Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Nitro Compounds”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,279 records · Page 71Linked to original sources
PubMed2006

Resistance and cross-resistance to neonicotinoid insecticides and spinosad in the Colorado potato beetle, Leptinotarsa decemlineata (Say) (Coleoptera: Chrysomelidae).

The Colorado potato beetle, Leptinotarsa decemlineata (Say), has developed resistance to many insecticides used for its control, recently including imidacloprid, a neonicotinoid compound. Other neonicotinoids are now being deployed to control this pest. A key point in the strategies of resistance management is the monitoring of resistance and cross-resistance. In the summer of 2003, imidacloprid-resistant adult Colorado potato beetles collected from Long Island, New York, USA were bioassayed using topical applications of imidacloprid and nine other neonicotinoids. Compared to a standard susceptible strain, the Long Island beetles showed 309-fold resistance to imidacloprid, and lower levels of cross-resistance to all other neonicotinoids, despite these never having been used in the field, i.e., 59-fold to dinotefuran, 33-fold to clothianidin, 29-fold to acetamiprid, 28-fold to N-methylimidacloprid, 25-fold to thiacloprid, 15-fold to thiamethoxam, 10-fold to nitenpyram, but less than 2-fold to nicotine. In injection bioassays, high resistance to imidacloprid was also found (116-fold). Piperonyl butoxide partially suppressed resistance to imidacloprid, but the resistance level was still over 100-fold, indicating that other mechanisms were primarily responsible for resistance. Low levels of resistance (8- to 10-fold) were found to the nicotinic activator, spinosad, in an imidacloprid-resistant strain collected from the same field in 2004. The cross-resistance seen with all the neonicotinoids tested suggests that the rotation of imidacloprid with other neonicotinoids may not be an effective long-term resistance management strategy. Rotation with spinosad also carries some risk, but it is unlikely that spinosad resistance in this case is mechanistically related to that for the neonicotinoids.

Anabasine↗
PubMed2006

Cystamine and cysteamine prevent 3-NP-induced mitochondrial depolarization of Huntington's disease knock-in striatal cells.

Abstract Cystamine significantly improved motor deficits and extended survival in mouse models of Huntington's disease (HD); however, the precise mechanism(s) by which cystamine and the related compound cysteamine are beneficial remain to be elucidated. Using clonal striatal cell lines from wild-type (STHdhQ7/HdhQ7) and mutant huntingtin knock-in (STHdhQ111/HdhQ111) mice, we have tested the hypothesis that cystamine and cysteamine could be beneficial by preventing the depolarization of mitochondria in cell cultures. Treatment with 3-nitroproprionic acid (3-NP), a mitochondrial complex II inhibitor, induces mitochondrial depolarization and cell death of mutant HD striatal cells but not of wild-type cells. The 3-NP-mediated decrease in the mitochondrial membrane potential was attenuated by 50 microm cystamine and completely inhibited by 250 microm cystamine. Similar results were obtained using cysteamine (50-500 microm). In addition, both cystamine and cysteamine significantly attenuated the 3-NP-induced cell death. Treatment of mutant HD striatal cells with 3-NP resulted in a robust decrease in the cellular and mitochondrial levels of glutathione (GSH) compared with cells exposed to the vehicle alone. Pre-treatment of the cells with cystamine and cysteamine completely prevented the 3-NP-mediated decrease in cellular and mitochondrial GSH levels. Incubation with L-buthionine (S,R) sulfoximine (BSO) 250 microm in combination with cystamine (250 microm) or cysteamine (250 microm) prior to being treated with 3-NP completely prevented the beneficial effects of cystamine and cysteamine on the 3-NP-mediated mitochondrial depolarization. These results demonstrate that cystamine and cysteamine prevent the 3-NP-induced mitochondrial depolarization of HD striatal cell cultures.

Animals↗
PubMed2001

Risk posed to honeybees (Apis mellifera L, Hymenoptera) by an imidacloprid seed dressing of sunflowers.

