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PubMed1995

Effects of alkyl substituents of xanthine on phosphodiesterase isoenzymes.

The structure-activity relationships of a series of alkylxanthine derivatives were investigated. The partition coefficient of alkylxanthines enlarged with an elongation of the alkyl chain at the 1-, 3-, or 7-position of xanthine. There was a mild correlation between the apparent partition coefficient and the tracheal relaxant activity or the inhibitory activity on phosphodiesterase (PDE) IV isoenzyme, while the tracheal relaxant activity closely correlated with the PDE IV inhibitory activity. Regarding substituents at different positions, the alkylation at the 3-position increased the inhibitory activity on every PDE isoenzyme. The alkylation at the 1-position potentiated the inhibitory activity on PDE IV with the alkyl chain length, but decreased the activities on other PDE isoenzymes. The alkylation at the 7-position was characteristic in its decrease in inhibitory activity on PDE III. These results suggested that the potency of the inhibitory activity of xanthine derivatives on PDE isoenzymes is not dependent simply upon their hydrophobicity but upon change in the affinity for the active sites on PDE isoenzymes by the introduction of the alkyl group at particular positions of the xanthine skeleton.

3',5'-Cyclic-AMP Phosphodiesterases↗

PubMed1999

Mutagenicity of potassium alkanediazotates in Chinese hamster V79 cells and their alkylating activity.

Alkanediazohydroxides are the key intermediates of carcinogenic N-nitroso compounds, and exist as geometrical isomers. In this paper, the mutagenicity and cytotoxicity of (E)- and (Z)-potassium alkanediazotates, precursors of alkanediazohydroxides, in Chinese hamster V79 cells were investigated. Mutagenic and cytotoxic activities of (E)-diazotates were dose-dependent, and activity decreased with an increase in the alkyl chain length; methyl>ethyl>propyl, butyl. On the other hand, (Z)-diazotates were less mutagenic and cytotoxic than (E)-diazotates, however (Z)-potassium methanediazotate did show weak mutagenicity. To compare chemical reactivity with biological activity, alkylating activity towards nicotinamide in an aqueous phosphate buffer system was evaluated as an index of the chemical reactivity of diazotates. Using a fluorometric HPLC method, alkylated nicotinamides were detected with high sensitivity in the reaction with all diazotates tested. The alkylating activity of (Z)-methanediazotate was higher than that of the corresponding (E)-diazotate, but the other isomers with ethyl, propyl and butyl groups had similar reactivity under the conditions used. The activity decreased by increasing the alkyl chain-length, which correlated well with the mutagenicity in V79 cells and also with that in Salmonella typhimurium, which we reported earlier. The results for (E)-diazotates were similar to the corresponding N-nitroso-N-(hydroxymethyl)alkylamines, further supporting the notion that alpha-hydroxy nitrosamines decompose through alkanediazohydroxide and alkylate DNA, and suggests that geometrical isomerism influences the carcinogenicity of -nitroso compounds in mammals.

Alkylating Agents↗

PubMed2006

Characterization of alkylphenol degradation gene cluster in Pseudomonas putida MT4 and evidence of oxidation of alkylphenols and alkylcatechols with medium-length alkyl chain.

Alkylphenols (APs) are ubiquitous contaminants in aquatic environments and have endocrine disrupting and toxic effects on aquatic organisms. To investigate biodegradation mechanisms of APs, an AP degradation gene cluster was cloned from a butylphenol (BP)-degrading bacterium, Pseudomonas putida MT4. The gene cluster consisted of 13 genes named bupBA1A2A3A4A5A6CEHIFG. From the nucleotide sequences, bupA1A2A3A4A5A6 were predicted to encode a multicomponent phenol hydroxylase (PH), whereas bupBCEHIFG were expected to encode meta-cleavage pathway enzymes. A partial sequence of a putative NtrC-type regulatory gene, bupR, was also found upstream of the gene bupB. This result indicates that APs can be initially oxidized into alkylcatechols (ACs), followed by the meta-cleavage of the aromatic rings. To confirm this pathway, AP degradation tests were carried out using the recombinant P. putida KT2440 harboring the PH genes (bupA1A2A3A4A5A6). The recombinant strain oxidized 4-n-APs with an alkyl chain of up to C7 (< or = C7) efficiently and also several BPs including those with an alkyl chain with some degree of branching. Therefore, it was found that PH had a broad substrate specificity for APs with a medium-length alkyl chain (C3-C7). Moreover, the cell extract of a recombinant Escherichia coli harboring bupB (a catechol 2,3-dioxygenase gene) converted 4-n-ACs with an alkyl chain of < or = C9 into yellow meta-cleavage products with a maximum absorbance at 379 nm, indicating that the second step enzyme in this pathway is also responsible for the degradation of ACs with a medium-length alkyl chain. These results suggest that MT4 is a very useful strain in the biodegradation of a wide range of APs with a medium-length alkyl chain, which known nonylphenol-degrading Sphingomonas strains have never degraded.

