Organic esters or salts of sulfonic acid derivatives containing an aliphatic hydrocarbon radical.

Characterization of a two-component alkanesulfonate monooxygenase from Escherichia coli. (1/165)

The Escherichia coli ssuEADCB gene cluster is required for the utilization of alkanesulfonates as sulfur sources, and is expressed under conditions of sulfate or cysteine starvation. The SsuD and SsuE proteins were overexpressed and characterized. SsuE was purified to homogeneity as an N-terminal histidine-tagged fusion protein. Native SsuE was a homodimeric enzyme of M(r) 58,400, which catalyzed an NAD(P)H-dependent reduction of FMN, but it was also able to reduce FAD or riboflavin. The SsuD protein was purified to >98% purity using cation exchange, anion exchange, and hydrophobic interaction chromatography. The pure enzyme catalyzed the conversion of pentanesulfonic acid to sulfite and pentaldehyde and was able to desulfonate a wide range of sulfonated substrates including C-2 to C-10 unsubstituted linear alkanesulfonates, substituted ethanesulfonic acids and sulfonated buffers. SsuD catalysis was absolutely dependent on FMNH(2) and oxygen, and was maximal for SsuE/SsuD molar ratios of 2.1 to 4.2 in 10 mM Tris-HCl, pH 9.1. Native SsuD was a homotetrameric enzyme of M(r) 181,000. These results demonstrate that SsuD is a broad range FMNH(2)-dependent monooxygenase catalyzing the oxygenolytic conversion of alkanesulfonates to sulfite and the corresponding aldehydes. SsuE is the FMN reducing enzyme providing SsuD with FMNH(2).  (+info)

The Escherichia coli ssuEADCB gene cluster is required for the utilization of sulfur from aliphatic sulfonates and is regulated by the transcriptional activator Cbl. (2/165)

The growth properties of an Escherichia coli strain carrying a chromosomal deletion of the ssuEADCB genes (formerly designated ycbPONME) indicated that the products of this gene cluster are required for the utilization of sulfur from aliphatic sulfonates. Sequence similarity searches indicated that the proteins encoded by ssuA, ssuB, and ssuC are likely to constitute an ABC type transport system, whereas ssuD and ssuE encode an FMNH(2)-dependent monooxygenase and an NAD(P)H-dependent FMN reductase, respectively (Eichhorn, E., van der Ploeg, J. R., and Leisinger, T. (1999) J. Biol. Chem. 274, 26639-26646). Synthesis of beta-galactosidase from a transcriptional chromosomal ssuE'-lacZ fusion was repressed by sulfate or cystine and depended on the presence of a functional cbl gene, which encodes a LysR-type transcriptional regulator. Electrophoretic mobility shift assays with the ssu promoter region and measurements of beta-galactosidase from plasmid-encoded ssuE'-'lacZ fusions showed that full expression of the ssu operon required the presence of a Cbl-binding site upstream of the -35 region. CysB, the LysR transcriptional regulator for the cys genes, was not required for expression of a chromosomal ssuE'-lacZ fusion although the ssu promoter region contained three CysB-binding sites. Integration host factor could also occupy three binding sites in the ssu promoter region but had no influence on expression of a chromosomal ssuE'-lacZ fusion.  (+info)

Deletion analysis of the Escherichia coli taurine and alkanesulfonate transport systems. (3/165)

The Escherichia coli tauABCD and ssuEADCB gene clusters are required for the utilization of taurine and alkanesulfonates as sulfur sources and are expressed only under conditions of sulfate or cysteine starvation. tauD and ssuD encode an alpha-ketoglutarate-dependent taurine dioxygenase and a reduced flavin mononucleotide-dependent alkanesulfonate monooxygenase, respectively. These enzymes are responsible for the desulfonation of taurine and alkanesulfonates. The amino acid sequences of SsuABC and TauABC exhibit similarity to those of components of the ATP-binding cassette transporter superfamily, suggesting that two uptake systems for alkanesulfonates are present in E. coli. Chromosomally located in-frame deletions of the tauABC and ssuABC genes were constructed in E. coli strain EC1250, and the growth properties of the mutants were studied to investigate the requirement for the TauABC and SsuABC proteins for growth on alkanesulfonates as sulfur sources. Complementation analysis of in-frame deletion mutants confirmed that the growth phenotypes obtained were the result of the in-frame deletions constructed. The range of substrates transported by these two uptake systems was largely reflected in the substrate specificities of the TauD and SsuD desulfonation systems. However, certain known substrates of TauD were transported exclusively by the SsuABC system. Mutants in which only formation of hybrid transporters was possible were unable to grow with sulfonates, indicating that the individual components of the two transport systems were not functionally exchangeable. The TauABCD and SsuEADCB systems involved in alkanesulfonate uptake and desulfonation thus are complementary to each other at the levels of both transport and desulfonation.  (+info)