In a greenhouse metabolism study, sunflowers were seed-treated with radiolabelled imidacloprid in a 700 g kg-1 WS formulation (Gaucho WS 70) at 0.7 mg AI per seed, and the nature of the resulting residues in nectar and pollen was determined. Only the parent compound and no metabolites were detected in nectar and pollen of these seed-treated sunflower plants (limit of detection < 0.001 mg kg-1). In standard LD50 laboratory tests, imidacloprid showed high oral toxicity to honeybees (Apis mellifera), with LD50 values between 3.7 and 40.9 ng per bee, corresponding to a lethal food concentration between 0.14 and 1.57 mg kg-1. The residue level of imidacloprid in nectar and pollen of seed-treated sunflower plants in the field was negligible. Under field-growing conditions no residues were detected (limit of detection: 0.0015 mg kg-1) in either nectar or pollen. There were also no detectable residues in nectar and pollen of sunflowers planted as a succeeding crop in soils which previously had been cropped with imidacloprid seed-treated plants. Chronic feeding experiments with sunflower honey fortified with 0.002, 0.005, 0.010 and 0.020 mg kg-1 imidacloprid were conducted to assess potential long-term adverse effects on honeybee colonies. Testing end-points in this 39-day feeding study were mortality, feeding activity, wax/comb production, breeding performance and colony vitality. Even at the highest test concentration, imidacloprid showed no adverse effects on the development of the exposed bee colonies. This no-adverse-effect concentration of 0.020 mg kg-1 compares with a field residue level of less than 0.0015 mg kg-1 (= limit of detection in the field residue studies) which clearly shows that a sunflower seed dressing with imidacloprid poses no risk to honeybees. This conclusion is confirmed by observations made in more than 10 field studies and several tunnel tests.

Alkenes↗
PubMedDate not supplied

Subchronic inhalation toxicity of nitromethane and 2-nitropropane.

Nitromethane (NM) and 2-nitropropane (2-NP) and versatile compounds employed in a wide variety of industrial applications, thus providing ample opportunity for occupational exposure. The purpose of this study was to determine the subchronic inhalation toxicity of NM and 2-NP in order to recommend acceptable exposure levels in the workplace. Fifty male rats and 15 male rabbits were exposed to either 98 ppm or 745 ppm of NM or 27 or 207 ppm of 2-NP 7 hours/day, 5 days/week, for periods up to 24 weeks. Fifty rats and 15 rabbits were exposed to filtered air for similar lengths of time and served as controls. Ten rats from each exposure and control group were sacrificed following 2 days, 10 days, 1 month, 3 months, and 6 months of exposure. Five rabbits from each exposure or control group were sacrificed at 1, 3, and 6 months of exposure. Effects relatable to exposure to NM were decreased body weight gain in rats following 8 weeks of exposure to 745 ppm, and a thyroid effect evidenced by an increased thyroid weight and decreased serum thyroxin levels, most notable in rabbits. Liver weights were significantly elevated in rats exposed to 207 ppm of 2-NP for 1, 3, and 6 months. No exposure-related gross or microscopic alterations were seen in any of the tissues examined for rats and rabbits exposed to 745 and 98 ppm of NM and 27 ppm of 2-NP or in tissues of rabbits exposed to 207 ppm of 2-NP. Liver neoplasms were seen in all 10 rats killed following 6 months of exposure to 207 ppm of 2-NP, indicating that 2-NP is a potent carcinogen in the rat.

Animals↗
PubMed2004

Creatine protects against 3-nitropropionic acid-induced cell death in murine corticostriatal slice cultures.

