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PubMed2003

Field and laboratory tests of new insecticides against the apple maggot, Rhagoletis pomonella (Walsh) (Diptera: Tephritidae).

Laboratory bioassays and field tests were conducted to compare the effectiveness of the new insecticides, imidacloprid, indoxacarb, pyriproxyfen, spinosad, thiacloprid, and thiamethoxam, against apple maggot. The activity ranking of the compounds in reducing oviposition in laboratory bioassays was: imidacloprid, 95% reduction at 11 ppm > thiamethoxam, 91% and thiacloprid, 89% reduction at 100 ppm > spinosad, 98% reduction at 316 ppm > indoxacarb, 80% reduction at 1000 ppm > pyriproxyfen, 0% reduction at 38 ppm. In laboratory bioassays, the only insecticides that were toxic to flies at concentrations equal to or below the recommended field rates were imidacloprid, (50% of flies at 11 ppm), spinosad (90% of flies at rates > 10 ppm), and thiamethoxam (approximately 50% of flies at 32 ppm). In field trials, thiacloprid was the only material that consistently controlled apple maggot fruit infestation that was comparable to standard treatments of organophosphate insecticides. Spinosad applied at weekly intervals, and indoxacarb applied as biweekly sprays provided adequate control of apple maggot damage when infestation levels in the field were low, but were not effective in preventing damage in small plots when apple maggot pressure was high.

Animals↗
PubMed2003

Glutamate uptake inhibitor L-trans-pyrrolidine 2,4-dicarboxylate becomes neurotoxic in the presence of subthreshold concentrations of mitochondrial toxin 3-nitropropionate: involvement of mitochondrial reducing activity and ATP production.

An increased concentration of extracellular glutamate is associated with neuronal damage induced by cerebral ischemia. We have demonstrated previously that exposure of cultured cerebellar granule neurons to L-trans-pyrrolidine-2,4-dicarboxylate (PDC), a glutamate uptake inhibitor, increases extracellular glutamate levels but does not induce neuronal damage. Coincubation of PDC, however, with a subthreshold concentration of the mitochondrial toxin, 3-nitropropionic acid (3-NP), results in severe damage to these neurons. We have investigated the time course of changes in mitochondrial reducing capacity and ATP levels in cerebellar granule cells after simultaneous exposure to 3-NP and PDC, and its relation to cell viability and nuclear condensation. Although individually, 3-NP and PDC treatments are not harmful to neurons, the simultaneous exposure to both compounds results in a progressive decline in mitochondrial reducing capacity during the first 4 hr, and a rapid decrease in ATP levels. At 4 hr, cells lose plasma membrane integrity and show condensed nuclei. In the presence of the energy substrates pyruvate and acetoacetate, the N-methyl-D-apartate (NMDA) receptor antagonist, MK-801, and the spin trapper alpha-phenyl-N-tert-butylnitrone (PBN), the decline in mitochondrial activity and ATP levels is prevented, the number of condensed nuclei is reduced, and plasma membrane integrity is preserved. In contrast, the broad-spectrum caspase inhibitor Z-Asp-DCB (Z-Asp-CH2-DCB) prevents nuclear condensation but has no effect on mitochondrial reducing capacity or cell survival. Our results show that glutamate uptake impairment rapidly induces neuronal death during inhibition of succinate dehydrogenase by a mechanism involving mitochondrial dysfunction that, if not prevented, leads to cell death.

Adenosine Triphosphate↗
PubMed1985

Pre-clinical toxicology of nitazoxanide--a new antiparasitic compound.

The acute and subchronic toxicological effects of nitazoxanide were investigated at levels near and in excess of the therapeutic dose in rats, mice, dogs and cats. Single oral gavage doses of 0.625-10 g per kg body weight were administered to rats and mice. Single oral doses of 1-10 g per kg body weight were administered in capsules to dogs and cats. Acute oral LD50 values were greater than 10 g kg-1 in rats, dogs and cats, and 1.4 g kg-1 in mice. Systemic toxicity was evaluated in a repeated dose study in rats at doses of 50, 150 and 450 mg per kg per day for 14 weeks. The highest dose group exhibited intense salivation, increased liver and spleen weight, and decreased thymus weights. Variances between control and treated organ weights were not confirmed by histopathological evaluation. Nitazoxanide was negative when tested in the Ames Salmonella assay using five tester strains with and without metabolic activation at levels from 1 to 100 mg per plate. The drug was also shown to be non-irritating in a test for eye irritation potential.