Ethane sulfonate metabolite of alachlor: assessment of oncogenic potential based on metabolic and mechanistic considerations. (4/165)

Chronic administration of alachlor has been shown to produce neoplastic responses in the nasal turbinate mucosa, glandular stomach mucosa, and thyroid follicular epithelium of rats. Subsequent studies have shown that specific metabolic activation of alachlor is required for nasal tumor formation, and that non-genotoxic, threshold-sensitive processes produce all three tumors. The herbicide alachlor is degraded in the soil by microbial action to the tertiary ethane sulfonate metabolite (ESA). The acute and subchronic toxicity of ESA is very low, and the metabolite did not produce developmental toxicity or genotoxicity. The studies described here were conducted to determine whether ESA shares a common mechanism of oncogenicity with alachlor in rats. Specifically, we studied ESA's pharmacokinetics and ability to produce changes that are causally associated with the oncogenicity of alachlor. These studies demonstrated that ESA was poorly absorbed and underwent minor metabolism, which contrasted with the significant absorption and substantial metabolism observed with alachlor. ESA was also excreted more quickly than alachlor and showed no evidence of accumulation in the nasal turbinates, a site of oncogenicity for alachlor in the rat. In addition, ESA did not elicit the characteristic preneoplastic changes observed in the development of alachlor-induced nasal, stomach, and thyroid tumors. The results of these studies support the conclusion that ESA does not share a common oncogenic mechanism with alachlor and would not be expected to produce the same oncogenic responses observed following chronic alachlor exposure in rats.  (+info)

Characterization of a sulfur-regulated oxygenative alkylsulfatase from Pseudomonas putida S-313. (5/165)

The atsK gene of Pseudomonas putida S-313 was required for growth with alkyl sulfate esters as sulfur source. The AtsK protein was overexpressed in Escherichia coli and purified to homogeneity. Sequence analysis revealed that AtsK was closely related to E. coli taurine dioxygenase (38% amino acid identity). The AtsK protein catalyzed the alpha-ketoglutarate-dependent cleavage of a range of alkyl sulfate esters, with chain lengths ranging from C(4) to C(12), required oxygen and Fe(2+) for activity and released succinate, sulfate, and the corresponding aldehyde as products. Enzyme activity was optimal at pH 7 and was strongly stimulated by ascorbate. Unlike most other characterized alpha-ketoglutarate-dependent dioxygenases, AtsK accepted a range of alpha-keto acids as co-substrates, including alpha-ketoglutarate (K(m) 140 microm), alpha-ketoadipate, alpha-ketovalerate, and alpha-ketooctanoate. The measured K(m) values for hexyl sulfate and SDS were 40 and 34 microm, respectively. The apparent M(r) of the purified enzyme of 121,000 was consistent with a homotetrameric structure, which is unusual for this enzyme superfamily, members of which are usually monomeric or dimeric. The properties and amino acid sequence of the AtsK enzyme thus define it as an unusual oxygenolytic alkylsulfatase and a novel member of the alpha-ketoglutarate-dependent dioxygenase family.  (+info)

In vitro activity of a novel antimycobacterial compound, N-octanesulfonylacetamide, and its effects on lipid and mycolic acid synthesis. (6/165)

