Polymerisation of trioxane; kinetics of the reaction initiated by BF3·OEt2 and the system FeCl3/trityl chloride

The kinetics of polymerisation of trioxane has been determined in a variety of solvents. The reaction, catalysed by boron trifluoride, is shown to be comparatively simple in o-dichlorobenzene and trichloroethylene. In both cases the reaction is shown to be complex kinetically due to the occurrence of several equilibria which precede the propagation reaction. Rate and equilibrium parameters have been evaluated and their significance has been discussed.     

Polymerisation of vinyl monomers by transition metal benzyl compounds. Part II. Polymerisation of styrene by tetrabenzyl zirconium

The polymerisation of styrene by tetrabenzyl zirconium in toluene in the dark at 30 and 40°C has been studied using kinetics, spectroscopic and radiochemical techniques. From the data obtained, together with information derived from molecular weight measurements, a mechanism has been obtained which is in accord with the experimental findings. The polymerisation is of the coordinated anionic type in which only one of the four zirconium benzyl bonds is activated for polymerisation. Each active metal centre grows only one chain and is terminated by a β-hydrogen abstraction process or by a bimolecular reaction involving monomer. Transfer reactions are absent. Only a small fraction of the catalyst participates in polymerisation and the concentration of active polymerisation centres is very low. A complex between tetrabenzyl zirconium and coordinated monomer could not be detected experimentally. Values for the velocity constants for initiation, propagation and termination are determined.     

Suppression of the anaphylactic reaction of isolated smooth-muscle organs by potassium arsenite

The possibility of suppressing the anaphylactic reaction of human and guinea pig smooth muscle by means of inorganic arsenic was studied. Potassium arsenite (in the form of Fowler's solution) inhibited the development of anaphylactic contraction of human smooth muscle (ileum). Potassium arsenite completely blocked the development of anaphylactic bronchospasm and the liberation of biologically active substances from the lungs of guinea pigs.Allergologic Research Laboratory, Academy of Medical Sciences of the USSR, Moscow. (Presented by Academician of the Academy of Medical Sciences of the USSR A. D. Ado.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 84, No. 9, pp. 341–343, September, 1977.     

Neoplastic transformation of human bronchial cells by lead chromate particles

Particulate hexavalent chromium (Cr(VI)) is a well-established human lung carcinogen with widespread exposure among people in occupational settings and the general public. However, no studies have examined the chromate-induced malignant transformation of human lung epithelial cells, its predominant target. Human papillomavirus-immortalized human bronchial epithelial (BEP2D) cells were used to better understand the mechanisms involved in human bronchial carcinogenesis induced by particulate chromate. We found that aneuploid cells increased in a concentration-dependent manner after chronic exposure to lead chromate. Moreover, chronic exposure to lead chromate induced BEP2D cell transformation. Transformed BEP2D cells developed through a series of sequential steps, including altered cell morphology, loss of cell contact inhibition and anchorage-independent growth. Specifically, a 5-day exposure to lead chromate induced foci formation with 0, 1, 5, and 10 microg/cm2 lead chromate inducing 0, 7, 3, and 15 foci in 10 dishes. Anchorage independence was observed in cell lines derived from these foci. These foci-derived cells also showed centrosome amplification and increases in aneuploid metaphases. Our study demonstrates that particulate Cr(VI) is able to transform human bronchial epithelial cells, and that chromosome instability may play an important role in particulate Cr(VI)-induced neoplastic transformation.     

Polymerisation of trioxane, 2. Kinetics of the reaction initiated by chlorosulphonic acid

The kinetics of polymerisation of trioxane, initiated by chlorosulphonic acid have been studied in o-dichlorobenzene, trichloroethylene, and carbon tetrachloride. The reaction is shown to be simple, though the kinetics are different in the above solvents. With very pure and dry substrates, no induction period is observed. Rate parameters have been evaluated.     