Animals↗
PubMed2005

Feasibility study on the removal of nitrous compounds with a hollow-fiber membrane biofilm reactor.

The objective of this study was to develop an integrated nitrogen treatment system using autotrophic organisms. A treatment system consists of an aerobic hollow-fiber membrane biofilm reactor (HfMBR) and anaerobic HfMBR. In the aerobic HfMBR, a mixture gas of air and O2 was supplied through the fibers for nitrification. Denitrification occurred in the anaerobic HfMBR using H2 as the electron donor. The treatment system was continuously operated for 190 days. NH4-N removal efficiencies ranging from 95% to 97% were achieved at NH4-N concentrations of influent ranging from 50 to 100 mg N/L. When glucose was added to the influent, the simultaneous nitrification and denitrification occurred in the aerobic HfMBR, and nitrogen removal rates were changed according to the COD/NH4-N ratio of influent. In the anaerobic HfMBR, autotrophic denitrification using H2 occurred and the removal rates achieved in this study were 23-58 mg N/m2 d. In this study, the achieved removal efficiency was lower than other study findings; however, the result suggested that this hybrid HfMBR system can be used effectively for nitrogen removal in oligotrophic water.

Aerobiosis↗
PubMed1999

Reaction of organic nitrate esters and S-nitrosothiols with reduced flavins: a possible mechanism of bioactivation.

Organic nitrate esters, such as glyceryl trinitrate and isosorbide dinitrate, are a class of compounds used to treat a variety of vascular ailments. Their effectiveness relies on their ability to be bioactivated to nitric oxide (NO) which, in turn, relaxes vascular smooth muscle. Although there have been many biological studies that indicate that NO can be formed from organic nitrate esters in a biological environment, the chemical mechanism by which this occurs has yet to be established. Previous studies have implicated both flavins and thiols in organic nitrate ester bioactivation. Thus, we examined the chemical interactions of flavins and thiols with organic nitrate esters as a means of determining the role these species may play in NO production. Based on these studies we concluded that a reasonable chemical mechanism for organic nitrate ester bioactivation involves reduction to the organic nitrite ester followed by conversion to a nitrosothiol. The release of NO from nitrosothiols can occur via a variety of processes including reaction with dihydroflavins and NADH.

Biotransformation↗
PubMed2002

Development of a catalytic enantioselective conjugate addition of 1,3-dicarbonyl compounds to nitroalkenes for the synthesis of endothelin-A antagonist ABT-546. Scope, mechanism, and further application to the synthesis of the antidepressant rolipram.

The enantioselective synthesis of endothelin-A antagonist ABT-546 has been accomplished via the discovery and development of a highly selective catalytic asymmetric conjugate addition of ketoesters to nitroolefins. Employing just 4 mol % bis(oxazoline)-Mg(OTf)(2) complex with an amine cocatalyst, we obtained the product nitroketone with 88% selectivity at the aryl-bearing stereocenter and in good yield on scales ranging to 13 mol. The effects of ligand structure, metal salt, and solvent on the reaction are described. Particularly important to the reaction is the water content. While water is necessary during the generation of the catalyst, the water must be then removed to maximize stereoselectivity and reactivity. The reaction has been extended to other dicarbonyl substrates, and a variety of substitution patterns are tolerated on the nitroolefin partner. The reaction has also been employed in the synthesis of the antidepressant rolipram. Investigations relating to the mechanism of the reaction are also described.

Alkenes↗
PubMed2001

Genotoxic evaluation of the furylethylene derivative 2-furyl-1-nitroethene in cultured human lymphocytes.