Alkylation↗

PubMed2000

Mechanisms of action of quinone-containing alkylating agents. I: NQO1-directed drug development.

Alkylating agents have been used to treat cancer since the 1940s. Quinone-containing alkylating agents represent a class of drugs called "bioreductive alkylating agents." These drugs require reduction of the quinone moiety for activation of their alkylating substituents. Despite active research in this area, mitomycin C is the only bioreductive alkylating agent approved for general use. The "enzyme-directed" approach to bioreductive drug development involves identification of reductases which are overexpressed in tumors when compared to uninvolved tissues. Bioreductive drugs which are substrates for these reductases should be selectively toxic to tumors with high reductase levels. NAD(P)H:quinone oxidoreductase (NQO1, DT-diaphorase, EC 1.6.99.2) is a two-electron reductase found primarily in the cytosol. NQO1 has received considerable attention because of the high levels of this enzyme in tumors particularly in tumors of the lung, colon and breast. In this review, the current state of research on quinone-containing alkylating agents is discussed with the focus on NQO1-directed bioreductive drug development. Recent structure-activity studies on indolequinones, benzoquinones and other novel quinones are reviewed, and the status of drugs which have been studied in clinical trials is discussed. Finally, the limitations and possible future directions in this research area are presented.

Alkylating Agents↗

PubMed1982

Mutagenic properties of allylic and alpha, beta-unsaturated compounds: consideration of alkylating mechanisms.

1. Allyl and allylic compounds may exert alkylating activities by SN1, SN2 and SN2' mechanisms. This direct alkylating potential can be determined quantitatively by a modified 4-NBP (4-nitrobenzyl pyridine) test. 2. The alkylating activities in a systematically selected series of allyl and allylic compounds correlate well with the direct mutagenic potential as determined in the Ames test using Salmonella typhimurium TA 100 as tester strain. 3. The allylic structure is a prerequisite for these types of activities since structurally related molecules lacking the allylic moiety are inactive in this respect. 4. The potency of both the alkylating and mutagenic activity is determined by the strength of the leaving group: --OSO2CH3 greater than I greater than Br greater than Cl greater than--NCS. 5. Indirect mutagenicity, through metabolic activation of the olefinic bond (by addition of S9 mix to the tester medium), can be ruled out for practically all compounds, the only exception found being 2,3-dichloro-1-propene where an increase of mutagenicity is encountered after addition of S9 mix; mechanistic explanations for this exception are provided. 6. Analogous activation is demonstrated for benzyl halides, the alkylating potency of which is even higher than that of genuine allylic compounds. 7. A variety of methyl- and chlorine-substituted allyl compounds has been included in the study: both groups increase activity, either by +I (CH3) or by +M effects (Cl). 8. alpha, beta-Unsaturated carbonyl compounds, e.g. acrolein and crotonaldehyde, also display direct mutagenic activity which is due to a completely different mechanism: covalent binding to nucleophilic sites of DNA bases by Michael addition. Methyl and other alkyl substitutions decrease the mutagenic potential in this type of compound. The corresponding alcohols, also displaying mutagenic activity but to a lesser degree, are metabolically activated by ADH (alcohol dehydrogenase) of the tester strain microbes to the aldehydes or ketones.

Alkylating Agents↗

PubMed1976

Evaluation of extracorporeal alkylation of red cells as a potential treatment for sickle cell anemia.

