines einfach zugänglichen Phasentransferkatalysators bei Raumtemperatur mit bemerkenswerter Diastereo- und Enantioselektivität ab (siehe Schema). [source]

    ChemInform Abstract: Asymmetric Organocatalytic Michael-Type Reaction of Phosphorus Ylides to Nitroolefins: Synthesis of ,-Nitro-,-aryl-,-methylene Carboxylic Esters.

    CHEMINFORM, Issue 15 2010
    Suresh Allu
    Abstract ChemInform is a weekly Abstracting Service, delivering concise information at a glance that was extracted from about 100 leading journals. To access a ChemInform Abstract of an article which was published elsewhere, please select a "Full Text" option. The original article is trackable via the "References" option. [source]

    ChemInform Abstract: A Simple Synthesis of ,-Nitro-,-keto Nitrile.

    CHEMINFORM, Issue 26 2008
    Nagatoshi Nishiwaki
    Abstract ChemInform is a weekly Abstracting Service, delivering concise information at a glance that was extracted from about 200 leading journals. To access a ChemInform Abstract of an article which was published elsewhere, please select a "Full Text" option. The original article is trackable via the "References" option. [source]

    ChemInform Abstract: Nitration of Dimethyl 1-Substituted Indole-2,3-dicarboxylates: Synthesis of Nitro- and Aminoindole Derivatives.

    CHEMINFORM, Issue 11 2008
    Yasuyoshi Miki
    Abstract ChemInform is a weekly Abstracting Service, delivering concise information at a glance that was extracted from about 200 leading journals. To access a ChemInform Abstract of an article which was published elsewhere, please select a "Full Text" option. The original article is trackable via the "References" option. [source]

    Improved Synthesis of ,-Nitro-,-Amino Ester and Acid Derivatives.

    CHEMINFORM, Issue 28 2005
    Roberto Ballini
    Abstract For Abstract see ChemInform Abstract in Full Text. [source]

    4-(Nitro)-diphenylammonium Triflate(NDPAT) Catalyzed Esterification of Carboxylic Acids with Alcohols.

    CHEMINFORM, Issue 7 2005
    Xuan-Gan Liu
    Abstract For Abstract see ChemInform Abstract in Full Text. [source]

    Double Thioalkylation/Arylation of Nitroarenes with the Reduction of Nitro- to Amino Group.

    CHEMINFORM, Issue 20 2003
    Zbigniew Wrobel
    Abstract For Abstract see ChemInform Abstract in Full Text. [source]

    Heterogeneous Catalytic Transfer Hydrogenation of Aromatic Nitro and Carbonyl Compounds over Cobalt(II) Substituted Hexagonal Mesoporous Aluminophosphate Molecular Sieves.

    CHEMINFORM, Issue 6 2003
    Susanta K. Mohapatra
    Abstract For Abstract see ChemInform Abstract in Full Text. [source]

    Systemic nitric oxide clamping in normal humans guided by total peripheral resistance

    ACTA PHYSIOLOGICA, Issue 2 2010
    J. A. Simonsen
    Abstract Aim:, We wanted to stabilize the availability of nitric oxide (NO) at levels compatible with normal systemic haemodynamics to provide a model for studies of complex regulations in the absence of changes in NO levels. Methods:, Normal volunteers (23,28 years) were infused i.v. with the nitric oxide synthase (NOS) inhibitor NG -nitro- l -arginine methyl ester (l -NAME) at 0.5 mg kg,1 h,1. One hour later, the NO donor sodium nitroprusside (SNP) was co-infused in doses eliminating the haemodynamic effects of l -NAME. Haemodynamic measurements included blood pressure (MABP) and cardiac output (CO) by impedance cardiography. Results:,l -NAME increased MABP and total peripheral resistance (TPR, 1.02 ± 0.05 to 1.36 ± 0.07 mmHg s mL,1, mean ± SEM, P < 0.001). With SNP, TPR fell to a stable value slightly below control (0.92 ± 0.05 mmHg s mL,1, P < 0.05). CO decreased with l -NAME (5.8 ± 0.3 to 4.7 ± 0.3 L min,1, P < 0.01) and returned to control when SNP was added (6.0 ± 0.3 L min,1). A decrease in plasma noradrenaline (42%, P < 0.01) during l -NAME administration was completely reversed by SNP. Plasma renin activity decreased during l -NAME administration and returned towards normal after addition of SNP. In contrast, plasma aldosterone was increased by l -NAME and remained elevated. Conclusions:, Concomitant NOS inhibition and NO donor administration can be adjusted to maintain TPR at control level for hours. This approach may be useful in protocols in which stabilization of the peripheral supply of NO is required. However, the dissociation between renin and aldosterone secretion needs further investigation. [source]