The compound 2-furyl-1-nitroethene (G-0) was evaluated for genotoxicity in cultured human peripheral blood lymphocytes, at concentrations ranging from 1 to 15microg/ml. Micronuclei (MN) and sister-chromatid exchanges (SCEs) were scored as genetic endpoints. In order to detect the role of metabolic enzymes on the genotoxicity of this furylethylenic derivative, the cultures for MN and SCE demonstrations were also treated with S9 microsomal fraction. The results indicate that, under the conditions of the study, the test agent does not seem to induce significant increases in the frequency of micronucleated cells, irrespective of the presence of metabolic activation. Nevertheless, a slight increase in the SCE frequency was observed in those cultures treated without the S9 mix; although this increase disappeared in presence of the microsomal fraction. In addition, cytostatic effects of 2-furyl-1-nitroethene were observed mainly in cultures without S9 fraction, as indicated by the reduction of cell proliferation.

Animals↗
PubMed2001

Biorational agents--mechanism and importance in IPM and IRM programs for controlling agricultural pests.

Among the new approaches for controlling agricultural pests is the development of novel compounds affecting specific processes in insects such as chitin synthesis inhibitors, juvenile hormone mimics and ecdysone agonists. In addition, efforts have been made to develop compounds acting selectively on groups of insects by inhibiting or enhancing biochemical sites such as respiration (diafenthiuron), the nicotinyl acetylcholine receptors (imidacloprid and acetamiprid), the GABA receptors (avermectins), the salivary glands of sucking pests (pymetrozine) and others. Among the most recent novel insecticides with selective properties are novaluron, thiamethoxam, emamectin and spinosad. Novaluron (Rimon) is a novel chitin synthesis inhibitor that acts by both ingestion and contact. It is a powerful suppressor of lepidopteran larvae such as Spodoptera littoralis and Helicoverpa armigera (by ingestion) and of whiteflies such as Bemisia tabaci and Trialeurodes vaporariorum (by contact). Thiamethoxam (Actarn), a novel neonicotinoid acts specifically on aphids and whiteflies. Emamectin (Proclaim), an avermectin derivative acts on GABA receptor affecting diversity of insects such as mites, lepidopterans and thrips. Spinosad (Tracer) seems to act on both acetylcholine and GABA receptors affecting diversity of insect species and is considered an important agent for controlling the western flower thrips.

Animals↗
PubMed1996

The superoxide production mediated by the redox cycling of xenobiotics in rat brain microsomes is dependent on their reduction potential.

Several exogenous molecules undergo enzymatic one-electron reduction leading to radicals which can rapidly react with molecular oxygen to form superoxide anions. We have previously shown that under aerobic conditions a significant superoxide anion production occurred during the NADPH-dependent one-electron reduction of some drugs and xenobiotics by rat brain preparations. We report here for several compounds a fairly good correlation between the reduction potentials (Epc vs. SCE) which ranged between - 230 and - 700 mV in aqueous medium (pH 7.4) or between -700 mV and -1100 mV in the aprotic solvent N,N-dimethylformamide, and the rate of superoxide anion production during their metabolism by rat brain microsomes. The data obtained suggest that the redox potential of most of the molecules assayed was related to their ability to undergo one-electron reduction mediated by flavoenzymes in the rat brain. The main range of reduction potentials corresponding to a large superoxide anion production suggests that the redox cycling of these chemicals was mediated by NADPH-cytochrome P-450 reductase. Therefore the measurement of reduction potentials of drugs and xenobiotics able to reach the brain, and chemically related to quinones, nitroaromatics, nitroheterocyclics and iminiums, may provide information both on their electron affinity and the possibility of one-electron transfer in vivo, and thus on their possible neurotoxicity due to the production of oxygenated free radicals.

Animals↗
PubMed1975

Electron transfer oxidation of DNA radicals by paranitroacetophenone.

