[Retarded action of polyvinylpyrrolidone (P.V.P.) on some plant organs].
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Povidone↗
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Evaluation of the genetic effects induced by vinyl chloride monomer (VCM) under mammalian metabolic activation: studies in vitro and in vivo.
As part of a programme of investigations on the biological effects of the industrial compound vinyl chloride monomer (VCM), the raw material for the production of polyvinyl chloride (PVC), analyses on the genetic effects by this compound have been done by experiments (in vitro) which have taken mammalian metabolism into account. Vinyl chloride in the presence of purified microsomes (sedimented at 105,000 g) obtained from mouse liver was converted into an active metabolite(s) which produced gene mutations in the yeast Schizosaccharomyces pombe (forward mutation) and gene conversions in two loci of a diploid Saccharomyces cerevisiae. Moreover, the compound was active in the host-mediated assay, when mice were treated with an oral dose of 700 mg/kg. The role is discussed of mutagenicity tests for the prediction of both genetic and carcinogenic risks of chemical compounds in industrial use.
Animals↗
1,3-dialkyl- and 1,3-diaryl-3,4,5,6-tetrahydropyrimidin-2-ylidene rhodium(i) and palladium(II) complexes: synthesis, structure, and reactivity.
The synthesis of novel 1,3-diaryl- and 1,3-dialkylpyrimidin-2-ylidene-based N-heterocyclic carbenes (NHCs) and their rhodium(i) and palladium(II) complexes is described. The rhodium compounds bromo(cod)[1,3-bis(2-propyl)-3,4,5,6-tetrahydropyrimidin-2-ylidene]rhodium (7), bromo(cod)(1,3-dimesityl-3,4,5,6-tetrahydropyrimidin-2-ylidene)rhodium (8) (cod=eta(4)-1,5-cyclooctadiene, mesityl=2,4,6-trimethylphenyl), chloro(cod)(1,3-dimesityl-3,4,5,6-tetrahydropyrimidin-2-ylidene)rhodium (9), and chloro(cod)[1,3-bis(2-propyl)-3,4,5,6-tetrahydropyrimidin-2-ylidene]rhodium (10) were prepared by reaction of [[Rh(cod)Cl](2)] with lithium tert-butoxide followed by addition of 1,3-dimesityl-3,4,5,6-tetrahydropyrimidinium bromide (3), 1,3-dimesityl-3,4,5,6-tetrahydropyrimidinium tetrafluoroborate (4), 1,3-di-2-propyl-3,4,5,6-tetrahydropyrimidinium bromide (6), and 1,3-di-2-propyl-3,4,5,6-tetrahydropyrimidinium tetrafluoroborate, respectively. Complex 7 crystallizes in the monoclinic space group P2(1)/n, and 8 in the monoclinic space group P2(1). Complexes 9 and 10 were used for the synthesis of the corresponding dicarbonyl complexes dicarbonylchloro(1,3-dimesityl-3,4,5,6-tetrahydropyrimidin-2-ylidene)rhodium (11), and dicarbonylchloro[1,3-bis(2-propyl)-3,4,5,6-tetrahydropyrimidin-2-ylidene]rhodium (12). The wavenumbers nu(CO I)/nu(CO II) for 11 and 12 were used as a quantitative measure for the basicity of the NHC ligand. The values of 2062/1976 and 2063/1982 cm(-1), respectively, indicate that the new NHCs are among the most basic cyclic ligands reported so far. Compounds 3 and 6 were additionally converted to the corresponding cationic silver(i) bis-NHC complexes [Ag(1,3-dimesityl-3,4,5,6-tetrahydropyrimidin-2-ylidene)(2)]AgBr(2) (13) and [Ag[1,3-bis(2-propyl)-3,4,5,6-tetrahydropyrimidin-2-ylidene](2)]AgBr(2) (14), which were subsequently used in transmetalation reactions for the synthesis of the corresponding palladium(II) complexes Pd(1,3-dimesityl-3,4,5,6-tetrahydropyrimidin-2-ylidene)(2) (2+)(Ag(2)Br(2)Cl(4) (4-))(1/2) (15) and Pd[1,3-bis(2-propyl)-3,4,5,6-tetrahydropyrimidin-2-ylidene)(2)]Cl(2) (16). Complex 15 crystallizes in the monoclinic space group P2(1)/c, and 16 in the monoclinic space group C(2)/c. The catalytic activity of 15 and 16 in Heck-type reactions was studied in detail. Both compounds are highly active in the coupling of aliphatic and aromatic vinyl compounds with aryl bromides and chlorides with turnover numbers (TONs) up to 2000000. Stabilities of 15 and 16 under Heck-couplings conditions were correlated with their molecular structure. Finally, selected kinetic data for these couplings are presented.