    B2 kinin receptors mediate the Indian red scorpion venom-induced augmentation of visceral reflexes via the nitric oxide cyclic guanosine monophosphate pathway

    ACTA PHYSIOLOGICA, Issue 4 2009
    S. Kanoo
    Abstract Aim:, This study was performed to delineate the kinin (receptor)-dependent pathways in the Indian red scorpion (Mesobuthus tamulus; MBT) venom-induced pulmonary oedema as well as the augmentation of cardio-pulmonary reflexes evoked by phenyldiguanide (PDG). Methods:, In urethane-anaesthetized adult rats, the effect of venom on the PDG reflex responses (blood pressure, heart rate and respiration rate) and the pulmonary water content was ascertained using various antagonists(des- Arg, B1 receptor antagonist; Hoe 140, B2 receptor antagonist; N, -nitro- l -arginine methyl ester (l -NAME), nitric oxide (NO) synthase inhibitor; methylene blue, soluble guanylate cyclase inhibitor; and glibenclamide, K+ATP channel blocker). The effect of phosphodiesterase V inhibitor (sildenafil citrate) on the reflex response and the pulmonary water content was also examined and compared with venom-induced responses. Results:, Intravenous injection of PDG (10 ,g kg,1) evoked apnoea, bradycardia and hypotension lasting >60 s. Exposure to MBT venom (100 ,g kg,1) for 30 min augmented the PDG reflex responses by two times and increased the pulmonary water content, significantly. Hoe 140 blocked the venom-induced responses (augmentation of PDG reflex and increased pulmonary water content) whereas des-Arg did not. l -NAME, methylene blue or glibenclamide also blocked the venom-induced responses. Furthermore, sildenafil citrate (that increases cGMP levels) produced augmentation of PDG reflex response and increased the pulmonary water content as seen with venom. Conclusion:, The results indicate that venom-induced responses involve B2 kinin receptors via the NO-dependent guanylate cyclase-cGMP pathway involving K+ATP channels. [source]

    Nitric oxide, superoxide and renal blood flow autoregulation in SHR after perinatal L -arginine and antioxidants

    ACTA PHYSIOLOGICA, Issue 4 2007
    M. P. Koeners
    Abstract Aim:, Nitric oxide (NO) and superoxide are considered to be regulatory in renal blood flow (RBF) autoregulation, and hence may contribute to development of hypertension. To extend our previous observations that dynamic NO release is impaired in the spontaneously hypertensive rat (SHR) we investigated, firstly, if superoxide dependency of RBF autoregulation is increased in SHR and, secondly, if the beneficial effect of perinatal supplementation in SHR is partly as a result of early correction of RBF autoregulation. We hypothesized that perinatal supplementation by restoring dynamic NO release and/or decreasing superoxide dependency and would improve life-long blood pressure regulation. Methods:, Autoregulation was studied using stepwise reductions in renal perfusion pressure in anaesthetized male SHR, SHR perinatally supplemented with arginine and antioxidants (SHRsuppl) and Wistar-Kyoto (WKY), prior to and during i.v. N, -nitro- l -arginine (NO synthase inhibitor) or tempol (superoxide dismutase mimetic). Results:, Spontaneously hypertensive rat displayed a wider operating range of RBF autoregulation as compared with WKY (59 ± 4 vs. 33 ± 2 mmHg, respectively; P < 0.01). Perinatal supplementation in SHR decreased mean arterial pressure, renal vascular resistance and the operating range of RBF autoregulation (43 ± 3 mmHg; P < 0.01). In addition autoregulation efficiency decreased. RBF autoregulation characteristics shifted towards those of normotensive WKY. However, dynamic NO release was still impaired and no clear differences in superoxide dependency in RBF autoregulation between groups was observed. Conclusion:, Perinatal supplements shifted RBF autoregulation characteristics of SHR towards WKY, although capacity of the SHRsuppl kidney to modulate NO production to shear stress still seems impaired. The less strictly controlled RBF as observed in perinatally supplemented SHR could result in an improved long-term blood pressure control. This might partly underlie the beneficial effects of perinatal supplementation. [source]