The Neurospora crassa chr-1 gene is up-regulated by chromate and its encoded CHR-1 protein causes chromate sensitivity and chromium accumulation

The ChrA membrane protein belongs to the CHR superfamily of chromate ion transporters, which includes homologues from bacteria, archaea and eukaryotes. Bacterial ChrA homologues confer chromate resistance by exporting chromate ions from the cell’s cytoplasm. The Neurospora crassa strain 74-A chr-1 gene encodes a putative CHR-1 protein of 507 amino acid residues, which belongs to the CHR superfamily. RT-PCR assays showed that expression of the chr-1 gene was up-regulated by chromate exposure of N. crassa cultures. Introduction in N. crassa of sense and antisense fragments of the chr-1 gene, as part of a silencing module within the pSilent-1 vector, produced transformants with a phenotype of resistance to chromate and diminished accumulation of chromium, as compared with the control strain containing only the vector. A chromate-resistance phenotype was also observed in N crassa strains deleted in the genomic chr-1 gene, thus confirming that the absence of CHR-1 protein confers chromate resistance to the fungus. The cDNA from N. crassa chr-1 gene (Ncchr-1) was cloned into the pYES2 vector under the control of a GAL promoter and the resulting recombinant plasmid was transferred to the yeast Saccharomyces cerevisiae. Galactose-induced S. cerevisiae transformants expressing Ncchr-1 were more sensitive to chromate and accumulated 2.5 times more chromium than the induced strain containing only the vector. Excess sulfate, a chromate analog, was unable to protect S. cerevisiae chr-1 transformants from chromate toxicity. These data indicate that the N. crassa CHR-1 protein functions as a transporter that takes up chromate; it also appears that this transport occurs in a sulfate-independent fashion. This is the first report assigning a role as a chromate transporter to a nonbacterial CHR protein.     

Highly Filled Polystyrene/Laponite Hybrid Nanoparticles Prepared Using the Ad‐miniemulsion Polymerisation Technique

The preparation of highly filled polystyrene/Laponite (PS/Lap) hybrid nanoparticles by the ad‐miniemulsion polymerisation technique, using conventional free‐radical polymerisation, is described. Laponite (Lap) is first modified with a polymerisable cationic surfactant. Then, using a second surfactant dispersions are prepared under sonication. A stable hybrid miniemulsion is obtained after mixing and co‐sonicating both miniemulsions. The polymerisation is conducted using an oil‐soluble initiator to obtain hybrid nanoparticles. PS/Lap hybrid nanoparticles are effectively prepared with clay contents as high as 50 wt%. TEM reveals that the highly filled hybrid latexes (≥30 wt%) exhibit encapsulated morphology with homogeneously distributed clay platelets.     

Specificity of arsenite in potentiating cytogenetic damage induced by the DNA crosslinking agent diepoxybutane.

In the present study, the induction of sister chromatid exchanges (SCEs) and chromosomal aberrations were measured in normal human lymphocytes treated with low concentrations of arsenite alone (0.5-2.0 microM) and arsenite in combination with the potent DNA crosslinking agent diepoxybutane (DEB). Experiments were carried out with lymphocytes from blood donors with different sensitivities to SCE induction by DEB. Arsenite, beginning at concentrations as low as 1 microM, increased SCE frequencies; chromosomal aberration frequencies were increased at 2 microM of arsenite. DEB treatments alone increased SCE frequencies and chromosomal aberrations. The yields of chromatid deletions and exchanges in lymphocytes exposed to both arsenite and DEB were markedly increased above the levels expected if the effects of the two agents had been simply additive. The frequencies of chromatid deletions were 4- to 8-fold greater than expected and chromatid exchanges were increased 7- to 40-fold. Chromatid exchanges detected in cells treated with arsenite and DEB were predominately incomplete exchanges. The most dramatic increases in chromatid aberrations were observed in lymphocytes from an individual sensitive to SCE induction by DEB, indicating that individuals may vary in their sensitivity to the co-clastogenic effects of arsenite. At concentrations that dramatically affect aberrations, arsenite had no effect on the induction of SCEs by DEB. These studies suggest a specific interaction of arsenite with the induction or repair of DNA damage produced by DEB that leads to chromosomal aberrations but not to SCEs. Based on the selective chemical reactivity of low concentrations of arsenite with proteins containing vicinal dithiols and the occurrence of these groups within DNA repair proteins, it is proposed that the specific co-clastogenic effects of arsenite may be mediated by its interference with DNA repair activities.     