Nitrogen mustard and nor-nitrogen mustard inhibit sickling, but the concentrations required would be associated with unacceptable toxicity if these agents were administered to patients. Red cells could be treated extracorporeally and infused back into donors, if the alkylating agent could be removed or inactivated, if the treatment per se did not significantly shorten red cell survival, and if viable alkylated lymphocytes could be eliminated from the treated blood. To estimate whether these conditions could be met in a clinical trial, red cells from four dogs were alkylated at 6-wk intervals. No toxic reactions were observed, although not all nor-nitrogen mustard was removed by the washing procedure. Red cell survival was shortened to about half that of control cells, using concentrations of alkylating agent which reduce sickling by 50%. Lymphocytes from treated blood could still exclude trypan blue, but could not be shown to circulate after reinfusion into donor dogs. If alkylating agents are used to treat patients' cells, inhibition of sickling may outweigh the shortening of red cell life span induced by the treatment; blood should probably be irradiated before infusion to avoid administration of alkylated and potentially mutated, but viable, lymphocytes.

Alkylating Agents↗

PubMed1989

Alkylation of cysteine 41, but not cysteine 200, decreases the ADP-ribosyltransferase activity of the S1 subunit of pertussis toxin.

Sulfhydryl-alkylating reagents are known to inactivate the NAD glycohydrolase and ADP-ribosyltransferase activities of the S1 subunit of pertussis toxin, a protein which contains two cysteines at positions 41 and 200. It has been proposed that NAD can retard alkylation of one of the two cysteines of this protein (Kaslow, H.R., and Lesikar, D.D. (1987) Biochemistry 26, 4397-4402). We now report that NAD retards the ability of these alkylating reagents to inactivate the S1 subunit. In order to determine which cysteine is protected by NAD, we used site-directed mutagenesis to construct analogs of the toxin with serines at positions 41 and/or 200. Sulfhydryl-alkylating reagents reduced the ADP-ribosyltransferase activity of the analog with a single cysteine at position 41; NAD retarded this inactivation. In contrast, sulfhydryl-alkylating reagents did not inactivate analogs with serine at position 41. An analog with alanine at position 41 possessed substantial ADP-ribosyltransferase activity. We conclude that alkylation of cysteine 41, and not cysteine 200, inactivates the S1 subunit of pertussis toxin, but that the sulfhydryl group of cysteine 41 is not essential for the ADP-ribosyltransferase activity of the toxin. These results suggest that the region near cysteine 41 contributes to features of the S1 subunit important for ADP-ribosyltransferase activity. Using site-directed mutagenesis, we found that changing aspartate 34 to asparagine, arginine 39 to lysine, and glutamine 42 to glutamate had little effect on ADP-ribosyltransferase activity. However, substituting an asparagine for the histidine at position 35 markedly decreased, but did not eliminate, ADP-ribosyltransferase activity. Chou-Fasman analysis predicted no significant modifications in secondary structure of the S1 peptide with the change of histidine 35 to asparagine. Thus, histidine 35 may interact with a substrate of the S1 subunit without being essential for catalysis.

Acylation↗

PubMed1986

DNA alkylation by enzyme-activated mitomycin C.

After anaerobic reductive activation by either NADPH cytochrome P-450 reductase (EC 1.6.2.4) or xanthine oxidase (EC 1.2.3.2), mitomycin C readily alkylated DNA. When the mitomycin C-alkylated DNA is digested by DNase, snake venom phosphodiasterase, and alkaline phosphatase, only partial release of the monofunctionally linked mitomycin C nucleotide adduct occurs. Cross-linked adducts are not released into dinucleotides but resist nuclease digestion and remain in oligonucleotides and insoluble precipitates. Kinetic analyses show that the nuclease-resistant fraction which is indicative of DNA cross-linking by mitomycin C takes place quite readily. This nuclease-resistant fraction is particularly significant when the amount of total bound mitomycin C is less than 15 mumol/mmol of DNA. The cross-linked mitomycin C product accounts for more than half of the total alkylation under all pH conditions tested. Our data suggest that particular DNA sites are available for DNA cross-linking by mitomycin C, and these sites are probably the preferred and immediate alkylating targets. Furthermore, DNA cross-links by mitomycin C are not the secondary product of monofunctional adducts. Activity of both flavoenzymes is pH dependent, hence, mitomycin C activation and the rate of DNA alkylation are pH dependent. At elevated mitomycin C alkylation of DNA, the highest amount of cross-linking occurs at neutral pH. High pressure liquid chromatographic separation of the nuclease-digested DNA detected one major and two less prominent mitomycin C adducts. These were verified to be mononucleotide mitosene types by UV spectra showing maximum absorbance at 312 and 250 nm. The major adduct was purified and identified as O6-(2'-deoxyguanosyl)-2,7-diaminomitosene by NMR, indicating that the O6 position of guanine is a preferred site in DNA for at least monofunctional linkage formation.