    Role of neuronal nitric oxide synthase in response to hypertonic saline loading in rats

    ACTA PHYSIOLOGICA, Issue 4 2004
    R. Wangensteen
    Abstract Aims:, This study analyses the influence of neuronal nitric oxide synthase (nNOS) blockade with 7-nitroindazole (7NI) on the haemodynamic and renal response to a hypertonic saline load (HSL). We also evaluated the effects of non-specific NOS inhibitor N, -nitro- l -arginine methyl ester (l -NAME). Methods:, The following groups were used: controls, rats treated with 7NI at 0.5 or 5 mg kg,1, and rats treated with l -NAME at 0.5 or 5 mg kg,1. A further five groups received an isotonic saline load (ISL). Results:, Mean arterial pressure (MAP) was significantly increased in control rats after HSL. MAP was further increased in both 7NI-treated groups, and the l -NAME groups showed marked dose-related pressor responses. During ISL, MAP was only significantly increased in the group treated with 5 mg kg,1 of l -NAME. The pressure,natriuresis relationship during the experimental period after the HSL was reduced in the 7NI group treated with 5 mg kg,1 and severely attenuated in both l -NAME groups. The increase in plasma sodium was significantly greater after the HSL in both 7NI groups and both l -NAME groups compared with controls. Conclusions:, The present results suggest that nNOS and other NOS isozymes play a counter-regulatory role in the pressor response to HSL. Moreover, the blockade of nNOS with the higher dose of 7NI produces a blunted pressure,natriuresis relationship in response to the HSL. Finally, it is concluded that nNOS participates in the homeostatic cardiovascular and renal response to hypertonic saline loading by attenuating the blood pressure increase and hypernatremia, and facilitating natriuresis. [source]

    Changes in reactivity of rat arteries subjected to dynamic stretch

    ACTA PHYSIOLOGICA, Issue 1 2000
    Dvoretsky
    The effect of dynamic stretch on the reactivity of the rat tail and mesenteric artery segments was studied. Segments mounted on a myograph were stretched by a computer-controlled motorized micromanipulator. Dynamic stretch (1, 5 or 7 Hz) inhibited the artery constriction induced by noradrenaline (10 ,M), 5-hydroxytryptamine (0.7 ,M), or electrical field stimulation of intramural nerves. In contrast, dynamic stretch enhanced the tetrodotoxin-insensitive dilation induced by electrical field stimulation of noradrenaline-contracted arteries. Maximal increase of dilation evoked by electrical field stimulation (24.5 ± 5.0% in mesenteric and 50.3 ± 15.6% in the tail artery) was observed at a dynamic stretch-frequency of 5 Hz. An inhibitor of nitric oxide synthesis, NG -nitro- L -arginine (100 ,M), abolished the difference in reactivity between static and dynamic conditions. The results indicate that dynamic stretch of the arteries activates nitric oxide synthesis/secretion, thus reducing constrictor and increasing dilator responses to the stimuli used. [source]

    Study of the Responses of a Sonogel-Carbon Electrode Towards Phenolic Compounds

    ELECTROANALYSIS, Issue 9 2005
    Cordero-Rando, Ma del
    Abstract The electrochemical behavior of a sonogel-carbon electrode towards nine phenolic compounds (chloro-, nitro- and alkyl-phenols) was studied; one of them (4-chloro-3-methylphenol) was used to evaluate characteristics of the electrode, such as accumulation and cleaning procedure of the electrode surface, reproducibility of the measurements, and influence of time from fabrication on electrochemical response. A polyethyleneglycol-modified sonogel-carbon electrode was found to improve the electrochemical response towards the analyte. A linear relationship between peak height and concentration in the range 0.005,0.5,mg L,1 was obtained, with a detection limit of 2.8,,g L,1. The studies of electrochemical parameters, as well as interferences, are also included. [source]

    A preliminary characterization of the mutagenicity of atmospheric particulate matter collected during sugar cane harvesting using the Salmonella/microsome microsuspension assay