Active oxygen species are involved in the induction of micronuclei by arsenite in XRS-5 cells

The human carcinogen, arsenic, is genotoxic to mammalian cellsin vitro. The mechanism is largely unknown, although the involvementof free radicals has been suggested. Since the X-ray sensitiveChinese hamster ovary cell line, XRS-5, is also sensitive toseveral free-radical generating agents, including H₂O₂, we haveused this cell line to test whether the genotoxic effect ofarsenite is mediated via the generation of active-oxygen species.The results indicate that the XRS-5 cells are more sensitiveto arsenite in terms of cell-killing and micronucleus inductioncompared to the parental CHO-K1 cells. The level of arsenicuptake and release, the levels of elementary components forarsenic detoxification, glutathione and glutathione S-transferaseactivities in these two cell lines are very similar. The XRS-5cells, however, were shown to have 6-fold lower catalase activityin comparison to CHO-K1 cells. Moreover, catalase could effectivelyreduce the frequency of arsenite-induced micronuclei. Theseresults indicate that the low catalase activity may be an importantreason why XRS-5 cells are more sensitive to the toxic effectsof arsenite, and arsenite probably induces micronuclei via theoverproduction of H₂O₂. The XRS-5 cells had a higher backgroundlevel of micronuclei, and were also more sensitive to     

Polymerisation of trioxane, 3. Kinetics of the reaction initiated by stannic chloride and phosphorous oxychloride

The kinetics of polymerisation of 1,3,5-trioxane initiated by stannic chloride and phosphorous oxychloride were investigated in the solvents chlorobenzene, o-dichlorobenzene, trichloroethylene, and tetrachloroethylene. With pure reactants no induction periods were observed. The kinetic and equilibrium parameters were evaluated.     

Multifunctional Poly(vinyl ethers) by Controlled Cationic Polymerisation in a Fluorinated Solvent

The living nature of the cationic polymerisation of butyl vinyl ether (BVE) in the fluorinated solvent 1,1,2‐trichloro trifluoroethane was studied, using the initiating system composed of ethyl aluminium dichloride (EtAlCl₂) as the activator and 1‐butoxyethyl acetate (BEA) as the initiator. BVE homopolymerises in a seemingly living fashion at T ≤ 0°C in the presence of 1,4‐dioxane (DO) as a stabilising Lewis base, although the fluorinated solvent slows down the polymerisation appreciably. Less than quantitative reinitiation has been observed when a second BVE feed was added to the living macrocation at nearly quantitative monomer conversion. The functional monomers 2‐chloroethyl vinyl ether (CLEVE), 3‐cyano‐3‐ethoxycarbonylpropyl vinyl ether (CNEVE) and 1H,1H,2H,2H‐perfluorodecyl vinyl ether (XFDVE) were submitted to polymerisation under the same conditions that allow to achieve a quasi‐living BVE polymerisation. CLEVE gave a homopolymer with relatively narrow molecular‐weight distribution (MWD), while efficient polymerisation of XFDVE was only achieved with BF₃ etherate as the initiator. Copolymerisation of the various functional vinyl ethers with BVE takes place in a more controlled fashion, yielding products with narrow MWD index (M_w/M_w = 1.2–1.35), at moderate functional vinyl ether conversions. Block copolymers could be synthesised from poly(BVE) living macrocations; these are probably characterised by a hybrid structure, consisting of a pure BVE block and a second block of BVE‐functional vinyl ether copolymer.     

Polymerisation via macrozwitterions, 2. Ethyl and butyl cyanoacrylates polymerised by pyridine and polyvinylpyridine

Anionic polymerisations of ethyl and butyl cyanoacrylates in THF initiated by pyridine and polyvinylpyridine were studied between 42 and ?95°C. The polymers showed the UV absorption of quaternised pyridine, indicating that they had grown as macrozwitterions. Pyridine consumption was very low (few %) and the polymer molecular weights high (3 · 10⁵ – 10⁶) irrespective of reaction conditions. Overall rates increased as reaction temperature was reduced, approaching those found in phosphine-initiated polymerisations by ?78°C. At 20°C the kinetics were complex, e.g. sigmoid conversion curves which reached an internal first order, yet showing apparent 2nd order external order. A qualitative kinetic interpretation is given, postulating absence of intrinsic termination processes, and a complex initiation process involving (exothermic) equilibrium formation of a precursor betaine. Polyvinylpyridine initiates graft copolymers; but only in presence of chain-terminating agents, e.g. acids, lactones or sultones, can the grafted side chains be kept short, and their number raised towards the potentially complete grafting of all pyridine groups.     