In murine corticostriatal slice cultures, we studied the protective effects of the bioenergetic compound creatine on neuronal cell death induced by the mitochondrial toxin 3-nitropropionic acid (3-NP). 3-NP caused a dose-dependent neuronal degeneration accompanied by an increased lactate dehydrogenase (LDH) activity in the cell culture medium. An increased ratio of lactate to pyruvate concentration in the medium suggested that metabolic activity shifted to anaerobic energy metabolism. These effects were predominantly observed in the 24-h recovery period after 3-NP exposure. Creatine protected against 3-NP neurotoxicity: LDH activity was reduced and aerobic respiration of pyruvate was stimulated, which resulted in lower lactate levels and less cell death. In both striatum and cortex, apoptosis in 3-NP-exposed slices was demonstrated by increased activation of the pro-apoptotic protein caspase-3 and by numerous cells exhibiting DNA fragmentation detected by the terminal transferase-mediated biotinylated-UTP nick end-labeling (TUNEL) technique. Creatine administration to the 3-NP-exposed corticostriatal slices resulted in a reduced number of TUNEL-positive cells in the recovery period. However, in the striatum, an unexpected increase of both TUNEL-positive cells and caspase-3-immunostained cells was observed in the exposure phase in the presence of creatine. In the recovery phase, caspase-3-immunostaining decreased to basal levels in both striatum and cortex. These findings suggest that 3-NP-induced neuronal degeneration in corticostriatal slices results from apoptosis that in the cortex can be prevented by creatine, while in the more vulnerable striatal cells it may lead to an accelerated and increased execution of apoptotic cell death, preventing further necrosis-related damage in this region.

Animals↗
PubMed2001

Lack of gastric toxicity of nitric oxide-releasing indomethacin, NCX-530, in experimental animals.

The effects of a nitric oxide (NO) releasing derivative of indomethacin (NCX-530) on gastric ulcerogenic and healing responses were evaluated in rats and mice, in comparison with the parent compound indomethacin. Indomethacin (per os) produced damage in the rat stomach in a dose-dependent manner. NCX-530 (per os) itself, however, was not ulcerogenic and even showed a dose-dependent protection against HCl/ethanol-induced lesions in the rat stomach. Likewise, indomethacin given repeatedly delayed healing of gastric ulcers induced in mice by thermal cauterization, while NCX-530 did not affect the healing response and significantly promoted the healing as compared to indomethacin. These actions of NCX-530 were mimicked by the combined administration of a NO donor NOR-3 with indomethacin. The amount of NO metabolites was increased in both the gastric contents and serum when NCX-530, but not indomethacin, was given in pylorus-ligated stomachs. Neither indomethacin nor NCX-530 influenced gastric acid secretion and transmucosal potential difference, yet NCX-530 caused a marked increase of gastric mucosal blood flow, which was preventable by carboxy-PTIO, a scavenger of NO. Gastric motility was increased by indomethacin but not by NCX-530. In addition, NCX-530 inhibited PGE2 generation in both the intact and ulcerated gastric mucosa and showed antiinflammatory action on carrageenan-induced rat paw edema, as effectively as indomethacin. These results suggest that unlike indomethacin, NCX-530 caused neither an irritating action on the stomach nor healing impairment effect on the preexisting gastric ulcers, but conferred gastric protection against HCl/ethanol, despite causing cyclooxygenase inhibition and antiinflammatory action, as effectively as indomethacin. This NO-releasing indomethacin, probably by releasing NO, exerts protective influences, such as an increase of gastric mucosal blood flow, that counteract the potential damaging effects of cyclooxygenase inhibition by indomethacin.

Acetates↗
PubMed2005

Longevity of granular iron in groundwater treatment processes: corrosion product development.