beta-Sulfonyl carboxamides have been proposed to serve as transition-state analogues of the beta-ketoacyl synthase reaction involved in fatty acid elongation. We tested the efficacy of N-octanesulfonylacetamide (OSA) as an inhibitor of fatty acid and mycolic acid biosynthesis in mycobacteria. Using the BACTEC radiometric growth system, we observed that OSA inhibits the growth of several species of slow-growing mycobacteria, including Mycobacterium tuberculosis (H37Rv and clinical isolates), the Mycobacterium avium complex (MAC), Mycobacterium bovis BCG, Mycobacterium kansasii, and others. Nearly all species and strains tested, including isoniazid and multidrug resistant isolates of M. tuberculosis, were susceptible to OSA, with MICs ranging from 6.25 to 12.5 microg/ml. Only three clinical isolates of M. tuberculosis (CSU93, OT2724, and 401296), MAC, and Mycobacterium paratuberculosis required an OSA MIC higher than 25.0 microg/ml. Rapid-growing mycobacterial species, such as Mycobacterium smegmatis, Mycobacterium fortuitum, and others, were not susceptible at concentrations of up to 100 microg/ml. A 2-dimensional thin-layer chromatography system showed that OSA treatment resulted in a significant decrease in all species of mycolic acids present in BCG. In contrast, mycolic acids in M. smegmatis were relatively unaffected following exposure to OSA. Other lipids, including polar and nonpolar extractable classes, were unchanged following exposure to OSA in both BCG and M. smegmatis. Transmission electron microscopy of OSA-treated BCG cells revealed a disruption in cell wall synthesis and incomplete septum formation. Our results indicate that OSA inhibits the growth of several species of mycobacteria, including both isoniazid-resistant and multidrug resistant strains of M. tuberculosis. This inhibition may be the result of OSA-mediated effects on mycolic acid synthesis in slow-growing mycobacteria or inhibition via an undescribed mechanism. Our results indicate that OSA may serve as a promising lead compound for future antituberculous drug development.  (+info)

Short-chain aliphatic polysulfonates inhibit the entry of Plasmodium into red blood cells. (7/165)

Several steps in the pathogenesis of a Plasmodium falciparum infection depend on interactions of parasite surface proteins with negatively charged sugars on the surface of host cells such as sialate residues or glycosaminoglycans. For these reasons, our previous studies examining agents that interfere with heparan sulfate-protein binding during amyloidogenesis suggested that short-chain aliphatic polysulfonates may prove useful as antimalarial agents. A series of related polysulfonates were synthesized and assessed both in tissue culture with the asexual stages of P. falciparum in human red blood cells and in vivo by use of Plasmodium berghei infections in mice. Poly(vinylsulfonate sodium salt) (molecular weight range, 1,500 to 3,000) proved effective in interfering with P. falciparum merozoite entry into human red blood cells and significantly delaying the increase in the level of P. berghei parasitemia in mice. The concept that anionic molecules that mimic large polysaccharide structures may have antimalarial properties has been suggested and examined previously. Our results suggest that related anionic agents [poly(vinylsulfonate sodium salt)-like molecules] orders of magnitude smaller than those previously considered may prove useful in abrogating merozoite entry into erythrocytes and may potentially block sporozoite entry into liver cells. Structure-activity studies conducted to enhance these properties may provide compounds with scope for significant further analysis and development.  (+info)

AZ 242, a novel PPARalpha/gamma agonist with beneficial effects on insulin resistance and carbohydrate and lipid metabolism in ob/ob mice and obese Zucker rats. (8/165)

Abnormalities in fatty acid (FA) metabolism underlie the development of insulin resistance and alterations in glucose metabolism, features characteristic of the metabolic syndrome and type 2 diabetes that can result in an increased risk of cardiovascular disease. We present pharmacodynamic effects of AZ 242, a novel peroxisome proliferator activated receptor (PPAR)alpha/gamma agonist. AZ 242 dose-dependently reduced the hypertriglyceridemia, hyperinsulinemia, and hyperglycemia of ob/ob diabetic mice. Euglycemic hyperinsulinemic clamp studies showed that treatment with AZ 242 (1 micromol/kg/d) restored insulin sensitivity of obese Zucker rats and decreased insulin secretion. In vitro, in reporter gene assays, AZ 242 activated human PPARalpha and PPARgamma with EC(50) in the micro molar range. It also induced differentiation in 3T3-L1 cells, an established PPARgamma effect, and caused up-regulation of liver fatty acid binding protein in HepG-2 cells, a PPARalpha-mediated effect. PPARalpha-mediated effects of AZ 242 in vivo were documented by induction of hepatic cytochrome P 450-4A in mice. The results indicate that the dual PPARalpha/gamma agonism of AZ 242 reduces insulin resistance and has beneficial effects on FA and glucose metabolism. This effect profile could provide a suitable therapeutic approach to the treatment of type 2 diabetes, metabolic syndrome, and associated vascular risk factors.  (+info)