Alkylating Agents↗

PubMed1986

Alkylating agents: in vitro studies of cross-resistance patterns in human cell lines.

The alkylating agents represent one of the most important classes of antitumor agents and play a major role in combination with other agents in the curative chemotherapy of selected human cancers. By repeatedly exposing cells to escalating doses of an alkylating agent, we have developed four human tumor cell lines which are relatively stably resistant to the drug with which the culture was treated. The response of these cell lines to a variety of alkylating agents was compared to the response of the parent cell lines to the same drug. The Raji/HN2 line was 7-fold resistant to nitrogen mustard and about 3-fold resistant to 4-hydroxyperoxycyclophosphamide, but it was not resistant to N,N'-bis(2-chloroethyl)-N-nitrosourea (BCNU), melphalan (MEL), busulfan, trimethyleneiminethiophosphoramide, 4-hydroperoxyifosfamide, or cisplatin [cis-diamminedichloroplatinum(II)] (CDDP). The Raji/BCNU line was 5.3-fold resistant to BCNU and 4-fold resistant to both MEL and CDDP. The Raji/CP line was 7-fold resistant to CDDP and 3-fold resistant to both nitrogen mustard and BCNU, but it was not resistant to busulfan, trimethyleneiminethiophosphoramide, or 4-hydroperoxyifosfamide. The SCC-25/CP line, which was 12-fold resistant to CDDP, was 5-fold resistant to MEL and 3-fold resistant to 4-hydroxyperoxycyclophosphamide. The SCC-25/CP line was almost 24-fold resistant to methotrexate after 30-min treatment and about 7-fold resistant to methotrexate after continuous treatment. None of the other cell lines was resistant to methotrexate. The survival of SCC-25 and SCC-25/CP cells exposed to several antineoplastic agents was examined over several logs of survival. The SCC-25/CP cells are highly resistant to CDDP; the ratio of the slopes of the survival curves (SCC-25/CP to SCC-25) of the two lines was 43. At survivals of 1%, resistance to MEL and BCNU became evident in the SCC-25/CP line. At survivals of 0.1%, resistance to mitomycin C and, to a lesser degree, to Adriamycin and vincristine was evident. It is more difficult to produce resistance to alkylating agents, even with extended selection pressure, than to other antineoplastic drugs such as antimetabolites and natural products. We found no evidence of pleiotropic resistance in any alkylating agent-resistant cell line. Our results suggest that a judicious choice of alkylating agents given in sequential or concurrent combination may be a rational treatment strategy with potential applications in the clinic.

Alkylating Agents↗

PubMed1979

Enhancement of the nuclear reactivity of alkylating agents by prednisolone.

We have compared the nuclear reactions of the alkylating agents chlorambucil, melphalan, and cyclophosphamide used alone, with those produced when the same drugs were used in combination with the corticosteroid prednisolone. Studies were performed in vivo in Wistar rats bearing ascites forms of either the Yoshida sarcoma or the Walker carcinosarcoma. Strains of both tumor lines, which were sensitive to alkylating agents, showed loss of condensed chromatin, increased phosphorylation of nuclear proteins, and increased DNA cross-linking after exposure to the alkylating agents alone; these changes were generally enhanced in the presence of prednisolone. When paired tumor lines which exhibited acquired resistance to alkylating agents were studied, no nuclear changes were detected when individual alkylating agents were given alone. However, in combination with prednisolone, each of the three alkylating agents produced loss of condensed chromatin, increased nuclear protein phosphorylation, and DNA cross-linking. These chromatin changes were associated with tumor cell death and may determine drug sensitivity in the tumors studied.