Permeable reactive barriers employing iron as a reactive surface have received extensive attention. A remaining issue, however, relates to their longevity. As an integral part of a long-term column study conducted to examine the influence of inorganic cosolutes on iron reactivity toward chlorinated solvents and nitroaromatic compounds, Master Builder iron grains were characterized via scanning and transmission electron microscopy, electron energy loss spectroscopy (EELS), micro-Raman spectroscopy, and X-ray diffraction. Prior to exposure to carbonate solutions, the iron grains were covered by a surface scale that consisted of fayalite (Fe2SiO4), wüstite (FeO), magnetite (Fe3O4), maghemite (gamma-Fe2O3), and graphite. After 1100 days of exposure to solutions containing carbonate, other inorganic solutes, and organic contaminants, the wüstite, fayalite, and graphite of the original scale partially dissolved, and magnetite and iron carbonate hydroxide (Fe3(OH)2.2CO3) precipitated on top of the scale. Raman results indicate the presence of green rust (e.g., [Fe4(2+)Fe2(3+)(OH)12]-[CO3 x 2H2O]) toward the column outlet after 308 days of operation, although this mineral phase disappears at longer operation times. Grains extracted from a column exposed to a high concentration (20 mM) of sodium bicarbonate were more extensively weathered than those from columns exposed to 2 mM sodium bicarbonate. An iron carbonate hydroxide layer up to 100 microm thick was observed. Even though EELS analysis of iron carbonate hydroxide indicates that this is a redox-active phase, the thickness of this layer is presumed responsible for the previously observed decline in the reactivity of this column relative to low-bicarbonate columns. A silica-containing feed resulted in reduced reactivity toward TCE. Grains from this column had a strong enrichment of silicon in the precipitates, although no distinct silica-containing mineral phases were identified. The substitution of 2 mM calcium carbonate for 2 mM sodium bicarbonate in the feed did not produce a measurable reactivity loss, asthe discrete calcium carbonate precipitates that formed in this system did not severely restrict access to the reactive surface.

Calcium Carbonate↗
PubMed2002

In-vitro transfer of nitazoxanide across the intestinal epithelial barrier.

Nitazoxanide is a thiazolide compound that exhibits antimicrobial properties against helminths, protozoa, anaerobic bacteria and also Helicobacter pylori. The mucosal diffusion of this new drug has not been studied. The aim of this study was to examine the transport of radiolabelled nitazoxanide across the epithelial barrier according to the mode (mucosal or serosal) of drug administration. HT29-19A intestinal epithelial cells, grown as monolayers on microporous filters, were used as an epithelial model. In a short-term (100 min) transport study, the apical to basal and the basal to apical transport of nitazoxanide across the monolayers was studied in an Ussing chamber. In a long-term (24 h) study, the transport of the drug and its intracellular accumulation were studied in filter-grown epithelial monolayers kept in culture plates. In the short-term transport study, both the apical and basal fluxes achieved a steady state after 70 min and there was no significant difference between the apical to basal (3991+/-1001 ng h(-1) cm(-2)) and the basal to apical (4246+/-856 ng h(-1) cm(-2)) nitazoxanide fluxes. In the long-term transport study, after apical or basal drug application, a gradual increase in the drug concentration in the opposite compartment was noted, which reached similar values for apical and basal fluxes (2497+/-125 and 2309+/-81 ng mL(-1), respectively) after 24 h. Moreover, a rapid, although transitory, intracellular accumulation of nitazoxanide was observed at 10 min after apical (299+/-25 ng/10(6) cells) and basal (124+/-10 ng/10(6) cells) drug application, but decreased thereafter. There is an important transepithelial transport of nitazoxanide across the digestive epithelial monolayer with a rapid intracellular accumulation of the drug. No difference between the apical to basal and basal to apical fluxes of the drug was observed, suggesting that both topical and systemic modes of action of this antibiotic are successful.

Anti-Bacterial Agents↗
PubMed1991

Complexes of .NO with nucleophiles as agents for the controlled biological release of nitric oxide. Vasorelaxant effects.

