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PubMed2002

Analytical method for the determination of metolachlor, acetochlor, alachlor, dimethenamid, and their corresponding ethanesulfonic and oxanillic acid degradates in water using SPE and LC/ESI-MS/MS.

A Good Laboratory Practices (GLP) validated, multiresidue analytical method is presented for the determination of the chloroacetanilide herbicides metolachlor, acetochlor, and alachlor, the chloroacetamide herbicide dimethenamid, and their respective ethanesulfonic (ESA) and oxanillic (OA) acid degradates in ground and surface water. A 50-mL water sample is subjected to purification using a C-18 SPE column. The four parent components and their eight ESA and OA degradates are isolated using 80/20 methanol/water (v/v) for elution. The eluate is reduced to < 1.0 mL and reconstituted in 10/90 acetonitrile/water (v/v) to the desired final fraction volume. Final analysis is accomplished using liquid chromatography/electrospray ionization-mass spectrometry/mass spectrometry in the + (parent compounds) and - (ESA and OA degradates) ion modes by monitoring appropriate precursor/product ion pairs for each of the 12 analytes. The method limit of quantification is 0.10 ppb and the limit of detection is 0.125 ng injected for each analyte. Average procedural recovery data range from 95 to 105% for fortification levels of 0.10-100 ppb. The method validation study was performed following GLP guidelines.

Acetamides↗
PubMed1997

Effects of non-steroidal antiallergic eyedrops on the complement-mediated histamine release from human cells.

Leukocytes from ten allergic patients (five allergic to dust-mites and five allergic to pollen) were treated with N-acetyl aspartyl glutamic acid (NAAGA) 4.9%, disodium cromoglycate (DSCG) 2%, lodoxamide (LODO) 1%, and levocabastine (LEVO) 0.5% (concentrations representing the pharmaceutical eyedrop preparations) for 20 minutes. Degranulation was then induced with Complement (rHu5Ca). Histamine was measured in the supernatant with ELISA. LODO and LEVO were inactive in blocking histamine released from human cells, and paradoxical unexpected effects were found with these two agents. They both induced significant histamine release in almost 100% of the samples. DSCG was able to block histamine release in seven patients out of nine (ranging between 5 and 34%). NAAGA was the most active agent on human cells and was able to block basophil degranulation in nine patients out of nine (inhibition ranging between 4 and 66% of total histamine pool).

Allergens↗
PubMed2000

Simultaneous quantification of acetanilide herbicides and their oxanilic and sulfonic acid metabolites in natural waters.

This paper describes a procedure for simultaneous enrichment, separation, and quantification of acetanilide herbicides and their major ionic oxanilic acid (OXA) and ethanesulfonic acid (ESA) metabolites in groundwater and surface water using Carbopack B as a solid-phase extraction (SPE) material. The analytes adsorbed on Carbopack B were eluted selectively from the solid phase in three fractions containing the parent compounds (PCs), their OXA metabolites, and their ESA metabolites, respectively. The complete separation of the three compound classes allowed the analysis of the neutral PCs (acetochlor, alachlor, and metolachlor) and their methylated OXA metabolites by gas chromatography/mass spectrometry. The ESA compounds were analyzed by high-performance liquid chromatography with UV detection. The use of Carbopack B resulted in good recoveries of the polar metabolites even from large sample volumes (1 L). Absolute recoveries from spiked surface and groundwater samples ranged between 76 and 100% for the PCs, between 41 and 91% for the OXAs, and between 47 and 96% for the ESAs. The maximum standard deviation of the absolute recoveries was 12%. The method detection limits are between 1 and 8 ng/L for the PCs, between 1 and 7 ng/L for the OXAs, and between 10 and 90 ng/L for the ESAs.

Acetanilides↗
PubMedDate not supplied

Infiltration of acetochlor and two of its metabolites in two contrasting soils.