The reaction of a typical electron-affinic sensitizer, paranitroacetophenone (PNAP) with the model compounds thymine, thymidine, thymidylic acid, deoxyribose and single and double-stranded DNA has been investigated by pulse radiolysis. Radicals formed by one-electron reduction of the bases and of DNA react rapidly and efficiently with PNAP by electron transfer. A small yield of transfer (less than 10 per cent) is also observed arising from oxidation of the radicals formed by the small proportion of OH which react at the sugar moieties in DNA. In contrast, electron transfer oxidation by PNAP of radicals formed by the addition of OH to the base moieties, e.g. thymine, is not an efficient process. Further, addition of the sensitizer to the thymine OH-adduct proceeds at a rate that is too low to measure by pulse radiolysis. We conclude that, since the major sites of OH reaction with DNA are the heterocyclic bases (greater than 80 per cent), oxidation of the resultant radicals is unlikely to be a major step in the mechanism of sensitization by this typical hypoxic-cell sensitizer.

Acetophenones↗
PubMed1999

Possible novel mechanism for bitter taste mediated through cGMP.

Taste is the least understood among sensory systems, and bitter taste mechanisms pose a special challenge because they are elicited by a large variety of compounds. We studied bitter taste signal transduction with the quench-flow method and monitored the rapid kinetics of the second messenger guanosine 3',5'-cyclic monophosphate (cGMP) production and degradation in mouse taste tissue. In response to the bitter stimulants, caffeine and theophylline but not strychnine or denatonium cGMP levels demonstrated a rapid and transient increase that peaked at 50 ms and gradually declined throughout the following 4.5 s. The theophylline- and caffeine-induced effect was rapid, transient, concentration dependent and gustatory tissue-specific. The effect could be partially suppressed in the presence of the soluble guanylyl cyclase (GC) inhibitor 10 microM ODQ and 30 microM methylene blue but not 50 microM LY 83583 and boosted by nitric oxide donors 25 microM NOR-3 or 100 microM sodium nitroprusside. The proposed mechanism for this novel cGMP-mediated bitter taste signal transduction is cGMP production partially by the soluble GC and caffeine-induced inhibition of one or several phosphodiesterases.

Aminoquinolines↗
PubMedDate not supplied

[Effects of the novel synthetic fatty acid dinitroglycerol esters on aggregation of the human platelets in vitro].

A series of six new synthetic dinitroglycerol esters of fatty acids on the human platelet aggregation was studied in vitro. Inclusion of the dinitroglycerol moiety into the molecule of arachidonic acid deprived this acid from pro-aggregant activity. All six compounds produced moderate (dose-dependent) inhibition of the platelet aggregation process induced by arachidonic acid (1 x 10(-3) M). Platelet aggregation was most significantly affected by dinitroglycerol esters of arachidonic and docosahexaenoic acids. This is probably explained by the influence of these esters on the oxidative metabolism of arachidonic acid to eicosanoids playing the role of proaggregants. In the presence of vessel wall (rat aorta fragments), dinitroglycerol esters of arachidonic and docosahexaenoic acids incubated with platelets (5 min, 37 degrees C) significantly reduced their aggregation induced by arachidonic acid (1 x 10(-3) M) or docosahexaenoic acid (1 x 10(-5) M) under the conditions of endothelial cyclooxygenase suppressed by acetylsalicylic acid (10 mg/ml). The pronounced antiaggregant effect of the synthetic dinitroglycerol esters studied is probably related to their ability to act as NO donors suppressing the activity of thrombocytes (provided that the NO production activity is present in the system).

Animals↗
PubMed2003

A dual role of adenosine A2A receptors in 3-nitropropionic acid-induced striatal lesions: implications for the neuroprotective potential of A2A antagonists.

