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PubMed2000

Peptide thioester preparation by Fmoc solid phase peptide synthesis for use in native chemical ligation.

Established methodology for the preparation of peptide thioesters requires the use of t-butoxycarbonyl chemistry owing to the lability of thioester linkers to the nucleophilic reagents used in Fmoc solid phase peptide synthesis. Both the greater ease of use and the broad applicability of the method has led to the development of an Fmoc-based methodology for direct peptide thioester synthesis. It was found that successful preparation of a peptide thioester could be achieved when the non-nucleophilic base, 1,8-diazabicyclo[5.4.0]undec-7-ene, together with 1-hydroxybenzotriazole in dimethylformamide, were used as the N(alpha)-Fmoc deprotection reagent. Native chemical ligation of the resulting thioester product to an N-terminal cysteine-containing peptide was successfully performed in aqueous solution to produce a fragment peptide of human alpha-synuclein. The formation of aspartimide (cyclic imide) in a base-sensitive hexapeptide fragment of scorpion toxin II was found to be significant under the deprotection conditions used. However, this could be controlled by the judicious protection of sensitive residues using the 2-hydroxy-4-methoxybenzyl group.

Amino Acids↗

PubMed1980

Maturation-induction of tumor cells using a human colon carcinoma model.

The establishment of a maturation-induction model using human colon cancer cells as targets is reported. Two colon carcinoma cell lines were established from human tumors; one line was heterogeneous and was cloned into two distant subpopulations. Cells from these lines and clones and cells from an established human colon carcinoma cell line were treated in vitro with N,N-dimethylformamide (DMF) and were compared to untreated cells according to two general sets of criteria. One set contains characteristics that define a cell as transformed (i.e., anchorage independence and tumorigenicity for nude mice), and the second set contains three antigenic marker systems that would provide evidence that maturation is occurring in treated human colon cancer cells. These colon tissue-or tumor-related markers include carcinoembryonic antigen (CEA), colonic mucoprotein antigen (CMA), and the human blood group determinants. DMF-treated cells are less malignant than untreated cells; the treated cells show a marked reduction in tumorigenicity and in clonogenicity in soft agar. Each of the markers indicates that the treated cells are better differentiated than their untreated counterparts. For example, treated cells show increased expression of normal-CMA and decreased expression of tumor-CMA compared to untreated cells. Cells removed from DMF reverted to express the tumorigenicity, growth properties, and antigens characteristic of their untreated counterparts. Therefore, DMF reversibly induces in cultured colon cancer cells a less malignant phenotype with concomitant maturational effects. These results indicate that this model is appropriate for study of maturation-induction in human colon tumor cells, and has potential application to other types of human carcinomas.

Adenocarcinoma↗

PubMed2004

The acidity constants of some pyrimidine bases in various water-organic solvent media.

The acid ionization constants of some pyrimidine bases of nucleic acids were determined pH-metrically at 25 degrees C and at the constant ionic strength I = 0.10 mol l(-1) (KNO3) in pure water as well as in aqueous media containing variable mole percentages (5-30%) of organic solvents. The organic solvents used were methanol, ethanol, N,N-dimethylformamide (DMF), dimethylsulfoxide (DMSO), acetonitrile, acetone and dioxane. The results obtained indicated that the acidity constants are generally decreased as the content of an organic solvent in the medium is increased. It was deduced that the hydrogen bonding interactions and the solvent basicity in addition to the electrostatic effect are the major effects influencing significantly the acid ionization process of pyrimidine bases in the different water-organic solvent media. Some thermodynamic parameters (deltaH, deltaG degrees, deltaS degrees) of the ionization process over the temperature range 5-45 degrees C in pure water were also determined and discussed.

Acetone↗

PubMed2002

Structural and catalytic response to temperature and cosolvents of carboxylesterase EST1 from the extremely thermoacidophilic archaeon Sulfolobus solfataricus P1.