Alkylating Agents↗

PubMedDate not supplied

[Complementarily addressed alkylation and cleavage of T7 phage DNA adjacent to the oligothymidylic sequences].

Effect of temperature and reagent excess on the alkylation of the T7 phage DNA by an alkylating derivative of hexaadenylate that containes a modifying group on the 3'-terminus has been studied. Under condition of saturation at 20 degrees the reagent covalently binds adjacent to the 133 5'-PuN2--4Tn greater than or equal to 4 sequences in the T7 DNA; at 40 degrees the reagent alkylates 24 5'-PuN2Tn greater than or equal to 6 sequences. DNA containing specific apurinic sites has been prepared due to elimination of the alkylated purines. This DNA has been cleaved at the apurinic sites and specific DNA fragments have been obtained. Three types of DNA fragments are formed due to alkylation at 20 degrees: one fragment with 26,500 nucleotides in length, seven fragments with 4500 nucleotides in length and 103--111 fragments with an average length of 190 nucleotides. Alkylation at 40 degrees with following apurinization and cleavage yields 21--23 fragments with the lengths: 1--31,500; 1--19,000; 3--9500 and 17--19 with 1100 nucleotides in average.

Alkylation↗

PubMed1995

Design, synthesis, DNA sequence preferential alkylation and biological evaluation of N-mustard derivatives of distamycin and netropsin analogues.

The design and synthesis of certain oligopeptides structurally related to distamycin and netropsin, but bearing mixed heterocyclic moieties capable of recognizing alternative base sites and nitrogen mustard moieties capable of covalent binding to DNA, are described. The binding and thermally induced DNA cleavage, covalent interstrand cross-linking, DNA preferential alkylation and anticancer cytotoxicities of the new agents are described. In contrast to the mustard derivative derived directly from distamycin, the new agents give evidence of extensive DNA alkylation and interstrand cross-linking. In general, strong alkylation is observed at A residues for this class of agents, while the G residues that are alkylated appear to be more characteristic of individual compounds. Densitometric analysis of the frequency of bases adjacent to the alkylation sites (-3 to +3) revealed that the preferred bases are exclusively A/T with little preference shown for G bases and none for C sites. Further insight into the DNA alkylation processes afforded by the drugs was provided by an independent assay whereby heating the drug-DNA adduct with 10% aqueous piperidine only yielded strand breaks specifically at G-N7 sites in the major groove.

Alkylation↗

PubMed1993

Effect of pH on DNA alkylation by enzyme-activated mitomycin C and porfiromycin.

DNA adduct formation by enzyme-activated antibiotics, mitomycin C (MMC) or porfiromycin (PFM), at pH 7.6 or pH 6.0 under anaerobic conditions was analyzed by a 32P-postlabeling method. Antibiotic activation by rat liver NADPH-cytochrome P-450 reductase (EC 1.6.2.4) and bovine milk xanthine oxidase (EC 1.2.3.2) produced similar results. Five 32P-labeled MMC adducts were separated by thin layer chromatography and high performance liquid chromatography from DNA alkylated at either pH. Four of the radioactive spots separated by thin layer chromatography were identified as two monofunctional monoadducts [1" alpha and 1" beta forms of N2-(2" beta,7"-diaminomitosen-1"-yl)-2'-deoxyguanylic acid], one bifunctional monoadduct [N2-(10"-decarbamoyl-2",7"-diaminomitosen-1" alpha-yl)-2'-deoxyguanylic acid], and one cross-linked adduct [N2-(2" beta,7"-diamino-10"-deoxyguanyl-N2-yl-mitosen- 1" alpha-yl)-2'-deoxyguanylic acid]. One minor radioactive spot was not identified. By comparing DNA alkylated at the two pH values, based on equal amounts of 32P radioactivity, similar amounts of cross-links were detected. However, the DNA showed different ratios of the alpha and beta isomers of the monofunctional monoadduct. Furthermore, the DNA alkylated at pH 6.0 showed more bifunctional monoadducts than did the DNA alkylated at pH 7.6. Analysis of alkylated DNA by enzyme-activated PFM showed a similar spectrum of DNA adduct formation. The effect of pH on the distribution of the five PFM-DNA adducts was similar to that observed for the five MMC-DNA adducts. The distribution of adducts in DNA alkylated at the same pH was similar irrespective of which enzyme activated MMC or PFM. The pH of the reaction during DNA and MMC interaction was the determining factor for the quantitative distribution of the adducts. This pH effect may be important for the cytotoxicity of MMC and PFM in tumor cells that have high levels of reductive enzymes with low optimal pH values.