To obtain data concerning the risk of leaching of acetochlor (2-chloro-2'-methyl-6'-ethyl-N-ethoxymethyl-acetanilide) and its major metabolites, ethanesulfonic acid (ESA) and oxanilic acid (OA), to ground water, we studied the fate of these products in two different soil types (luvisol and calcisol) under the same weather conditions. The metabolites were detected in the soils as early as 7 d after application, indicating a rapid onset of acetochlor degradation. Ethanesulfonic acid was predominant over OA in the calcisol, regardless of time or depth, whereas the ESA to OA ratio varied with both time and depth in the luvisol. The maximum depths at which they were detected were 60 to 70 and 10 to 20 cm for ESA and OA, respectively, in the luvisol, and 60 to 70 cm (maximum depth sampled) and 30 to 40 cm for ESA and OA, respectively, in the calcisol. Acetochlor was still detected in the surface layer of the two soils 344 d after its application, although the molecule was partially leached. The maximum depths at which acetochlor was detected (60-70 cm in the luvisol and 50-60 cm [maximum depth sampled] in the calcisol) were recorded during the first sampling 7 d after application. Acetochlor was not detected on later dates below the 30- to 40-cm layer in the calcisol or the 5- to 10-cm layer in the luvisol. The greater preferential flow in the luvisol, which would have favored leaching, might partially explain why the mass balances done 7 d after application were lower in the luvisol (approximately 26%) than in the calcisol (approximately 45%).

Alkanesulfonates↗
PubMed2002

Analysis and detection of the herbicides dimethenamid and flufenacet and their sulfonic and oxanilic acid degradates in natural water.

Dimethenamid [2-chloro-N-(2,4-dimethyl-3-thienyl)-N-(2-methoxy-1-methylethyl)acetamide] and flufenacet [N-(4-fluorophenyl)-N-(1-methylethyl)-2-(5-(trifluoromethyl)-1,3,4-thiadiazol-2-yl)oxy] were isolated by C-18 solid-phase extraction and separated from their ethanesulfonic acid (ESA) and oxanilic acid (OXA) degradates during their elution using ethyl acetate for the parent compound, followed by methanol for the polar degradates. The parent compounds were detected using gas chromatography-mass spectrometry in selected-ion mode. The ESA and OXA degradates were detected using high-performance liquid chromatography--electrospray mass spectrometry (HPLC-ESPMS) in negative-ion mode. The method detection limits for a 123-mL sample ranged from 0.01 to 0.07 microg/L. These methods are compatible with existing methods and thus allow for analysis of 17 commonly used herbicides and 18 of their degradation compounds with one extraction. In a study of herbicide transport near the mouth of the Mississippi River during 1999 and 2000, dimethenamid and its ESA and OXA degradates were detected in surface water samples during the annual spring flushes. For flufenacet, the only detections at the study site were for the ESA degradates in samples collected at the peak of the herbicide spring flush in 2000. The low frequency of detections in surface water likely is due to dimethenamid and flufenacet being relatively new herbicides. In addition, detectable amounts of the stable degradates have not been detected in ground water.

Acetamides↗
PubMed1998

Treatment of common ocular allergic disorders; a comparison of lodoxamide and NAAGA.

BACKGROUND/AIMS: Lodoxamide tromethamine and N-acetyl-aspartyl glutamic acid (NAAGA) are mast cell stabilisers, both of which have been shown to be effective in the treatment of allergic conjunctivitis. The aim of this study was to compare the two compounds in patients with common ocular allergic disorders. METHODS: 73 patients participated in a double masked, randomised multicentre study. Diagnoses were chronic allergic conjunctivitis, vernal conjunctivitis, seasonal and atopic conjunctivitis. 36 patients were treated with lodoxamide 0.1% and 37 with NAAGA 4.9%, the drops being instilled four times daily for up to 56 days. RESULTS: The overall opinion of the physicians and the patients was in favour of lodoxamide at day 10 of the study. At this time, 86% of lodoxamide treated and 49% of NAAGA treated patients considered they had improved. The patients' opinion favoured lodoxamide at day 28 and both physicians' and patients' evaluations were in favour of lodoxamide at day 42. Evaluation of signs and symptoms indicated superiority of lodoxamide at days 42 and 56. Both treatments were well tolerated. CONCLUSION: While both lodoxamide and NAAGA treatments are associated with clinical improvements in patients with allergic conjunctivitis, lodoxamide may have an earlier onset of action.