The interactive effects of temperature and cosolvents on the kinetic and structural features of a carboxylesterase from the extremely thermoacidophilic archaeon Sulfolobus solfataricus P1 (Sso EST1) were examined. While dimethylformamide, acetonitrile, and dioxane were all found to be deleterious to enzyme function, dimethyl sulfoxide (DMSO) activated Sso EST1 to various extents. This was particularly true at 3.5% (v/v) DMSO, where k(cat) was 20-30% higher than at 1.2% DMSO, over the temperature range of 50-85 degrees C. DMSO compensated for thermal activation in some cases; for example, k(cat) at 60 degrees C in 3.5% DMSO was comparable to k(cat) at 85 degrees C in 1.2% DMSO. The relationship between DMSO activation and enzyme structural characteristics was also investigated. Nuclear magnetic resonance spectroscopy and circular dichroism showed no gross change in enzyme conformation with 3.5% DMSO between 50 and 80 degrees C. However, low levels of DMSO were shown to have a small yet significant change in enzyme conformation. This was evident through the reduction of Sso EST1's melting temperature and changes in the microenvironment of the enzyme's tyrosine and tryptophan residues at 3.5% versus 1.2% (v/v) solvent. Finally, activation parameter analysis based on kinetic data, at 1.2% and 3.5% DMSO, implied an increase in conformational flexibility with additional cosolvent. These results suggest the activating effect of DMSO was related to small changes in the enzyme's structure resulting in an increase in its conformational flexibility. Thus, in addition to their use for solubilizing hydrophobic substrates in water, cosolvents may also serve as activators in applications involving thermostable biocatalysts at sub-optimal temperatures.

Acetonitriles↗

PubMed1994

Determination of amino- and amide-15N glutamine enrichment with tertiary butyldimethylsilyl derivatives.

We have developed a simple and rapid method for the selective synthesis of tetra-tertiarybutyldimethylsilyl (TBDMS) glutamine, which allows the simultaneous quantitation of glutamine (2-15N) and (5-15N) isotopic enrichment by selected ion monitoring (SIM) gas chromatographic/mass spectrometric analysis. The tetra-TBDMS glutamine (4S-gln) has an electron impact mass fragment at m/z 258 that contains only the amino-N and larger fragments (e.g., at m/z 545) that have both nitrogens. Derivatization with acetonitrile (ACN) and N-methyl-N-(tert-butyldimethylsilyl)trifluoroacetamide yields primarily tri-TBDMS glutamine (3S-gln) and quantities of 4S-gln too small to allow accurate SIM and tracer/tracee ratio determinations. However, when N,N-dimethylformamide, a more polar aprotic solvent, was substituted for ACN and the sample was heated for 30 min at 125 degrees C, greater than 80% of derivatized glutamine appeared as 4S-gln. Derivatized plasma samples that had been mixed with amide- and/or amino-15N glutamine and analyzed by SIM demonstrated strong agreement (r > or = 0.998, p = 0.0001) between theoretical and observed enrichment values for the 4S-gln fragments at m/z 258 and 545. Deamidation of glutamine to glutamate is negligible during sample processing and analysis. This procedure will facilitate the investigation of the specific sources and fates of glutamine amide and amino nitrogen as well as stable isotope studies involving amino acid transamination, ammonia clearance, urea production and other areas of nitrogen metabolism.

Acetamides↗

PubMed2002

Chirality and the origin of life: in situ enantiomeric separation for future space missions.

Two different methods of derivatization were studied in order to select and optimize one for the in situ enantiomeric separation of amino acids present in Martian samples. The method, using DMF-DMA [N,N-dimethylformamide dimethyl acetal], is simple and easily automated. However, byproducts of the reaction interfere in the gas chromatograms and mass spectrometry detection is needed for in situ analysis. The chloroformate derivatization has several advantages, including the use of achiral robust capillary column, room temperature reaction, and short analysis. The choice of the definitive derivatization method will depend on the energy and time devoted to the analysis of amino acids in the next Mars exploration missions.

Amino Acids↗

PubMed1988

Alterations in c-myc expression in relation to maturational status of human colon carcinoma cells.