    ENVIRONMENTAL AND MOLECULAR MUTAGENESIS, Issue 4 2008
    Gisela de Aragćo Umbuzeiro
    Abstract During sugar cane harvesting season, which occurs from May to November of each year, the crops are burnt, cut, and transported to the mills. There are reports showing that mutagenic activity and PAH content increase during harvesting season in some areas of Sćo Paulo State in comparison with nonharvesting periods. The objective of this work was to preliminarily characterize the mutagenic activity of the total organic extracts as well as corresponding organic fractions of airborne particulate matter (PM) collected twice from two cities, Araraquara (ARQ) and Piracicaba (PRB), during sugar cane harvesting season using the Salmonella/microsome microssuspension assay. One sample collected in Sćo Paulo metropolitan area was also included. The mutagenicity of the total extracts ranged from 55 to 320 revertants per cubic meter without the addition of S9 and from not detected to 57 revertants per cubic meter in the presence of S9 in areas with sugar cane plantations. Of the three fractions analyzed, the most polar ones (nitro and oxy) were the most potent. A comparison of the response of TA98 with YG1041 and the increased potencies without S9 indicated that nitro compounds are causing the observed effect. More studies are necessary to verify the sources of the mutagenic activity such as burning of vegetal biomass and combustion of heavy duty vehicles used to transport the sugar cane to the mills. The Salmonella/microsome assay can be an important tool to monitor the atmosphere for mutagenicity during sugar cane harvesting season. Environ. Mol. Mutagen. 2008. © 2008 Wiley-Liss, Inc. [source]

    Proteomic analysis of cellular responses to low concentration N -methyl- N,-nitro- N -nitrosoguanidine in human amnion FL cells

    ENVIRONMENTAL AND MOLECULAR MUTAGENESIS, Issue 2 2004
    Jinghua Jin
    Abstract We have shown previously that exposure to a low concentration of N -methyl- N,-nitro- N -nitrosoguanidine (MNNG) induces comprehensive changes in the protein expression profile of human amnion FL cells, including the induction, suppression, upregulation, and downregulation of various proteins. In addition, by proteomic analysis combining two-dimensional gel electrophoresis (2-DE) and mass spectrometry, some of the induced and suppressed proteins were identified. In this study, we identified an additional 18 proteins among those that were either up- or downregulated by MNNG treatment. The proteins identified were a heterogeneous group that included several zinc finger proteins, proteins involved in signal transduction, cytoskeletal proteins, cell-cycle regulation proteins, and proteins with unknown functions. The involvement of these proteins in the cellular responses to alkylating agents has not been reported before and their physiological relevance is not clear. Therefore, our findings may help better understand the global cellular stress responses to chemical carcinogens, and may lead to new studies on the functions of these MNNG-responsive proteins. Furthermore, some of these proteins may serve as biomarkers for detecting exposure of human populations to environmental carcinogens. Environ. Mol. Mutagen. 43:93,99, 2004. © 2004 Wiley-Liss, Inc. [source]

    Novel DNA repair alkyltransferase from Caenorhabditis elegans

    ENVIRONMENTAL AND MOLECULAR MUTAGENESIS, Issue 2-3 2001
    Sreenivas Kanugula
    Abstract O6 -Alkylguanine DNA-alkyltransferase (AGT) is a widely distributed DNA repair protein that protects living organisms from endogenous and exogenous alkylation damage to DNA at the O6 -position of guanine. The search of the C. elegans genome database for an AGT protein revealed the presence of a protein (cAGT-2) with some similarity to known AGTs in addition to the easily recognized cAGT-1 protein. The predicted protein sequence of cAGT-2 contains the amino acid sequence ,ProCysHisPro, at the presumed active site of the protein, whereas all other known AGTs have ,ProCysHisArg,. A truncated version of the cAGT-2 protein was expressed in E. coli. This purified recombinant protein was able to repair O6 -methylguanine and O4 -methylthymine adducts in DNA in vitro and also reacted with the bulky benzyl adduct in O6 -benzylguanine. This fragment of cAGT-2 (104 amino acids) is the smallest protein possessing AGT activity yet described. The full-length cAGT-2 protein (274 amino acids) totally lacks the N-terminal domain present in all other known AGTs but has a long C-terminal extension that has significant homology to histone 1C. Expression of cAGT-2 in an E. coli strain lacking endogenous AGT activity provided modest but statistically significant resistance to the toxicity of N -methyl- N,-nitro- N -nitrosoguanidine, confirming that cAGT-2 is an alkyltransferase. Environ. Mol. Mutagen. 38:235,243, 2001. © 2001 Wiley-Liss, Inc. [source]