Polymerisation via macrozwitterions, 1. Ethyl and butyl cyanoacrylates polymerised by triethyl and triphenylphosphines

Anionic polymerisation of ethyl and butyl cyanoacrylates in THF initiated by triethyl and triphenylphosphines were followed by adiabatic calorimetry at temperatures between 20 and ?95°C. The polymers showed UV absorptions characteristic of phosphonium and cyanoacrylate carbanion end groups, indicating that the growing chains were macrozwitterions. Monomer conversion was quantitative and of 1st order in both monomer and initiator. Other criteria of ‘living’ polymerisation were satisfied, e.g. molecular weights corresponded to one chain per initiator molecule, and indicated that monomer added subsequently was incorporated on to previously formed chains. Assuming the overall rate to be that of propagation yielded values of k_p = 1 – 3 · 10⁵ dm³ · mol^?1 · s^?1 at ?78°C, with very low activation energies, i.e. 2,2 and 5,5 kJ · mol^?1 for ECA and BCA, respectively. Of a range of inert salts only LiBr significantly reduced the rate of polymerisation.     

Polymerisation of Acrylates Catalysed by Methylaluminoxane Activated Ditertiary Phosphine Complexes of Iron and Cobalt Dichlorides

Summary: Diphosphane complexes of iron(II) are active catalysts for the polymerisation of methyl acrylate (MA) monomers in the presence of methylaluminoxane (MAO). High molar mass atactic MA polymers ( ～ 200 kg/mol) were obtained under mild conditions with relatively narrow polydispersities (PDI ～ 2). Polymerisation activity and polymer molar masses are strongly dependent on the ligand frame. The polymerisation requires the coordination of MA to a vacant coordination site at the metal centre, and processes with chain‐transfer to aluminium. Cobalt analogues proved to be less efficient catalysts, giving activities in the range of 50–250 kg/mol · h instead of 200–450 kg/mol · h for the iron complexes. MAO activated FeCl₂ and CoCl₂ salts also perform the polymerisation of MA with low activity.

Ditertiary phosphine complex of iron(II) chloride as methyl acrylate polymerisation catalyst.     

Sodium arsenite potentiates the clastogenicity and mutagenicity of DNA crosslinking agents

To see if sodium arsenite enhances the clastogenicity and the mutagenicity of DNA crosslinking agents, Chinese hamster ovary (CHO) cells and human skin fibroblasts were exposed to cis-diamminedichloroplatinum (II) (cis-Pt(II)) or 8-methoxypsoralen (8-MOP) plus long-wave ultraviolet light (UVA) and then to sodium arsenite. The results indicate that the clastogenicity of cis-Pt(II) and 8-MOP plus UVA are enhanced by the post-treatment with sodium arsenite. Chromatid breaks and exchanges are predominantly increased in doubly treated cells. Furthermore, the mutagenicity of cis-Pt(II) at the hypoxanthine-guanine phosphoribosyl transferase locus is also potentiated by sodium arsenite in CHO cells.     

Cationic vinyl polymerization by the initiator system diethylzinc/phosphoryl chloride

Et₂Zn in combination with POCl₃ induces the cationic polymerization of isobutyl vinyl ether and N-vinyl carbazole at ambient temperature. The rate is directly proportional to [Et₂Zn]. [POCl₃] up to a mole ratio of unity of the components, and thereafter it decreases. At a fixed ratio of [Et₂Zn]/[POCl₃] the rate is second order in [Isobutyl vinyl ether]. Rate and [η] decrease in the presence of basic additives, pyridine, and water. Unlike the system Et₃Al/POCl₃, the present combination does not lead to any stereoregular poly(isobutyl vinyl ether) at ambient or lower temperatures. A cationic mechanism is proposed and an appropriate kinetic scheme is suggested.