Previous work from this laboratory established a large bank of human colon carcinoma cell lines in culture and classified them with respect to growth regulatory phenotypes based on several biological and biochemical characteristics. In the present report, Northern analysis indicates that addition of the maturational agent N,N-dimethylformamide (DMF) (1.0%) to proliferating HCT 116 and MOSER cells resulted in a repression of c-myc proto-oncogene expression; retinoic acid (1.0 microM) was less effective in this regard. Repression of c-myc expression by DMF was observed in MOSER and HCT 116 cells, whether it was added to proliferating or late log phase cultures, and was associated with a corresponding reduction in cellular proliferation. The reduction in c-myc expression by DMF did not require new protein synthesis and occurred within a few minutes after its addition, resulting in a 70% reduction within approximately 2 hr. Previous work from this laboratory indicated that transforming growth factor-beta (TGF-beta) elicited alterations in MOSER cells similar to those observed following DMF treatment. The present report demonstrates that proliferating, but not late log phase, MOSER cells responded to TGF-beta with a repression of c-myc expression. Similarly, an inhibition of cellular proliferation was only observed when TGF-beta (10 ng/ml) was added to proliferating cells. Collectively, these findings indicate that repression of c-myc expression is associated with diminished cellular proliferation and the induction of a more benign phenotype in human colon carcinoma cells. Furthermore, this report is the first demonstration of a c-myc response to TGF-beta in an epithelial cell line.

Cell Division↗

PubMed1982

Stimulation of dome formation in MDCK kidney epithelial cultures by inducers of differentiation: dissociation from effects on transepithelial resistance and cyclic AMP levels.

Changes in transepithelial electrical resistance and cyclic nucleotide levels were monitored accompanying chemical induction of domes in a clonal subline of MDCK kidney epithelial cells. Confluent cell monolayers grown on nitrocellulose filters exhibited a relatively high mean transepithelial resistance (387 ohms X cm2). Hexamethylene bisacetamide, a potent inducer of dome formation (Lever, 1979b), stimulated significantly increased transmonolayer resistance as well as elevated levels of intracellular cyclic AMP. By contrast, dimethylformamide, an equally potent inducer of dome formation in MDCK cells, did not appreciably alter either resistance values or cyclic nucleotide levels. These results suggest that induction of dome formation in epithelial cell cultures by compounds generally known as inducers of differentiation may involve multiple and separate mechanisms.

Acetamides↗

PubMed1985

Variant (MDCK) kidney epithelial cells altered in response to inducers of dome formation and differentiation.

Confluent cultures of the MDCK kidney epithelial cell line exhibit dome formation, a result of transepithelial fluid transport influenced by cell-cell and cell-substratum interaction. Dome formation was inducible by hexamethylene bisacetamide (HMBA) or dimethylformamide (DMF), compounds known as inducers of cell differentiation (Lever, 1979b). Analysis of the incidence of the dome-forming phenotype in colonies derived nonselectively from the MDCK cell line suggested that inducers recruit an increased fraction of the cell population to express dome formation. Variant MDCK cell lines were isolated which differed from the parental line in response to inducers while retaining cuboidal epithelial morphology. In five independently isolated and cloned MDCK variants, dome formation was not inducible by DMF and only marginally increased by HMBA. This phenotype was also associated with increased cell adhesiveness to a plastic substratum. Results from cocultivation experiments suggested that the DMF-unresponsive phenotype of variant cells may be partially overcome by cell-cell contact with wild-type cells. Sodium pump transport activity assessed by ouabain-sensitive Rb+ uptake was partially inhibited by HMBA and by DMF in a "wild-type" inducer-responsive clone. By contrast, DMF did not inhibit ouabain-sensitive Rb+ uptake in DMF-unresponsive variant clones, and sodium pump inhibition by HMBA was greatly diminished. This close correspondence between altered sodium pump modulation by inducers in variant clones and their altered dome-forming response reinforces our previous conclusions (Kennedy and Lever, 1984) that sodium pump modulation is closely associated with mechanisms of inducer action. Taken together, these findings implicate cell-cell interaction, cell-substratum interaction and sodium pump modulation in regulation of the differentiated phenotype of this cell line.

Animals↗

PubMed1987

Apical trehalase expression associated with cell patterning after inducer treatment of LLC-PK1 monolayers.