Journal Article↗
Review of epidemiologic study results of vinyl chloride-related compounds.
Epidemiologic study results addressing the carcinogenicity of six compounds related to vinyl chloride (vinylidene chloride, trichloroethylene, perchloroethylene, carbon tetrachloride, ethylene dibromide and epichlorohydrin) are reviewed. The study results suggest an increased carcinogenic risk among workers exposed to epichlorohydrin and to dry cleaning and degreasing solvents. Although several studies report no significant excess of cancer mortality, an evaluation of the design of these investigations demonstrates that these negative cohort studies consisted of populations of insufficient sample size and latency to permit any meaningful conclusions regarding carcinogenic risk. Therefore, experimental studies must be relied upon to determine whether several of these substances pose a potential carcinogenic risk to humans. Available evidence indicates that all of these substances have demonstrated a carcinogenic response in experimental animals and most are mutagenic in experimental test systems.
Epidemiologic Methods↗
Synthesis and bioactivity of propranolol analogues with a rigid skeleton. I.
The synthesis of two kinds of propranolol analogues, A and B, with a rigid skeleton was investigated. The compounds were designed to help identify the conformation involved in beta-adrenergic receptor-propranolol interaction. The key intermediate, 2-hydroxy.2,3-dihydronaphtho[1,8-bc]pyran (5), was obtained starting from acenaphthenone (1). On sequential dehydration, hydroboration, and oxidation, 5 gave 2,3-dihydronaphtho[1,8-bc]pyran-3-one (8), which was converted to compound A. Compound 5 was also derived to 2-formyl-2,3-dihydronaphtho[1,8-bc]pyran (13) via the 2-vinyl compound (12). Condensation of nitromethane with 13 followed by reduction and alkylation produced the desired compound B. The beta-blocking activities of A and B were examined.
Adrenergic beta-Antagonists↗
Audiogenic seizure protection by elevated brain GABA concentration in mice: effects of gamma-acetylenic gaba and gamma-vinyl GABA, two irreversible GABA-T inhibitors.
gamma-Acetylenic GABA and gamma-vinyl GABA, two catalytic irreversible inhibitors of GABA-transaminase, produce marked and sustained elevations in mouse brain GABA concentrations and protect DBA/2 mice against audiogenically induced seizures in a similar dose and time-dependent manner. The acetylenic analog also inhibits GAD activity while the vinyl compound has minimal activity against this enzyme. The increase in brain GABA concentrations induced by these compounds correlates well with attenuation of audiogenic seizure intensity (r = 0.991 and 0.962 for gamma-acetylenic and gamma-vinyl GABA respectively) and with degree of seizure protection (r = 0.974 and 0.834). Seizure intensity is reduced by 50% when brain GABA is increased to 265% and 264% of control values by the two inhibitors and seizure incidence is halved at 322% and 324%. Thus, audiogenic seizure protection in genetically susceptible mice is apparently a function of whole brain GABA concentrations.
4-Aminobutyrate Transaminase↗
Structure-activity relationships of cephalosporins having a (dimethylisoxazolidinio)vinyl moiety at their 3-position.