Alkylation↗

PubMedDate not supplied

[The biochemical mechanisms of the action of N-alkyl-N-nitrosoureas. The possible reasons for drug resistance to these compounds].

N-alkyl-N-nitrosoureas exhibit a wide spectrum of antitumor activity. They react as alkylating agents at nucleophilic sites in purine and pyrimidine moieties of DNA. The predominant site of this alkylation is N7 of guanine, which is followed by the site N3 of adenine and 06 of guanine. The formation and persistence of 0(6)-alkylguanine (0(6)-AG) may be of primary importance in cytotoxicity of the nitrosoureas. 0(6)-AG adducts of DNA of the tumor cells are repaired by protein 0(6)-alkylguanine-DNA transferase (0(6)-AGT) which transfers the alkyl group to internal cysteine residue being the acceptor protein for the alkyl group in an irreversible transfer reaction. 0(6)-AGT can protect the tumor cells against 0(6)-AG adducts by the way of inhibiting the formation of the DNA interstrand cross-links 0(6)-AGT plays an important role in the drug resistance because it repairs the DNA alkyl adducts at the 0(6) position of guanine. The 0(6)-AGT activity inversely correlates with the cytotoxic effect of the nitrosoureas. The agents like 0(6)-methylguanosine, 0(6)-methyl-2'-deoxyguanosine, and some 0(6)-benzylated guanine derivatives are effective inactivators of 0(6)-AGT, and thus can be used to enhance the cytotoxicity of N-nitrosoureas. The activation of 0(6)-AGT and other repairing enzymes such as alpha and beta DNA-polymerases as well as an increase in the level of reduced glutathione may be used in developing the resistance to the nitrosoureas.

Animals↗

PubMedDate not supplied

Brain hypoplasia caused by exposure to trichlorfon and dichlorvos during development can be ascribed to DNA alkylation damage and inhibition of DNA alkyltransferase repair.

Treatment of pregnant guinea pigs with trichlorfon causes cerebellar hypoplasia in offspring. The most sensitive period for treatment is days 42-47 of gestation, which coincides with the rapid brain growth spurt and with the development of cerebellar granule cells. When rat granule cells were exposed in vitro to trichlorfon and dichlorvos for 24 hours they died, whereas trichloroethanol had no effect. When the cells were exposed to trichlorfon and dichlorvos for 3 hours, only dichlorvos was lethal indicating that the metabolite dichlorvos was more potent than trichlorfon itself. Cultured cerebellar granule cells were also found to be quite sensitive to other DNA-alkylating agents such as methylazoxymethanol and methylmethane sulphonate and to O6-benzylguanine; a potent and specific inhibitor of the DNA alkyltransferase involved in the repair of DNA alkylation damage. The organophosphorous compounds were also found to cause inhibition of the alkyltransferase and the lethal effects of the tested compounds on granule cell culture correlated well with the potency of inhibition. In a bacterial test system for monitoring alkylation effects on the DNA, dichlorvos was demonstrated to have a strong DNA alkylation effect. These results suggest that alkylation of DNA and inhibition of its repair can contribute to the brain hypoplasia observed after exposure to trichlorfon and dichlorvos during brain development.

Alkyl and Aryl Transferases↗

PubMed1999

Explorations of alkyl polyols as "class I" organic modifiers to adjust selectivity in micellar electrokinetic capillary chromatography.