Adolescent↗
PubMed2005

Enantiomeric separation of metolachlor and its metabolites using LC-MS and CZE.

The stereoisomers of metolachlor and its two polar metabolites [ethane sulfonic acid (ESA) and oxanilic acid (OXA)] were separated using liquid chromatography-mass spectrometry (LC-MS) and capillary zone electrophoresis (CZE), respectively. The separation of metolachlor enantiomers was achieved using a LC-MS equipped with a chiral stationary phase based on cellulose tris(3,5-dimethylphenyl carbamate) and an atmospheric pressure chemical ionization source operated under positive ion mode. The enantiomers of ESA and OXA were separated using CZE with gamma-cyclodextrin (gamma-CD) as chiral selector. Various CZE conditions were investigated to achieve the best resolution of the ESA and OXA enantiomers. The optimum background CZE electrolyte was found to consist of borate buffer (pH=9) containing 20% methanol (v/v) and 2.5% gamma-CD (w/v). Maximum resolution of ESA and OXA enantiomers was achieved using a capillary temperature of 15 degrees C and applied voltage of 30 kV. The applicability of the LC-MS and CZE methods was demonstrated successfully on the enantiomeric analysis of metolachlor and its metabolites in samples from a soil and water degradation study that was set up to probe the stereoselectivity of metolachlor biodegradation. These techniques allow the enantiomeric ratios of the target analytes to be followed over time during the degradation process and thus will prove useful in determining the role of chirality in pesticide degradation and metabolite formation.

Acetamides↗
PubMed1996

Efficacy of lodoxamide 0.1% versus N-acetyl aspartyl glutamic acid 6% ophthalmic solutions in patients with vernal keratoconjunctivitis.

In a double-masked, randomized and controlled clinical trial, the effectiveness and safety of lodoxamide 0.1% eye drops were compared with N-acetyl aspartyl glutamic acid 6% (NAAGA) drops in the treatment of 120 patients with vernal keratoconjunctivitis. There were 60 patients in each of the two study groups. The drugs were instilled 4 times daily for 60 days. Follow-up examinations were made on days 7, 30 and 60. Of the 120 patients, 98 (50 in lodoxamide and 48 in NAAGA groups) were still available for follow-up on day 7, 89 (45 in lodoxamide and 44 in NAAGA groups) on day 30 and 75 (38 in lodoxamide and 37 in NAAGA groups) on day 60. Lodoxamide was clinically more effective than NAAGA. Statistically significant trends toward improvement were noted in the lodoxamide group in resolving papillae on day 30, decreasing corneal staining on days 30 and 60, relieving photophobia on day 60, tearing on days 7, 30 and 60 and itching on days 30 and 60. Lodoxamide 0.1% was more effective in lowering the mean scores for corneal staining on days 30 and 60 (p < 0.05). The composite scores for clinical signs and symptoms calculated by averaging the mean scores for signs and symptoms showed clinically significant differences in favor of the lodoxamide group. More frequent follow-up visits might have resulted in better statistical correlations. Treatment-related adverse events were reported in both groups with similar frequency but none were permanent or serious.

Adolescent↗
PubMed2003

Chiral bis(amino alcohol)oxalamide gelators-gelation properties and supramolecular organization: racemate versus pure enantiomer gelation.