Selected nucleophile/nitric oxide adducts [compounds which contain the anionic moiety, XN(O-)N = O] were studied for their ability to release nitric oxide spontaneously in aqueous solution and for possible vasoactivity. The diversity of structures chosen included those in which the nucleophile residue, X, was that of a secondary amine [Et2N, as in [Et2NN(N = O)O]Na, 1], a primary amine [iPrHN, as in [iPrHNN(N = O)O]Na, 2], a polyamine, spermine [as in the zwitterion H2N(CH2)3NH2+(CH2)4N[N(N = O)O-](CH2)3NH2, 3], oxide [as in Na[ON(N = O)O]Na, 4], and sulfite [as in NH4[O3SN(N = O)O]NH4, 5]. The rate constants (k) for decomposition in pH 7.4 phosphate buffer at 37 degrees C, as measured by following loss of chromophore at 230-260 nm, were as follows: 1, 5.4 x 10(-3) s-1; 2, 5.1 x 10(-3) s-1; 3, 0.30 x 10(-3) s-1; 4, 5.0 x 10(-3) s-1; and 5, 1.7 x 10(-3) s-1. The corresponding extents of nitric oxide release (ENO) were 1.5, 0.73, 1.9, 0.54, and 0.001 mol/mol of starting material consumed, respectively, as determined from the integrated chemiluminescence response. Vasodilatory activities expressed as the concentrations required to induce 50% relaxation in norepinephrine-constricted aortic rings bathed in pH 7.4 buffer at 37 degrees C (EC50) were as follows: 1, 0.19 microM; 2, 0.45 microM; 3, 6.2 microM; 4, 0.59 microM; and 5, 62 microM. Vasorelaxant potency (expressed as 1/EC50) was strongly correlated with the quantity of .NO calculated from the physicochemical data to be released in the interval required to achieve maximum relaxation at the EC50 doses (r = 0.995). This suggests that such nucleophile/.NO adducts might generally be useful as vehicles for the nonenzymatic generation of nitric oxide, in predictable amounts and at predictable rates, for biological purposes. The particular significance for possible drug design is underscored in the very favorable potency comparison between several of these agents and the established nitrovasodilators sodium nitroprusside and glyceryl trinitrate (EC50 values of 2.0 and greater than 10 microM, respectively) in parallel aortic ring tests.

Animals↗
PubMed1986

Structure-activity relationships of nitro and methyl-nitro derivatives of indoline, indole, indazole and benzimidazole in Salmonella typhimurium.

The mutagenic activities of eleven nitro derivatives and eleven N-methyl-nitro derivatives of indoline, indole, indazole and benzimidazole were investigated in Salmonella TA98 and TA100. The presence of a nitro group at C4 or C7 resulted in only weakly or nonmutagenic compounds, while a nitro group at C2, C5 or C6 usually resulted in measurable mutagenic activity in the non-N-methylated compounds. Methylation of a ring nitrogen usually reduced the mutagenic activity of these nitroheterocyclics except 2-nitro-benzimidazole, which resulted in a better than 300-fold increase in mutagenic activity. A proposed mechanism for the increased mutagenic activity obtained by methylation of imidazole nitrogens may provide insights into the reasons for the potent mutagenicities observed for several similarly methylated cooked-food mutagens.

Benzimidazoles↗
PubMed2000

Characterization of nicotinic acetylcholine receptors from the insects Aphis craccivora, Myzus persicae, and Locusta migratoria by radioligand binding assays: relation to thiamethoxam action.

Thiamethoxam, a new neonicotinoid insecticide acting at nicotinic acetylcholine receptors, was characterized in competition binding assays with [3-H]-imidacloprid, a specific nicotinic ligand, using membranes from the aphids Aphis craccivora and Myzus persicae, and from the locust Locusta migratoria. In all insects, Scatchard analysis suggested two binding sites for imidacloprid with Kd values in the range of 1 nM and 10 nM, respectively. The Hill values were significantly below 1 (range of 0.63 to 0.85). In contrast to imidacloprid and nicotine, the potency of thiamethoxam to displace [3-H]-imidacloprid varied considerably among these insects. Thiamethoxam was more active than nicotine on Aphis receptors but 100-fold less in Locusta, a nontarget insect. Comparable relations were found to nithiazine. In Myzus, the inhibition curve for thiamethoxam was shallow. This suggested a heterogeneous receptor population displaying a range of binding affinities to thiamethoxam in this aphid. In all three insects, the other neonicotinoid insecticides studied competed with [3-H]-imidacloprid in the same order: thiacloprid > imidacloprid > or = acetamiprid > nitenpyram. N-Methylation of imidacloprid strongly reduced the affinity to the imidacloprid site, whereas N-demethylation of thiamethoxam resulted in a comparable increase of affinity. Supplementary assays were performed with (-)-[3-H]-nicotine and [3-H]-alpha-bungarotoxin on locust membranes. Overall, the data suggested that the outstanding insecticidal properties of thiamethoxam may be due to either a different binding site on nicotinic receptors, or receptor isoforms, or specific pharmakokinetic behavior, rather than to exceptional affinity to one of the examined binding sites.