The S1 secondary alkylsulphohydrolase of the detergent-degrading micro-organism, Pseudomonas C12B, was separated from other alkylsulphohydrolases and purified to homogeneity. Under the experimental conditions used the enzyme completely hydrolysed d-octan-2-yl sulphate (d-1-methylheptyl sulphate), but showed no activity towards the corresponding l-isomer. Additional evidence has been obtained to indicate that it is probably optically stereospecific for d-secondary alkyl sulphate esters with the ester sulphate group at C-2 and with a chain length of at least seven carbon atoms. Enzyme activity towards racemic samples of heptan-2-yl sulphate (1-methylhexyl sulphate), octan-2-yl sulphate and decan-2-yl sulphate (1-methylnonyl sulphate) increased with increasing chain length. l-Octan-2-yl sulphate is a competitive inhibitor of the enzyme, as are certain primary alkyl sulphates and primary alkanesulphonates. Inhibition by each of the last two types of compounds is characteristic of the behaviour of an ...
Agonists of peroxisome proliferator-activated receptors (PPARs) have emerged as important pharmacological agents for improving insulin action. A major mechanism of action of PPAR agonists is thought to involve the alteration of the tissue distribution of nonesterified fatty acid (NEFA) uptake and utilization. To test this hypothesis directly, we examined the effect of the novel PPARalpha/gamma agonist tesaglitazar on whole-body insulin sensitivity and NEFA clearance into epididymal white adipose tissue (WAT), red gastrocnemius muscle, and liver in rats with dietary-induced insulin resistance. Wistar rats were fed a high-fat diet (59% of calories as fat) for 3 wk with or without treatment with tesaglitazar (1 micromol.kg(-1).d(-1), 7 d). NEFA clearance was measured using the partially metabolizable NEFA tracer, (3)H-R-bromopalmitate, administered under conditions of basal or elevated NEFA availability. Tesaglitazar improved the insulin sensitivity of high-fat-fed rats, indicated by an increase in the
Abstract PPARs are transcription factors belonging to the superfamily of nuclear receptors. PPAR-alpha is involved in the regulation of fatty acid (FA) uptake and oxidation, inflam..
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A one-pot reaction between di-n-propyl/di-n-butyltin oxide, dialkyl sulfite, and triethylamine or tetra-n-alkylammonium iodide proceeds under ambient conditions (110-120 degrees C, 20 h) via sulfur-centered Arbuzov rearrangement to afford the corresponding dianionic tetraalkanesulfonato diorganostannates [R2Sn(OSO2Me)(4)]center dot 2Et(3)NMe [R = n-Pr (1), n-Bu (2)] as well as [n-Bu2Sn(OSO2R1)(4)]center dot 2R(4)(2)N [R-1 = Me, Et, n-Pr; R 2 = Et (3, 5, and 7), n-Bu (4, 6, and 8)]. X-ray crystal structures of 2 and 3 reveal a monomeric motif of the dianion, with methanesulfonate groups acting as unidentate ligands. The Sn-119 NMR spectral studies suggest the existence of pentacoordinated tin species in solution.. ...
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Structure, properties, spectra, suppliers and links for: 2-{[(3α,5β,6α,7α,17ξ)-3,6,7-Trihydroxy-24-oxocholan-24-yl]amino}ethanesulfonic acid.
Structure, properties, spectra, suppliers and links for: 2-{[(3α,5β,12α,17α,20S)-3,12-Dihydroxy-24-oxocholan-24-yl]amino}ethanesulfonic acid.
Primary alkyl amines released into the atmosphere are likely to be degraded by reaction with hydroxyl radicals, with a half-life around 7.5 h.Because there are no important releases into the atmosphere and volatilisation is expected to be negligible, this removal mechanism is considered not to be relevant. Primary alkyl amines are unlikely to undergo photolytical or hydrolytic degradation. Thus abiotic degradation in the environment is not expected. Based on the available studies on biodegradation, the substances are estimated to be readily biodegradable, fulfilling the 10-days-window criterion. An OECD 307 aerobic soil transformation study (3 soils) was carried out with [1-14C]-Hexadecanamine (Harlan, 2010). Although this C16 amine is strongly sorbing to soil (median Kpsoil of 3875 L/kg at lowest measured concentration) half-lives between 8.1 and 9 days at 20 degree C were determined. The median Half-life of 8.9 d at 20 degree C corresponds to a median Half-life of 16.9 d at an environmental ...