Four new chiral bis(amino alcohol)oxalamides (1-4: amino alcohol=leucinol, valinol, phenylglycinol, and phenylalaninol, respectively) have been prepared as low-molecular-weight organic gelators. Their gelation properties towards various organic solvents and mixtures were determined and these were then compared to related bis(amino acid) oxalamide gelators. Spectroscopic (FTIR, (1)H NMR) and X-ray diffraction studies revealed that the primary organization motif of (S,S)-1 and racemate 1 (rac-1) in lipophilic solvents involved the formation of inverse bilayers. The X-ray crystal structure of (S,S)-1 also shows this type of bilayer organization. The crystal structure of rac-2 reveals meso bilayers of hydrogen-bonded aggregates. Within the bilayers formed, the gelator molecules are connected by cooperative hydrogen bonding between oxalamide units and OH groups, while the interbilayer interactions are realized through lipophilic interactions between the iBu groups of leucinol. Oxalamide meso-1 lacks any gelation ability and crystallizes in monolayers. In dichloromethane rac-1 forms an unstable gel; this is prone to crystallization as a result of the formation of symmetrical meso bilayers. In contrast, in aromatic solvents rac-1 forms stable gels; this indicates that enantiomeric bilayers are formed. Oxalamide rac-1 is capable of gelling a volume of toluene three times larger than (S,S)-1. A tranmission electron microscopy investigation of rac-1 and (S,S)-1 toluene gels reveals the presence of thinner fibers in the former gel, and, hence, a more compact network that is capable of immobilizing a larger volume of the solvent. The self-assembly of these types of gelator molecules into bilayers and subsequent formation of fibrous aggregates can be explained by considering the strength and direction of aggregate forces (supramolecular vectors) in three-dimensional space.

Amino Alcohols↗
PubMed2003

[In vitro effects of antiallergic eyedrops on complement activation induced by particulate matter].

BACKGROUND: Recent decades have been marked by an increasing number of patients suffering from ocular allergic-like symptoms without being associated with an increase in IgE levels. These symptoms include heaviness of the lid, foreign body sensation, burning, stinging and photophobia. Both epidemiological studies and controlled human exposure clinical studies have shown cause-effect relationships between allergic-like symptoms and environmental factors such as outdoor air pollutants or poor indoor air quality. An ocular surface subclinical inflammation is thought to be responsible for pseudoallergic, pollution-related conjunctivitis. The complement system is considered as one of the major effector mechanisms involved in initiation of the subclinical inflammation that leads to IgE-independent eye irritation. PURPOSE: To study the capability of nine antiallergic eyedrops commonly used in the treatment of allergic conjunctivitis to inhibit complement activation induced in vitro by pollutants. METHODS: Normal human serum obtained from healthy individuals was used as a source of complement. Activation of complement was assessed using the complement hemolytic 50% (CH50) assay, in the absence or the presence of antiallergic eyedrops and in the absence or the presence of various stimuli, including sand, common house dust, eye mascara, and Dactylis glomerata pollen extract. Zymosan was used as a standardized complement activator. The following eyedrops were studied: Naabak (4.9% N-acetyl aspartic acid-glutamic acid, NAAGA, sodium salt), Almide (lodoxamide 0.1%), Levophta (0.05% levocabastine), Emadine (0.05% emedastine), Tilavist (2% nedocromil), Allergodil (0.05% azelastine), Patanol (olopatadine), and Zaditen (0.025% ketotifen). Effects of preservative-free lodoxamide and ketotifen were also assessed and compared to those of the preserved formulations. A solution of 0.01% benzalkonium chloride (BAC), the most widely used preservative in topical eyedrops, was also tested. RESULTS: Zymosan-induced activation of complement (30+/-6%) was significantly lowered by preincubation of serum with unpreserved NAAGA (16.6+/-4%, p=0.0026) or benzalkonium-preserved nedocromil (20+/-2%, p=0.022). Preserved levocabastine, emedastine, olopatadine and ketotifen did not interfere with zymosan-induced complement activation, whereas preserved azelastine, lodoxamide and benzalkonium chloride significantly aggravated complement activation induced by zymosan. Similar results were obtained when complement activation was triggered by sand, common house dust, mascara, or by an allergenic extract of Dactylis glomerata pollen. In the absence of complement activator, none of the antiallergic eyedrops induced a significant change in CH50 titer, indicating that the deleterious pro-inflammatory effect of preserved azelastine and lodoxamide may occur only once complement activation has been initiated, i.e., on an inflamed ocular surface. CONCLUSION: Among the antiallergic eyedrops tested in this study, only Naabak and Tilavist were found to significantly inhibit complement activation triggered by particulate matters or pollen allergenic extract. Such an anticomplement activity confers these two molecules a potential in the therapeutic management of pollution-related pseudoallergic conjunctivitis.