Reduction of A2A receptor expression is one of the earliest events occurring in both Huntington's disease (HD) patients and mice overexpressing the N-terminal part of mutated huntingtin. Interestingly, increased activity of A2A receptors has been found in striatal cells prone to degenerate in experimental models of this neurodegenerative disease. However, the role of A2A receptors in the pathogenesis of HD remains obscure. In the present study, using A2A-/- mice and pharmacological compounds in rat, we demonstrate that striatal neurodegeneration induced by the mitochondrial toxin 3-nitropropionic acid (3NP) is regulated by A2A receptors. Our results show that the striatal outcome induced by 3NP depends on a balance between the deleterious activity of presynaptic A2A receptors and the protective activity of postsynaptic A2A receptors. Moreover, microdialysis data demonstrate that this balance is anatomically determined, because the A2A presynaptic control on striatal glutamate release is absent within the posterior striatum. Therefore, because blockade of A2A receptors has differential effects on striatal cell death in vivo depending on its ability to modulate presynaptic over postsynaptic receptor activity, therapeutic use of A2A antagonists in Huntington's as well as in other neurodegenerative diseases could exhibit undesirable biphasic neuroprotective-neurotoxic effects.

Adenosine↗
PubMed2005

Celastrol protects against MPTP- and 3-nitropropionic acid-induced neurotoxicity.

Oxidative stress and inflammation are implicated in neurodegenerative diseases including Parkinson's disease (PD) and Huntington's disease (HD). Celastrol is a potent anti-inflammatory and antioxidant compound extracted from a perennial creeping plant belonging to the Celastraceae family. Celastrol is known to prevent the production of proinflammatory cytokines, inducible nitric oxide synthase and lipid peroxidation. Mice were treated with celastrol before and after injections of MPTP, a dopaminergic neurotoxin, which produces a model of PD. A 48% loss of dopaminergic neurons induced by MPTP in the substantia nigra pars compacta was significantly attenuated by celastrol treatment. Moreover, celastrol treatment significantly reduced the depletion in dopamine concentration induced by MPTP. Similarly, celastrol significantly decreased the striatal lesion volume induced by 3-nitropropionic acid, a neurotoxin used to model HD in rats. Celastrol induced heat shock protein 70 within dopaminergic neurons and decreased tumor necrosis factor-alpha and nuclear factor kappa B immunostainings as well as astrogliosis. Celastrol is therefore a promising neuroprotective agent for the treatment of PD and HD.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMedDate not supplied

Nitazoxanide, a nitrothiazolide antiparasitic drug, is an anti-Helicobacter pylori agent with anti-vacuolating toxin activity.

Nitazoxanide (NTZ), a synthesized drug of the nitrothiazolide class, was initially developed as an antiparasitic compound. This compound has recently been shown to have antibacterial activities against some bacterial pathogens. In the present study, NTZ and its main metabolite tizoxanide (TIZ) were found to have strong minimum inhibitory concentrations (MICs) against both metronidazole (MTZ)-resistant strains and sensitive clinical isolates of Helicobacter pylori. The MIC90 of both NTZ and TIZ against 37 clinical isolates was 8 microg/ml. Vacuolating toxin activity of H. pylori assayed by HeLa cell vacuole formation was inhibited by NTZ at a sub-MIC. In contrast, urease production by H. pylori was not specifically affected by the sub-MIC of NTZ. An acidic pH (pH 5.0) medium reduced the antimicrobial activity of the drug in terms of growth inhibition due to the low growth rate of the bacteria, but killing activity of NTZ against the bacteria was still observed. Thus, it was apparent that both NTZ and TIZ are highly effective against H. pylori, even when the bacteria are resistant to MTZ.

Anti-Bacterial Agents↗
PubMed2004

Thermochemical properties and non-isothermal decomposition reaction kinetics of 3,4-dinitrofurazanfuroxan (DNTF).

The constant-volume combustion energy, DeltacU (DNTF, s, 298.15K) and kinetic behavior of the exothermic decomposition reaction of the title compound (DNTF) are determined by a precise rotating bomb calorimeter and DSC, respectively. Its standard enthalpy of combustion, DeltacHmtheta (DNTF, s, 298.15K), standard enthalpy of formation, DeltacHmtheta (DNTF, s, 298.15K) and kinetic parameters of the major exothermic decomposition reaction in a temperature-programmed mode [the apparent activation energy (Ea) and pre-exponential factor (A)] are calculated. The values of DeltacU (DNTF, s, 298.15K), DeltacHmtheta (DNTF, s, 298.15K), and DeltacHmtheta (DNTF, s, 298.15K) of DNTF are -9733.96 +/- 8.59 Jg(-1), -3018.29 +/- 2.68 kJ mol(-1), and 657.23 +/- 2.70 kJ mol(-1), respectively. The kinetic model function in integral form and the value of E(a) and A of the major exothermic decomposition reaction of DNTF are 1-(1-alpha)1/3, 177.03 kJ mol(-1) and 10(13.68)s(-1), respectively. The critical temperature of thermal explosion of DNTF is 240.6 degrees C.