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The Beta distribution is given by $\frac{\Gamma(\alpha+\beta)}{\Gamma(\alpha)\Gamma(\beta)}x^{\alpha-1}(1-x)^{\beta-1}$. Define $\frac{\Gamma(\alpha)\Gamma(\beta)}{\Gamma(\alpha+\beta)} \triangleq \mathcal{B}(\alpha,\beta)$, which is the normalization constant. Notice that this definition makes $\int_0^1 x^{\alpha-1}(1-x)^{\beta-1}\mathrm{d}x = \mathcal{B}(\alpha,\beta)$. Together with $\Gamma(x+1) = x\Gamma(x)$ we can use these identities to obtain the requested statistics: $$\begin{align*} \mathbb{E}[x] &= \frac{1}{\mathcal{B}(\alpha,\beta)}\int_0^1 x x^{\alpha-1}(1-x)^{\beta-1}\mathrm{d}x \\ &= \frac{1}{\mathcal{B}(\alpha,\beta)}\int_0^1x^{\alpha}(1-x)^{\beta-1}\mathrm{d}x \\ &= \frac{\mathcal{B}(\alpha+1,\beta)}{\mathcal{B}(\alpha,\beta)} \\ &= \frac{\Gamma(\alpha+1)\Gamma(\alpha+\beta)}{\Gamma(\alpha)\Gamma(\alpha+\beta+1)}\\ &= \frac{\alpha \Gamma(\alpha)\Gamma(\alpha+\beta) }{(\alpha+\beta)\Gamma(\alpha)\Gamma(\alpha+\beta)}\\ &= \frac{\alpha}{\alpha+\beta} \\ \mathbb{V}[x] &= ...
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US EPA PC Code ); 187022-11-3 (CAS number); 187022113 (CAS number without hyphens); 2-[(2-ethyl-6-methylphenyl)(ethoxymethyl) amino]-2-oxoethanesulfonic acid; 621600 (US EPA PC Code Text ); ABN (PDP Code); Acetochlor breakdown product; Acetochlor ESA; Acetochlor ethanesulfonic acid; Acetochlor ethanesulfonic acid (ESA); ...
Sulfonate sphingoids or sulfonolipids are bioactive unusual compounds found in members of the Bacteroidetes family. The present report describes the structures of sulfonolipids of halophilic bacteria, sharing structural similarity with compounds of fungal origin inhibiting the serine palmitoyl transferase and with capnines, known as antagonists of von Willebrandt factor. Two sulfonolipids (SL1 and SL2) were isolated from the lipid extract of the halophile Salisaeta longa and analyzed by ESI-MS/MS. SL1 and SL2 structures have in common the long chain aminosulfonate 2-carboxy-2-amino-3,4-hydroxy-17 methyloctadec-5-ene-1-sulfonic for which the common name of halocapnine is suggested. The hydroxyl group on carbon 3 of aminosulfonate moiety is acylated: iso C15 and iso hydroxy C15 chains are present in SL1 and SL2, respectively. The levels of the two different sulfonolipids in the bacterium were found to be modulated by the proportion of sodium and magnesium ions in the environment ...
Results of the irradiations indicate that, in aerated solutions, the major mode of degradation is by desulfonation of the molecule. Degradation was accompanied by significant losses in oxygen, possibly a result of direct oxidation of the solute by radiation, rather than by free radical reactions. Enols were also found to occur, but at very low concentrations. The product formed as a result of desulfonation of benzenesulfonic acid appeared to be quinonoid rather than phenolic in nature ...
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This polymer supported strong alkyl sulfonic acid and can be used instead of soluble organic acids for quenching or catalysis of reactions. It can be also used for scavenging and catch and release applications. ...
InCHi String: canonical and isomeric SMILES: CCS(=O)(=O)[O-]. PUBCHEM iupac NAME: PUBCHEM iupac OPENEYE NAME: PUBCHEM iupac CAS NAME: PUBCHEM iupac SYSTEMATIC NAME ...
Fatty Methyl Ester Sulfonates Market (FMES Market) was valued at USD 0.57 billion in 2014 and is anticipated to reach USD 1.58 billion by 2020, expanding at a CAGR of 18.6% between 2015 and 2020
Information on Registered Substances comes from registration dossiers which have been assigned a registration number. The assignment of a registration number does however not guarantee that the information in the dossier is correct or that the dossier is compliant with Regulation (EC) No 1907/2006 (the REACH Regulation). This information has not been reviewed or verified by the Agency or any other authority. The content is subject to change without prior notice ...