Air Pollutants↗
PubMed2005

Urea lesion formation in DNA as a consequence of 7,8-dihydro-8-oxoguanine oxidation and hydrolysis provides a potent source of point mutations.

The DNA oxidation product 7,8-dihydro-8-oxoguanine (8-oxoG) forms several mutagenic oxidation products, including a metastable oxaluric acid (Oa) derivative. We report here that a synthetic oligonucleotide containing Oa hydrolyzes under simulated "in vivo" conditions to form a mutagenic urea (Ua) lesion. Using the Oa 2'-deoxyribonucleoside as a model, the hydrolysis rate depended strongly upon the concentrations of bicarbonate and divalent magnesium. In buffered solutions containing physiologically relevant levels of these species, the half-life of Oa nucleoside was approximately 40 h at 37 degrees C. The mutagenic properties of Ua in DNA were investigated using a M13mp7L2 bacteriophage genome containing Ua at a specific site. Transfection of the lesion-containing genome into wild-type AB1157 Escherichia coli allowed determination of the mutation frequency and DNA polymerase bypass efficiency from the resulting progeny phage. Ua was bypassed with an efficiency of 11% as compared to a guanine control and caused a 99% G-->T mutation frequency, assuming the lesion originated from G, which is at least an order of magnitude higher than the mutation frequency of 8-oxoG under the same conditions. SOS induction of bypass DNA polymerase(s) in the bacteria prior to transfection caused the mutation frequency and type to shift to 43% G-->T, 46% G-->C, and 10% G-->A mutations. We suggest that Ua is instructional, meaning that the shape of the lesion and its interactions with DNA polymerases influence which nucleotide is inserted opposite the lesion during replication and that the instructional nature of the lesion is modulated by the size of the binding pocket of the DNA polymerase. Replication past Ua, when formed by hydrolysis of the 8-oxoG oxidation product Oa, denotes a pathway that nearly quantitatively generates point mutations in vivo.

DNA↗
PubMed1989

Xanthine oxidase activity in rat pulmonary artery endothelial cells and its alteration by activated neutrophils.

The possibility that endothelial cell-derived oxidants could contribute to neutrophil-mediated endothelial cell injury and cytotoxicity has been a subject of speculation. Rat pulmonary artery endothelial cells (RPAECs) were examined for the presence of xanthine oxidase (XO) activity, a well-known source of O2-. Using a sensitive assay based on measurements of radioactive xanthine conversion to uric acid by high performance liquid chromatography (HPLC), RPAEC extracts were found to contain both XO and xanthine dehydrogenase (XD) activities. Extracts from early passage cells have 55.3 +/- 11.7 (mean +/- SE) units/10(6) cells of total (XO + XD) activity, one unit of activity being defined as the conversion of 1% of substrate to product in 30 minutes of incubation. XO comprised 31.6 +/- 3.1% of this total activity. Addition of human neutrophils stimulated with phorbol myristate acetate (PMA) caused a rapid and dose-dependent increase in RPAEC XO activity from 31.6 +/- 3.1% to 71.7 +/- 4.8% of total without altering total (XO + XD) activity. The neutrophil dose-response curve for increase in XO paralleled closely the curve for neutrophil-mediated RPAEC cytotoxicity. The basal XO and XD activities and the neutrophil-induced increase in XO activity were inhibited by treating RPAECs with allopurinol, oxypurinol, and lodoxamide, which also inhibited cytotoxicity, but not by catalase, superoxide dismutase, or deferoxamine. Addition of H2O2 failed to cause an increase in RPAEC XO activity or XD to XO conversion. The results suggest that during neutrophil-mediated injury, rapid conversion of RPAEC XD to XO occurs, resulting in increased XO, catalyzed endogenous oxidant production, which may contribute to the oxidant burden in the killing mechanism initiated by activated neutrophils. Although the mechanism for conversion of XD to XO is uncertain, it appears that neutrophil-derived H2O2 is not sufficient to cause this phenomenon. Furthermore, neither O2- nor chelatable iron is required for neutrophil-induced XD to XO conversion. Supernatant fluids from activated neutrophils failed to induce XD to XO conversion in RPAECs. This in vitro system provides an opportunity to define the cellular and molecular mechanisms underlying the in vivo phenomenon of XD to XO conversion associated with ischemic/reperfusion or inflammatory tissue injury.