    Role of Nitric Oxide in Pentylenetetrazol-Induced Seizures: Age-Dependent Effects in the Immature Rat

    EPILEPSIA, Issue 4 2000
    Anne Pereira de Vasconcelos
    Summary: Purpose: Seizure susceptibility and consequences are highly age dependent. To understand the pathophysiologic mechanisms involved in seizures and their consequences during development, we investigated the role of nitric oxide (NO) in severe pentylenetetrazol (PTZ)-induced seizures in immature rats. Methods: Four cortical electrodes were implanted in 10-day-old (P10) and 21-day-old (P21) rats, and seizures were induced on the following day by repetitive injections of subconvulsive doses of PTZ. The effects of NG -nitro- l -arginine methyl ester (l -NAME; 10 mg/kg) and 7-nitroindazole (7NI; 40 mg/kg), two NO synthase (NOS) inhibitors, and l -arginine (l -arg; 300 mg/kg), the NOS substrate, were evaluated regarding the mean PTZ dose, seizure type and duration, and mortality rate. Results: At P10, the postseizure mortality rate increased from 18,29% for the rats receiving PTZ only to 100% and 89% for the rats receiving l -NAME and 7NI, respectively; whereas l -arg had no effect. Conversely, at P21, NOS inhibitors did not affect the 82,89% mortality rate induced by PTZ alone, whereas l -arg decreased the mortality rate to 29%. In addition, all NO-related drugs increased the duration of ictal activity at P10, whereas at P21, L -arg and L -NAME affected the first seizure type, producing clonic seizures with L -arg and tonic seizures with L -NAME. Conclusions: The relative natural protection of very immature rats (P10) against PTZ-induced deaths could be linked to a high availability of L -arg and, hence, endogenous NO. At P21, the modulation of seizure type by NO-related compounds may be related to the maturation of the brain circuitry, in particular the forebrain, which is involved in the expression of clonic seizures. [source]

    A 4-trifluoromethyl derivative of salicylate, triflusal, stimulates nitric oxide production by human neutrophils: role in platelet function

    EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 9 2000
    De Miguel
    Background The thrombotic process is a multicellular phenomenon in which not only platelets but also neutrophils are involved. Recent in vitro studies performed in our laboratory have demonstrated that triflusal, a 4-trifluoromethyl derivative of salicylate, reduced platelet aggregation not only by inhibiting thromboxane A2 production but also by stimulating nitric oxide (NO) generation by neutrophils. The aim of the present study was to evaluate whether oral treatment of healthy volunteers with triflusal could modify the ability of their neutrophils to produce NO and to test the role of the NO released by neutrophils in the modulation of ADP-induced platelet aggregation and ,-granule secretion. Methods The study was performed in 12 healthy volunteers who were orally treated with triflusal (600 mg day,1) for 5 days. Flow cytometric detection of platelet surface expression of P-selectin was used as a measure of the ability of platelets to release the contents of their ,-granules. Results After treatment with triflusal, there was an increase in NO production by neutrophils and an increase in endothelial nitric oxide synthase (eNOS) protein expression in neutrophils. A potentiation of the inhibition of platelet aggregation by neutrophils was reversed by incubating neutrophils with both an l -arginine antagonist, NG -nitro- l -arginine methyl ester ( l -NAME) and an NO scavenger, 2-(4-carboxyphenyl)-4,4,5,5 tetramethylimidazoline 1-oxyl 3-oxide (C-PTIO). A slight decrease in P-selectin surface expression on platelets was found which was not modified by the presence of neutrophils and therefore by the neutrophil-derived NO. Exogenous NO released by sodium nitroprusside dose-dependently inhibited both ADP-stimulated ,-granule secretion and platelet aggregation. Therefore, platelet aggregation showed a greater sensitivity to be inhibited by exogenous NO than P-selectin expression. Conclusion Oral treatment of healthy volunteers with triflusal stimulated NO production and eNOS protein expression in their neutrophils. After triflusal treatment, the neutrophils demonstrated a higher ability to prevent ADP-induced platelet aggregation. However, the neutrophils and the endogenous NO generated by them failed to modify P-selectin expression in ADP-activated platelets. [source]