Explosions↗
PubMed1998

Nitazoxanide, a potential drug for eradication of Helicobacter pylori with no cross-resistance to metronidazole.

Nitazoxanide, a thiazolide compound, and its desacetyl derivative, tizoxanide, have antimicrobial properties against anaerobic bacteria, as well as against helminths and protozoa. Because the treatment of Helicobacter pylori infection may be jeopardized by metronidazole resistance, nitazoxanide and tizoxanide were tested in vitro against these bacteria. The MICs of these two compounds were determined by agar dilution and were compared to those of metronidazole. Exposure to subinhibitory concentrations of nitazoxanide was also carried out by the method of Szybalski (W. Szybalski and V. Bryson, J. Bacteriol. 64:489-499, 1952). The MICs of nitazoxanide and tizoxanide for 103 strains ranged from 0.25 to 8 microg/ml, with the MIC at which 50% of strains are inhibited (MIC50) being 1 microg/ml and the MIC90 being 4 microg/ml, and no resistant strain was detected, whereas strains resistant to metronidazole were detected. When 10 strains were successively subcultured on medium containing nitazoxanide, no significant change in the MICs of this compound was observed. A pilot study of nitazoxanide for the treatment of H. pylori infection was carried out with 86 patients in association with 20 mg of omeprazole. An eradication rate of 83% (95% confidence interval, 64% to 94%) was obtained in a per-protocol analysis in the group receiving 1 g of nitazoxanide orally twice daily, and a few side effects were observed. The failures could not be explained by the selection of resistant strains since the MICs of nitazoxanide were similar for six pairs of isolates (proven to be the same strain by random amplified polymorphic DNA analysis in four cases) cultured before and after the treatment failure. Nitazoxanide exhibits good antimicrobial activity against H. pylori without the problem of acquired resistance which is encountered with metronidazole and has been demonstrated to have a satisfactory effect in a dose-ranging pilot study. It is therefore a good candidate to be included in treatment regimens aimed at the eradication of H. pylori.

Anti-Bacterial Agents↗
PubMed2002

The adenosine A1 receptor agonist adenosine amine congener exerts a neuroprotective effect against the development of striatal lesions and motor impairments in the 3-nitropropionic acid model of neurotoxicity.

Huntington's disease is a genetic neurodegenerative disorder characterized clinically by both motor and cognitive impairments and striatal lesions. At present, there are no pharmacological treatments able to prevent or slow its development. In the present study, we report the neuroprotective effect of adenosine amine congener (ADAC), a specific A1 receptor agonist known to be devoid of any of the side effects that usually impair the clinical use of such compounds. Remarkably, in a rat model of Huntington's disease generated by subcutaneous infusion of the mitochondrial inhibitor 3-nitropropionic acid (3NP), we have observed that an acute treatment with ADAC (100 microg x kg(-1) x d(-1)) not only strongly reduces the size of the striatal lesion (-40%) and the remaining ongoing striatal degeneration (-30%), but also prevents the development of severe dystonia of hindlimbs. Electrophysiological recording on corticostriatal brain slices demonstrated that ADAC strongly decreases the field EPSP amplitude by 70%, whereas it has no protective effect up to 1 microm against the 3NP-induced neuronal death in primary striatal cultures. This suggests that ADAC protective effects may be mediated presynaptically by the modulation of the energetic impairment-induced striatal excitotoxicity. Altogether, our results indicate that A1 receptor agonists deserve further experimental evaluation in animal models of Huntington's disease.

Adenosine↗