Animals↗
PubMed2002

Nitrates for achalasia.

BACKGROUND: Achalasia is a disease that impairs oesophageal motility. Though nitrates have been used to treat achalasia for a long time, the effectiveness of nitrates for achalasia is still controversial. OBJECTIVES: To quantify short-term and long-term effects of nitrate therapy in patients with achalasia. SEARCH STRATEGY: Trials were identified by searching the Cochrane Controlled Trials Register (Issue 4-2001), MEDLINE (1966-2001), EMBASE (1980-2001), LILACS - Latin American and Caribbean health science literature (1982-2001) and CBM-Chinese Biomedical database(1980-2000). Additionally, all references in the identified trials were checked for further relevant trials. SELECTION CRITERIA: All randomised controlled trials involving achalasic patients given any type of nitrates were included. DATA COLLECTION AND ANALYSIS: Data were extracted by two independent observers based on the intention to treat principle. MAIN RESULTS: Two randomised cross-over studies were found, but no results are included. Due to the design of the studies and the method of reporting the results in the original paper it was not possible to extract the necessary information to examine any of the outcomes. REVIEWER'S CONCLUSIONS: We can conclude no implications for practice at this stage. Appropriately designed parallel group randomised controlled trials with long term follow-up are needed to determine the effects of nitrates.

Esophageal Achalasia↗
PubMed2004

Nitrates for achalasia.

BACKGROUND: Achalasia is a disease that impairs oesophageal motility. Though nitrates have been used to treat achalasia for a long time, the effectiveness of nitrates for achalasia is still controversial. OBJECTIVES: To quantify short-term and long-term effects of nitrate therapy in patients with achalasia. SEARCH STRATEGY: Trials were identified by searching the Cochrane Controlled Trials Register (Issue 4-2001), MEDLINE (1966-2001), EMBASE (1980-2001), LILACS - Latin American and Caribbean health science literature (1982-2001) and CBM-Chinese Biomedical database(1980-2000). Additionally, all references in the identified trials were checked for further relevant trials. An updated search was run on the Cochrane Library, MEDLINE, and EMBASE in September 2003 - no new trials were found. SELECTION CRITERIA: All randomised controlled trials involving achalasic patients given any type of nitrates were included. DATA COLLECTION AND ANALYSIS: Data were extracted by two independent observers based on the intention to treat principle. MAIN RESULTS: Two randomised cross-over studies were found, but no results are included. Due to the design of the studies and the method of reporting the results in the original paper it was not possible to extract the necessary information to examine any of the outcomes. REVIEWER'S CONCLUSIONS: We can conclude no implications for practice at this stage. Appropriately designed parallel group randomised controlled trials with long term follow-up are needed to determine the effects of nitrates.

Esophageal Achalasia↗
PubMed2000

Temporal changes of cerebral metabolites and striatal lesions in acute 3-nitropropionic acid intoxication in the rat.

To investigate the mechanisms of neuronal death in neurodegeneration, in vivo localized proton magnetic resonance spectroscopy ((1)H-MRS) and diffusion-weighted MRI (DWI) were used to evaluate temporal changes in rat striata after administration of 3-nitropropionic acid. It was found that N-acetylaspartate (NAA) reduction, with nearly simultaneous evidence of striatal lesions in DWI, was preceded by a significant and progressive increase of acetate. Shortly before the NAA levels decreased to the lowest point, acetate levels peaked and began to gradually decline toward the control levels. These results suggest that acetate increase may arise from fatty acid degradation, inhibition of succinate dehydrogenase and possible NAA hydrolysis. The elevated acetate may provide a source of acetyl group for membrane repair during excitotoxic brain injury. Magn Reson Med 44:29-34, 2000.

Acetates↗