    Pro-VGF-derived peptides induce penile erection in male rats: possible involvement of oxytocin

    EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 11 2004
    Salvatora Succu
    Abstract The effect of five peptides derived from the C-terminal portion of rat pro-VGF (VGF577-617, VGF588-617, VGF599-617, VGF556-576 and VGF588-597) on penile erection was studied after injection into the hypothalamic paraventricular nucleus of male rats. VGF577-617, VGF588-617, VGF599-617 and, to a lower extent, VGF588-597 (0.1,2 µg) induced penile erection episodes in a dose-dependent manner when injected into the paraventricular nucleus, while VGF556-576 was ineffective. VGF588-617 -induced penile erection was reduced by nitro, - l -arginine methylester (L-NAME; 20 µg), by morphine (5 µg) and by muscimol (1 µg), but not by dizocilpine [(+)MK-801; 1 µg], nor by cis -flupenthixol (10 µg) given into the paraventricular nucleus 10 min before the VGF peptide. d(CH2)5Tyr(Me)-Orn8 -vasotocin (1 µg) effectively reduced VGF588-617 -induced penile erection when given into the lateral ventricles but not when injected into the paraventricular nucleus. Immunocytochemistry with antibodies specific for the C-terminal nonapeptide sequence of pro-VGF (VGF609-617) revealed numerous neuronal fibres and terminals within the paraventricular nucleus, including its parvocellular components. Here, many immunostained neuronal terminals impinged on parvocellular oxytocinergic neurons. The present results show for the first time that certain pro-VGF C-terminus-derived peptides promote penile erection when injected into the paraventricular nucleus and suggest that, within this nucleus, these or closely related pro-VGF-derived peptides may be released to influence sexual function by activating paraventricular oxytocinergic neurons mediating penile erection. [source]

    Palladium-Catalyzed C2 or C5 Direct Arylation of 3-Formylthiophene Derivatives with Aryl Bromides

    EUROPEAN JOURNAL OF ORGANIC CHEMISTRY, Issue 4 2010
    Jia Jia Dong
    Abstract The system Pd(OAc)2/dppb was found to be an efficient catalyst precursor for the direct arylation of 3-formylthiophene derivatives. When using 3-formylthiophene, the 2-arylated thiophenes were obtained with regioselectivities of 76,86,%, whereas the arylation of 3-formylthiophene diethyl acetal gave the 5-arylated thiophenes with regioselectivities of 64,88,%. These reactions were performed by using only 0.1 mol-% of the catalyst. Moreover, this procedure has been found to be tolerant to a variety of functional groups on the aryl bromide such as formyl, propionyl, benzoyl, nitrile, or nitro. [source]

    Stable Ion and Electrophilic Substitution (Nitration and Bromination) Study of A-Ring Substituted Phenanthrenes: Novel Carbocations and Substituted Derivatives; NMR, X-ray Analysis, and Comparative DNA Binding

    EUROPEAN JOURNAL OF ORGANIC CHEMISTRY, Issue 3 2007
    Cédric Brulé
    Abstract Persistent carbocations were generated from five A-ring mono- and di-substituted phenanthrenes [3-OMe; 4-OMe, 1,3-bis(OMe), 2,4-bis(OMe), and 1,3-bis(Me)]. In all cases protonation occurs in the A-ring, ortho/para relative to methoxy or methyl substituent(s). Complete NMR assignments of the resulting carbocations are reported and their charge delocalization modes are discussed. Mild nitration (with 20,50,% aqueous HNO3 at ,10 °C or at room temp.) and bromination (NBS/MeCN/room temp.) of these substrates resulted in the synthesis of several novel mononitro-/dinitro- as well as monobromo/dibromo derivatives, including those with nitro or bromo substituent in the bay-region. Correspondence between the site of attack in low-temperature protonation study and nitro substitution in ambient mild nitrations are examined. Complete NMR assignments for the new derivatives are reported as well as X-ray structures for 2,4-dimethoxy-1-nitro- and 1,3-dimethyl-4-nitrophenanthrenes. A comparative DNA binding study with MCF cells on three of the synthesized mononitro and one dinitro derivative showed that 1,3-dimethyl-9-nitro- (nitro at the meso position), 3-methoxy-4-nitro- (nitro in bay-region), and 1,3-dimethoxy-4,9-dinitrophenanthrenes (nitro in both meso and bay-regions) formed DNA adducts. (© Wiley-VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2007) [source]