A series of cephalosporins having a (dimethylisoxazolidinio)vinyl group at their 3-position were synthesized to investigate their structure-activity relationships. With regard to the olefin geometry, the (E)-vinyl compound exhibited higher in vitro activity than the (Z)-compound. Regarding the C-7 substituents, the replacement of 2-aminothiazole with 5-amino-1,2,4-thiadiazole increased the anti-pseudomonal activity. Determination of the absolute configuration of the C-3 substituent is also presented. Among the compounds synthesized, we selected 7 beta-[(Z)-2-(5-amino-1,2,4-thiadiazol-3-yl)-2-(fluoromethoxyimi no)acetamido]-3-[(E)-2-((S)-2,2-dimethyl-5-isoxazolidinio)vinyl ]-3-cephem-4-carboxylate (YM-40220), which showed well-balanced in vitro activity and an excellent in vivo efficacy against Staphylococcus aureus Smith, as a candidate for further development.
Animals↗
Deprotonation of cationic tungsten(IV) aqua-oxo-alkyne complexes to form dioxo-vinyl tungsten(VI) complexes.
Chiral tungsten(IV) aqua-oxo-alkyne complexes, [Tp'W(O)(H2O)(RC identical to CR)][OTf] (R = H (1); R = Me (2)); (Tp' = hydridotris(3,5-dimethylpyrazolyl)borate; OTf = trifluoromethanesulfonate), have been prepared by halide abstraction from iodide precursors. These cationic complexes have been characterized with triflate as the counteranion. The tautomeric dihydroxo isomer has not been observed. The neutral triflate adduct Tp'W(O)(OTf)(HC identical to CH) (3) has also been isolated. Cationic complexes 1 and 2 undergo deprotonation and isomerization when exposed to Al2O3 to give the dioxo-vinyl compounds Tp'W(O)2(CH=CH2) (6) and Tp'W(O)2[C(Me)=C(H)(Me)] (7), reflecting the conversion of the WIV(OH)(RC identical to CR) fragment to WVI(=O)(RC=CHR). The presumed intermediates, neutral oxo-hydroxo compounds Tp'W(O)(OH)(RC identical to CR) (R = H (9); R = Me (10)), can be accessed by deprotonation of 1 or 2 with NaOH. Conversion of 9 to 6 was achieved thermally upon heating at 100 degrees C for 2 days. X-ray structural data have provided solid-state structures of both the cationic aqua complex 2 and the dioxo-vinyl complex 6.
Journal Article↗
NTP Toxicology and Carcinogenesis Studies of Allyl Glycidyl Ether (CAS No. 106-92-3) in Osborne-Mendel Rats and B6C3F1 Mice (Inhalation Studies).
Allyl glycidyl ether is used as a resin intermediate and as a stabilizer of chlorinated compounds, vinyl resins, and rubber. NTP Toxicology and Carcinogenesis studies were conducted by exposing groups of Osborne-Mendel rats and B6C3F1 of each sex to allyl gylcidyl ether (greater than 97% pure) by inhalation for 6 hours per day, 5 days per week for 2 weeks, 13 weeks, or 2 years. Genetic toxicology studies were conducted in Salmonella typhimurium, Chinese hamster ovary (CHO) cells, and Drosophila melanogaster. Studies of reproductive effects were conducted in rats and mice exposed to allyl glycidyl ether for 8 weeks. Two-Week Studies: Exposure concentrations ranged up to 500 ppm in rats and 100 ppm in mice. All rats that were exposed to 500 ppm died; no deaths occurred at the next lower (200 ppm) exposure concentration. All male mice and 3/5 female mice exposed to 100 ppm and 2/5 male mice and 1/5 female mice exposed to 50 ppm died. Compound-related lesions in rats and mice included acute inflammation of the nasal passage and major airways. Eight-Week Studies of Reproductive Effects: Rats were exposed to 0-200 ppm allyl glycidyl ether, and mice were exposed to 0-30 ppm, 6 hours per day, 5 days per week for 8 weeks. The mating performance of exposed male rats was markedly reduced; however, sperm motility and number were not affected. No deficiencies were seen in the reproductive performance of exposed female rats or male or female mice. Thirteen-Week Studies: Exposure concentrations ranged up to 200 ppm for rats and 30 ppm for mice. All rats lived to the end of the studies. The final mean body weights of male rats exposed to 10-200 ppm were 7%-24% lower than that of controls. Clinical signs attributable to irritation of the upper respiratory tract and eyes were seen in exposed animals. Histologic lesions included squamous metaplasia of the nasal passage in all exposure groups (4 ppm, lowest