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Three esterase-labile, but chemically-stable sulfonate protecting groups have been designed and synthesized. One of these sulfonate esters allowed the cytoplasmic delivery and unmasking of a sulfonated dye in live cells.
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Synonyms: TAURINE;TURIN;2-amino-ethanesulfonicaci;2-sulfoethylamine;Aminoethanesulfonic acid;beta-Aminoethylsulfonic acid;Ethanesulfonic acid, 2-amino-;Ethanesulfonicacid,2-amino- CAS: 107-35-7 MF: C2H7NO3S MW: 125.15 EINECS: 203-483-8 Chemical...
Ethanesulfonic acid, 2-((2-(bis(2-chloroethyl)amino)tetrahydro-2H-1,3,2-oxazaphosphorin-4-yl)thio)-, compd.with cyclohexanamine (1:1) ...
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Unexpected Reaction of 2,3-Epoxy Sulfonates: Novel Formation of Two Enones with Reversed Substituents at α- and β-Positions from the Single Isomer (2004 ...
"The Synthesis of Some Tritium-labelled Mutagenic Alkyl Alkanesulfonates". Acta Chemica Scandinavica. 20: 908-910. doi:10.3891/ ...
SIAM 25: Alkyl Sulfates, Alkane Sulfonates, and α-Olefin sulfonates" (PDF). OECD SIDS. Helsinki. DE/ICCA (2009). "SIDS Initial ... primary alkane sulfonates, and α-Olefin sulfonate". Ecotoxicology and Environmental Safety. 74 (5): 1089-1106. doi:10.1016/j. ... Assessment Profile SIAM 25: Alkyl Sulfates, Alkane Sulfonates, and α-Olefin sulfonates". OECD. Wibbertmann, A; Mangelsdorf, I ...
1996). "Regiochemical Analysis of Water Soluble Conductive Polymers: Sodium Poly(ω-(3-thienyl)alkanesulfonates)". ...
Technical alkane sulfonates - Methods of analysis ISO 894:1977 Surface active agents - Technical sodium primary alkylsulphates ...
... alkanesulfonates MeSH D02.455.326.146.100.050.490 - mesna MeSH D02.455.326.146.100.050.500 - mesylates MeSH D02.455.326.146. ... alkanesulfonates MeSH D02.886.645.600.055.050.500 - mesna MeSH D02.886.645.600.055.050.510 - mesylates MeSH D02.886.645.600. ...
Surface active agents - Technical alkane sulfonates - Determination of alkane monosulfonates content by direct two-phase ...
SIDS Category of Alkyl sulfates, Alkane sulfonates and Alpha-olefin sulfonates. Author:. OECD Year:. 2% ...
... similarly composed secondary alkane sulfonates (UVCBs); slight differences are caused by the production processes - for the ... similarly composed secondary alkane sulfonates (UVCBs); slight differences are caused by the production processes - for the ... saponified and the read across substance are very similarly composed secondary alkane sulfonates (UVCBs); slight differences ... saponified and the read across substance are very similarly composed secondary alkane sulfonates (UVCBs); slight differences ...
Alkanesulfonates - Preferred Concept UI. M0000720. Scope note. Organic esters or salts of sulfonic acid derivatives containing ...
Alkanesulfonates. General subdivision. adverse effects.. 650 02 - SUBJECT ADDED ENTRY--TOPICAL TERM. ...
... acetamido-alkane sulfonates, and (8) sarcosinates having from 8 to 22 carbons, e.g., sodium lauroyl sarcosinate. ...
Alkanesulfonates Utilization (22). Amino Acids and Derivatives (785). Glutamine, glutamate, aspartate, asparagine; ammonia ...
D02.455.326.146.100.050 Alkanesulfonates .. D02.455.326.146.100.050.500 Mesylates .. D02.455.326.146.100.050.500.500 Methyl ... D02.886.645.600.055.050 Alkanesulfonates .. D02.886.645.600.055.050.510 Mesylates .. D02.886.645.600.055.050.510.500 Methyl ...
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Alkanesulfonates. *Alkanesulfonic Acids. *Compounds used in a research, industrial, or household setting ...
Surface Activities, Foam Properties, HLB, and Krafft Point of Some n-Alkanesulfonates (C14-C18) with Different Isomeric ...
Alkanesulfonates KW - adverse effects KW - Environmental exposure KW - Guidelines N1 - First draft prepared at the National ...
This study presents the development of an ion pairing liquid chromatography with alkanesulfonates coupled to tandem mass ...
Alkanesulfonates * Benzamides * Blood Glucose * Diabetes Mellitus, Type 2 * Dose-Response Relationship, Drug ...
Organic Chemicals - Alkanesulfonates * Toluene - Toluidines * Toxic Actions - Herbicides * Water Pollutants, Chemical has ...

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