Allopurinol↗
PubMed2000

The role of mast cells in ischaemia-reperfusion injury in murine skeletal muscle.

To determine the role of mast cells in ischaemia-reperfusion (IR) injury to skeletal muscle, W(f)/W(f) mast cell-deficient and their corresponding wild-type mice were subjected to 70 min tourniquet ischaemia and 24 h reperfusion. As measured by nitroblue tetrazolium (NBT) staining, muscle viability was 9% in wild-type and 94% in mast cell-deficient animals (p<0.001). Assay of residual lactate dehydrogenase activity within the injured muscle (p<0.05) and histological examination confirmed the greater muscle necrosis in treated wild-type than in treated mast cell-deficient mice. There was no significant difference in the degree of neutrophil infiltration, tissue myeloperoxidase content or water content of IR-injured muscle in the two mouse phenotypes. To determine further the role of mast cells in IR injury, wild-type mice were treated 30 min prior to reperfusion with an intraperitoneal dose of either saline or the mast cell-stabilizing agent lodoxamide trometamol (2.5, 7.5, 25 or 75 mg/kg). Twenty-four hours after removal of the tourniquet, saline-treated gastrocnemius muscle had a mean viability of 14% compared with 28% (p<0.05) and 48% (p<0.01) after 25 mg/kg and 75 mg/kg of lodoxamide treatment, respectively. The ability of lodoxamide to stabilize mast cells was confirmed by histological examination. Ischaemic muscle reperfused for 1 h showed much less degranulation of mast cells in mice pretreated with lodoxamide (50 mg/kg) than in saline-treated controls. These findings suggest that mast cells are a major source of mediators of necrosis in IR injury to skeletal muscle.

Animals↗
PubMed2000

Expression of autocrine motility factor/phosphohexose isomerase in Cos7 cells.

Autocrine motility factor (AMF) is identical to the glycolytic enzyme phosphohexose isomerase (PHI) and overexpression of AMF/PHI is associated with tumor malignancy. In order to study the overexpression of AMF/PHI, an HA-tagged AMF construct was transiently transfected into Cos7 cells. Expression of a tagged AMF-HA allowed us to determine that over a period of 16 hours only a small amount (0.1-1%) of total cellular AMF-HA was secreted into the cell medium. Cell-associated AMF-HA was exclusively cytosolic as it could be completely extracted with Triton X-100 and concentrated within actin rich pseudopodial domains. Treatment of the cells with the glycolysis inhibitor oxamate disrupted the association of AMF-HA with actin concentrations demonstrating that glycolysis regulates the formation of these AMF/PHI-associated actin-rich protrusions. AMF/PHI is a well-characterized tumor cell secreted cytokine and we identify here an alternate intracellular function for this glycolytic enzyme/cytokine in cell motility.

Actins↗
PubMed1988

Do anti-allergic drugs or anticholinergic drugs have a role in the treatment of asthma?

After the successful introduction of sodium cromoglycate (SCG) for the treatment of asthma, emphasis was placed on its apparent novel mechanism of action, the inhibition of inflammatory mediator release from mast cells. This opened the flood gates for numerous SCG-derivatives, many with oral efficacy and improved potency. The majority of these compounds were ineffective clinically, casting doubts on SCG's mechanism of action and questioning the importance of mast cells in asthma. However, information on the heterogeneity of mast cells has directed recent drug screening to new, more relevant models of asthma involving other inflammatory cells. Consequently, nedocromil sodium has emerged to perhaps lead a new generation of antiallergic drugs. Bronchodilator anticholinergic drugs have met with a resurgence of interest of late with the development of a number of quaternary ammonium homologues of atropine. While not as effective as beta-adrenoceptor agonists in asthma they are particularly effective in chronic obstructive pulmonary disease. Drugs with anticholinergic properties and associated beneficial effects are also under investigation.

Animals↗