    Nitric oxide and thyroid gland: modulation of cardiovascular function in autonomic-blocked anaesthetized rats

    EXPERIMENTAL PHYSIOLOGY, Issue 3 2004
    Andrea Lorena Fellet
    We have previously reported that acute administration of NG -nitro- l -arginine methyl ester (l -NAME) increases the mean arterial pressure (MAP) and heart rate (HR) in autonomic-blocked (CAB) anaesthetized rats. In the present study we examined whether thyroid and adrenal glands are involved in these pressor and chronotropic responses. Sprague-Dawley rats were studied after bilateral vagotomy and ganglionic blockade with hexamethonium (10 mg kg,1), and stabilization of MAP with infusion of phenylephrine (PE) (6 ,g kg,1 min,1). The rats were divided into groups: L, CAB; PE, CAB + PE bolus (6 ,g kg,1); L-TX, thyroidectomy + CAB; L-AX, adrenalectomy + CAB; TX, only thyroidectomy; C, CAB. L, L-AX and L-TX groups received a bolus of l -NAME (7.5 mg kg,1). Triiodothyronine (T3), thyroxin (T4) and thyrotropin (TSH) levels were measured in L and L-TX rats before and after l -NAME administration. Reduced nicotamide adenine dinucleotide (NADPH) diaphorase activity was determined in heart and aorta of the TX group. The pressor response induced by l -NAME was similar in all groups. l -NAME-induced-tachycardia was associated with this rise in MAP. Adrenalectomy did not modify this chronotropic response, but it was attenuated by thyroidectomy. Thyroidectomy by itself decreased the circulating levels of T3 but it had no effect on the plasma levels of T4 and TSH. L and L-TX groups showed similar levels of circulating T4 and TSH, meanwhile the plasma level of T3 decreased in the L group. Nitric oxide synthase (NOS) activity in atria as well as in aorta was greater in the TX group compared with C. When autonomic influences are removed, the thyroid gland modulates intrinsic heart rate via a mechanism that involves, at least in part, the nitric oxide pathway. [source]

    Possible role of exogenous cAMP to improve vascular endothelial dysfunction in hypertensive rats

    FUNDAMENTAL & CLINICAL PHARMACOLOGY, Issue 6 2006
    Dhvanit I. Shah
    Abstract The study has been designed to investigate the effect of 8-Br-cAMP, an activator of protein kinase A, in hypertension-induced vascular endothelial dysfunction. Rats were uninephroctomized and desoxycortisone acetate (DOCA) (40 mg/kg, s.c.) was administered to rats to produce hypertension (mean arterial blood pressure > 140 mmHg). Vascular endothelial dysfunction was assessed using isolated aortic ring preparation, electron microscopy of thoracic aorta and serum concentration of nitrite/nitrate. The expression of mRNA for p22phox and eNOS was assessed by using reverse transcriptase-polymerase chain reaction. Serum thiobarbituric acid reactive substances concentration and aortic superoxide anion concentration were estimated to assess oxidative stress. 8-Br-cAMP (5 mg/kg, i.p.) or atorvastatin (30 mg/kg, p.o.) prevented hypertension-induced attenuation of acetylcholine-induced endothelium-dependent relaxation, impairment of vascular endothelial lining, decrease in expression of mRNA for endothelial nitric oxide synthase (eNOS), serum nitrite/nitrate concentration and increase in expression of mRNA for p22phox, superoxide anion and serum TBARS. The ameliorative effect of 8-Br-cAMP was prevented by N -nitro- l -arginine methyl ester (25 mg/kg, i.p.) and glibenclamide (30 mg/kg, i.p.). It may be concluded that 8-Br-cAMP may stimulate expression and activity of eNOS and suppress expression of p22phox subunit of NADPH oxidase to reduce oxidative stress and subsequently improve vascular endothelial dysfunction. [source]