concentration) and involved both the respiratory epithelium and the olfactory epithelium. The lesions were more severe anteriorly and dorsally and with increasing concentration. At 30 ppm and higher, erosion was seen in the nasal passage and squamous metaplasia was seen in the upper airways. There were no compound-related deaths in mice. The final mean body weights of mice exposed to 30 ppm were 12% lower than those of controls for both males and females. Mice exposed to 10 or 30 ppm allyl glycidyl ether had squamous metaplasia of the nasal passage, involving both the respiratory epithelium and the olfactory epithelium, which tended to be more severe in the anterior and dorsal portions of the nasal passage. In mice exposed to 30 ppm, epithelial erosions were also found. Body Weights and Survival in the Two-Year Studies: Two-year studies were conducted by exposing groups of 50 Osborne-Mendel rats and B6C3F1 mice of each sex to 0, 5, or 10 ppm allyl glycidyl ether by inhalation for 6 hours per day, 5 days per week for 102 or 103 weeks. Mean body weights of the exposed rats were within 8% of those of controls throughout the studies. Mean body weights of mice exposed to 5 or 10 ppm were 5%-20% lower than those of controls. Deaths were seen in all groups of male rats beginning at 1 year of age (final survival-- control, 12/50; 5 ppm, 11/50; 10 ppm, 8/50). Survival of female rats was not exposure related (24/50; 30/50; 25/50). Exposed mice had slightly increased survival (male mice: 38/50; 39/50; 46/50; female mice: 33/50; 42/50; 41/50). Nonneoplastic and Neoplastic Effects in the Two-Year Studies: In male rats exposed to 10 ppm allyl glycidyl ether, three apparently unrelated neoplasms of the nasal passage were found. Two neoplasms, a papillary adenoma and a squamous cell carcinoma, appeared to arise from different cell types in the respiratory epithelium. One poorly differentiated adenocarcinoma in the olfactory region was also found. One papillary adenoma of respiratory epithelial origin was found in a female rat exposed to 5 ppm. Exposure-related nonneoplastic lesions of the nasal passages in rats included inflammation, squamous metaplasiin rats included inflammation, squamous metaplasia, respiratory metaplasia (replacement of olfactory epithelium by ciliated epithelium), hyperplasia of the respiratory epithelium, and degeneration of the olfactory epithelium. In male mice exposed to 10 ppm allyl glycidyl ether, a hemangioma and three papillary adenomas were present in the nasal passage. In female mice exposed to 10 ppm, a hemangioma and an adenoma were found in the nasal passage. Nonneoplastic lesions of the nasal passages in mice included inflammation, squamous metaplasia, hyperplasia, basal cell hyperplasia, dysplasia of the respiratory epithelium, and metaplasia of the olfactory epithelium. In male mice, there was an exposure-related decrease in the incidences of hepatocellular neoplasms; in female mice, there was a decrease in the incidences of pituitary gland adenomas. Genetic Toxicology: Allyl glycidyl ether was mutagenic in S. typhimurium strains TA100 and TA1535 with and without exogenous metabolic activation; no mutagenic activity was observed in strains TA98 or TA1537. Allyl glycidyl ether induced sister chromatid exchanges and chromosomal aberrations in CHO cells both in the presence and the absence of metabolic activation. A significant increase in sex-linked recessive lethal mutations was recorded in the germ cells of male D. melanogaster fed a sucrose solution containing allyl glycidyl ether, but no increase in reciprocal translocations occurred in these cells. Conclusions: Under the conditions of these 2-year inhalation studies, there was equivocal evidence of carcinogenic activity of allyl glycidyl ether for male Osborne-Mendel rats, based on the presence of one papillary adenoma of respiratory epithelial origin, one squamous cell carcinoma of respiratory epithelial origin, and one poorly differentiated adenocarcinoma of olfactory epithelial origin, all occurring in the nasal passage of males exposed to 10 ppm. There was no evidence of carcinogenic activity of allyl glycidyl ether for female rats. One papillary adenoma of the