In this study, we investigated a novel series of micelle modifiers useful to alter selectivity in micellar electrokinetic capillary chromatography (MEKC). These modifiers were alkyl polyalcohols, including 1-octanol, 1,2-octanediol, 1,2,3-octanetriol, 1,2-hexanediol, and 1,2-butanediol, which act as class I organic modifiers in that their effects are on the sodium dodecyl sulfate (SDS) micelle rather than the surrounding aqueous phase. This characteristic allows the alkyl polyols to effect resolution when applied at concentrations as low as 20 mM (0.25% v/v) by altering the selectivity observed with SDS without a modifier. The effects of the alkyl polyols on the critical micelle concentration of SDS, electroosmotic flow, and electrophoretic mobility of the SDS micelle are presented. These modifiers had little impact on the migration time window at the concentrations explored. Changes in selectivity induced by the alkyl polyols for a large set of model compounds are presented. Trends indicate that solutes capable of forming hydrogen bonds tend to decrease their interactions with the micellar phase while nonhydrogen bonding solutes increase their interactions upon addition of the modifiers. The solvation parameter model was used to characterize the induced changes in selectivity. This model suggests that even though the modifiers are structurally similar, each produced a unique set of system constants. It was also demonstrated that the addition of alkyl polyols improved the correlation between the partition coefficients of SDS and water to 1-octanol and water. The usefulness of the alkyl polyols was demonstrated by examining their effects on the separation of 11 priority phenols.

1-Octanol↗

PubMed2004

Mass spectrometric investigation of noncovalent complexation between a tetratosylated resorcarene and alkyl ammonium ions.

Noncovalent complexation between tetratosylated tetraethyl resorcarene (1) and primary, secondary, and tertiary alkyl ammonium ions (mMe, dMe, tMe, mEt, dEt, tEt, dBu, and dHex) was studied by electrospray ionization Fourier transform ion cyclotron resonance (ESI-FTICR) mass spectrometry. Interactions of the noncovalent complexes were investigated by means of competition experiments, collision-induced dissociation (CID) experiments, ion-molecule reactions with tripropylamine and gas phase H/D-exchange reactions with deuteroammonia. Gas phase ion-molecule reactions gave especially valuable information about the structure and properties of the complexes. Resorcarene 1 formed relatively stable 1:1 complexes with all aliphatic alkyl ammonium ions. Steric properties of the alkyl ammonium ions and proton affinities of the conjugate amines noticeably affected the complexation properties, indicating the importance of hydrogen bonding in these complexes. According to the competition experiments, the thermodynamically most stable host-guest complexes were formed with alkyl ammonium ions that were most substituted and had the longest alkyl chains. In CID experiments, release of an intact free guest ion or dissociation of the host was observed to depend on the proton affinity of the amine and the strength of the hydrogen bond that was formed. In ion-molecule reactions with tripropylamine, a guest exchange reaction occurred with all alkyl ammonium ion complexes with reaction rates mostly dependent on the steric properties of the original guest ion. In H/D-exchange reactions the N-H hydrogen atoms of the guest ion were exchanged with deuterium, whereas the resorcinol hydrogen atoms remained unchanged.

Ions↗

PubMed1997

Blend of Electroactive Complexes of Polyaniline and Surfactant with Alkylated Polyacrylate

The cocrystallization of alkylated polyimides and polyesters, as shown by Ballauff et al., offers an opportunity to mix alkylated electrically conducting blends with the alkylated insulating materials. In this investigation we have used a flexible alkylated polymer to blend with a stiff alkylated conducting polymer. Comb-shaped poly(octadecyl acrylate) (PODA) was blended with polyaniline emeraldine base (PANI)/dodecyl benzenesulfonic acid (DBSA) complex to investigate the effect of long alkyl chain of flexible polymer on the electroactive rigid rod-like PANI(DBSA)4 (weight ratio) complex. Binary blend DBSA/PODA was also used as a model to investigate the intermolecular interaction between unprotonated excess amounts of DBSA and PODA in the ternary blend. Cross-polarized optical microscope (OM) and wide-angle X-ray diffraction (WAXD) were applied to observe the highly ordered mesophase structure of these blends. This newly formed mesomorphic structure of DBSA/PODA binary blend due to the hydrogen bonding was observed when the PODA content was below 40 wt% in binary blend and these blend samples show a homogeneous one phase above 68°C by OM. With addition of 10 wt% of PODA in ternary blend, the homogeneous smectic liquid crystalline structure was clearly confirmed by OM and WAXD. The intermolecular interactions that occurred in the blend systems was explained for each different characteristic peak with FT-IR spectra.

Journal Article↗