respiratory epithelium was present in a female rat exposed to 5 ppm. There was some evidence of carcinogenic activity of allyl glycidyl ether for male B6C3F1 mice, based on the presence of three adenomas of the respiratory epithelium, dysplasia in four males, and focal basal cell hyperplasia of the respiratory epithelium in seven males in the nasal passage of mice exposed to 10 ppm. There was equivocal evidence of carcinogenic activity of allyl glycidyl ether for female mice, based on the presence of one adenoma of the respiratory epithelium and focal basal cell hyperplasia of the respiratory epithelium in seven females exposed to 10 ppm. The sensitivity of the assay to detect potential carcinogenicity may have been reduced in male rats because of poor survival in all groups. In exposed mice, body weights were decreased 10% or more, mortality was decreased, and there were lower incidences of liver neoplasms (males) and pituitary gland adenomas (females) compared with controls. Significant exposure-related nonneoplastic lesions were restricted to the nasal passage in both rats and mice and induced inflammation, metaplasia, respiratory epithelial hyperplasia, and olfactory epithelial degeneration. Basal cell hyperplasia and dysplasia of the respiratory epithelium of the nasal passage were found only in the mice. Synonyms: allyl 2,3-epoxypropyl ether; 1-allyloxy-2,3-epoxypropane; 1,2-epoxy-3-allyloxypropane; glycidyl allyl ether; ((2-propenyloxy)methyl)oxirane; 1-(allyloxy)-2,3-epoxypropane
Journal Article↗
Asymmetric allylic alkylation of cyclic vinylogous esters and thioesters by Pd-catalyzed decarboxylation of enol carbonate and beta-ketoester substrates.
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Alkylation↗
Heck coupling with nonactivated alkenyl tosylates and phosphates: examples of effective 1,2-migrations of the alkenyl palladium(II) intermediates.
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Alkenes↗
[Organophosphorus compounds. I. Synthesis and reactions of vinylacylester phosphates].
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Acylation↗
Gas-phase protonation and deprotonation of acrylonitrile derivatives N[triple chemical bond]C--CH==CH--X (X=CH(3), NH(2), PH(2), SiH(3)).
A combined experimental and theoretical study on the gas-phase basicity and acidity of a series of cyanovinyl derivatives is presented. The gas-phase basicities and acidities of (N[triple chemical bond]C--CH==CH--X, X=CH(3), NH(2)) were obtained by means of Fourier transform ion cyclotron resonance (FT-ICR) mass spectrometry techniques. The corresponding calculated values were obtained at the G3B3 level of theory. The effects of exchanging CH(3) for SiH(3), and NH(2) for PH(2), were analyzed at the same level of theory. For the neutral molecules, the Z isomer is always the dominant species under standard gas-phase conditions at 298 K. The loss of the proton from the substituent X was found systematically to be much more favorable than deprotonation of the HC==CH linking group. The corresponding isomeric E ion is much more stable than the Z ion, so that only the former should be found in the gas phase. The most significant structural changes upon deprotonation occur for the methyl and amino derivatives because, in both cases, deprotonation of X leads to a significant charge delocalization in the corresponding anion. Protonation takes place systematically at the cyano group, whereby the isomeric E ion is again more stable than the Z ion. Push-pull effects explain the preference of aminoacrylonitrile to be protonated at the cyano group, which also explains the high basicity of this derivative relative to other members of the analyzed series that present rather similar gas-phase basicities, GB approximately 780 kJ mol(-1), indicating that the different nature of the substituents has only a weak effect on the intrinsic basicity of the cyano group. The cyanovinyl derivatives have a significantly stronger gas-phase acidity than that of the corresponding vinyl compounds CH(2)==CH--X. This acidity-strengthening effect of the cyano group is attributed to the greater stabilization of the anion with respect to the corresponding neutral compound.
Journal Article↗
Synthesis and stereochemistry of dispiro substituted pyridazines: application of ellipticity-absorbance ratio spectra for proving enantiomeric relationship by HPLC-CD/UV detection.
The aim of our study was to synthesize vinylic and pyrido-fused pyridazines with a spirano moiety and to investigate their stereochemistry by spectroscopic and HPLC analyses. The vinylic compounds 5 were obtained by Knoevenagel condensation of cyclohexylidene malonates 1 with pyridazinecarbaldehyde 2. Compound 5b exhibits geometric isomerism identified by NMR, HPLC, and X-ray methods. The thermal rearrangement reactions of compounds 5 easily led to the pyridopyridazine derivatives 6. In the case of 6b, possessing both central and axial chirality, both diastereomers and the respective enantiomers were detected. Their stereochemical relationships could be determined by HPLC-CD/UV analyses with application of anisotropy spectra in a novel way.
Journal Article↗
2-Oxoacid dehydrogenases of rat liver mitochondria as the site of action of S-(1,2 dichlorovinyl)-L-cysteine and S-(1,2-dichlorovinyl)-3-mercaptopropionic acid.
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Adenosine Triphosphate↗
Further studies on the site and mechanism of action of s-(1,2 dichlorovinyl)-l-systeine and s-(1,2 dichlorovinyl)-3-mercaptopropionic acid in rat liver.
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Ammonia↗
Reaction of vinylfurans with sulfhydryl and amino groups.
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Amines↗
Sulfur-containing proreactive intermediates: hydrolysis and mutagenicity of halovinyl 2-nitrophenyl disulfides.
Chemical cleavage of the sulfur-sulfur bond in halovinyl and fluoroalkyl 2-nitrophenyl disulfides is expected to yield halovinyl and fluoroalkyl thiols identical to those formed by cysteine conjugate beta-lyase catalyzed cleavage of the corresponding cysteine S-conjugates. To study the potential use of disulfides as precursors for these thiols, whose transformation to acylating agents is most likely responsible for cysteine S-conjugate mutagenicity, we determined the mutagenicity of several halovinyl and fluoroalkyl 2-nitrophenyl disulfides and identified products formed by hydrolysis of these disulfides, 1,2,3,4,4-Pentachlorobutadienyl 2-nitrophenyl disulfide, 1,2,2-trichlorovinyl 2-nitrophenyl disulfide, 1-fluro-2,2-dichlorovinyl 2-nitrophenyl disulfide and 1,2-dichloro-3,3,3-trifluropropenyl 2-nitrophenyl disulfide were mutagenic in nitroreductase deficient strains of Salmonella typhimurium TA100; as haloalkyl cysteine S-conjugates, 1,1-difluoro-2,2-dichloroethyl 2-nitrophenyl disulfide and 1-chloro-1,2,2-trifluroethyl 2-nitrophenyl disulfide were not mutagenic. Hydrolysis of 1,2,3,4,4-pentachlorobutadienyl 2-nitrophenyl disulfide and 1,2,2-trifluorethyl 2-nitrophenyl disulfide in presence of diethylamine resulted in tetrachlorothiobutenoic acid diethylamide and chlorofluorothionoacetic acid diethylamide. The differences in mutagenicity between halovinyl and fluoroalkyl disulfides are most likely responsible to their different abilities to react with DNA-constituents. Products formed from the mutagenic 1,2,3,4,4-pentachlorobutadienyl 2-nitrophenyl disulfide modified 2'-deoxyguanosine-3'-monophosphate and DNA as detected by 32Phosphorus-postlabeling, whereas products formed from the nonmutagenic 1-chloro-1,2,2-trifluoroethyl 2-nitrophenyl disulfide did not result in detectable 2'-deoxyguanosine-3'-monophosphate and DNA modification.
DNA↗