Trehalase, a differentiation-specific marker of renal proximal tubule brush border membrane, is expressed in confluent long-term cultures of the renal epithelial cell line LLC-PK1. The level of trehalase is greatly increased after treatment of cultures with differentiation inducers such as hexamethylene bisacetamide (HMBA), accompanied by increases in other apical membrane-associated differentiated functions (Yoneyama and Lever: J. Cell. Physiol. 121: 64-73, 1984). In the present study, we utilize a polyclonal antibody specific for renal trehalase to demonstrate that trehalase expression induced in LLC-PK1 cultures after HMBA treatment is localized in cells forming a three-dimensional network of strands across the confluent monolayer. The antitrehalase antibody recognized an apical membrane antigen of apparent molecular weight 100-110 kD both in LLC-PK1 cultures and in the corresponding pig renal brush border membranes. Strand formation and total trehalase activity increased in parallel as a function of inducer concentration and duration of exposure. Strand formation and trehalase expression were also greatly enhanced in monolayers grown on a Nuclepore filter support even in the absence of inducer. Strand formation was not a prerequisite for induced trehalase expression in culture, since strands did not develop in cultures treated with N, N'-dimethylformamide (DMF) and equally potent inducer of trehalase expression. In this case, cells which expressed increased levels of trehalase were dispersed at random over the monolayer. Induction of strand formation and trehalase expression by HMBA required a minimum exposure period of 48 hr and persisted up to a week after removal of inducer. By contrast, the response to DMF required continuous presence of inducer. Levels of trehalase declined even in the continuous presence of inducer in local regions of low cell density created by wound-repair of the monolayer. In addition to the membrane-bound form, trehalase activity was also recoverable from the culture medium, but release of trehalase was not affected by inducers. These observations are consistent with the view that a cell type committed to express a program of differentiation after HMBA treatment or growth on a permeable support is organized in specific cell patterns visible as strands over the confluent cell monolayer.

Acetamides↗

PubMed1990

Modulation of fibronectin synthesis and fibronectin binding during transformation and differentiation of mouse AKR fibroblasts.

In previous studies it was shown that transformation of AKR fibroblasts with 3-methylcholanthrene was associated with a loss of surface fibronectin and that induction of differentiation of the transformed cells with N,N-dimethylformamide (DMF) was associated with reacquisition of surface fibronectin (Chakrabarty et al., J. Cell. Physiol. 133:415, 1987). It is shown in the present study that changes in surface fibronectin reflect altered fibronectin synthesis and altered fibronectin binding. Both the nontransformed cells (AKR-2B) and their transformed counterparts (AKR-MCA) bound 125I-fibronectin in a receptor-like fashion, but the AKR-MCA cells had only 20% of the receptors found on the AKR-2B cells. Whole cell extracts prepared from the AKR-2B cells and separated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis under reducing conditions were examined for 125I-fibronectin binding. Under these conditions, the majority of binding occurred to moieties with molecular weights of 180 kD, 150 kD, and 97 kD. Binding to similar moieties on the AKR-MCA cells was virtually absent but occurred rapidly after treatment with DMF. The appearance of these moieties paralleled the acquisition of 125I-fibronectin binding activity by whole cells. Antibodies to the fibronectin receptor isolated from human placenta reacted with the DMF-sensitive moieties in immunoblot assays. Both the appearance of the fibronectin binding moieties and the acquisition of 125I-fibronectin binding activity by whole cells occurred within 6 hr of DMF treatment and increased over the subsequent 4 day period. The time course of these events paralleled closely the time course for induction of fibronectin biosynthesis by DMF. These changes in fibronectin binding and fibronectin production were associated with alterations in cell-substrate adhesion. The AKR-2B cells rapidly attached and spread on bovine serum albumin-coated dishes and on fibronectin-coated dishes, whereas the AKR-MCA cells were less adhesive on both substrates. Capacity to attach and spread was regained concomitantly with the induction of fibronectin binding and fibronectin production. Adhesion on both substrates was partially inhibited by antibodies to the fibronectin receptor and by RGDS. These studies suggest that fibronectin production and fibronectin binding are coregulated in AKR fibroblasts and that they function together to bring about changes in cell-substrate adhesion.

Animals↗

PubMed1990

Effects of differentiation-inducing agents on maturation of human MCF-7 breast cancer cells.

The effects of the differentiation inducing agents (DIAS), sodium butyrate (NaBu), retinoic acid (RA), dimethylformamide (DMF), hexamethylene bisacetamide (HMBA), forskolin, and 12-O-tetradecanoylphorbol-13-acetate (TPA), on the growth, morphology, and estrogen receptor (ER) content and epithelial membrane antigen (EMA) expression on a serumless human breast cancer cell line (MCF-7) were compared. All these agents reversibly caused a concentration-dependent growth inhibition in monolayers and markedly reduced colony-forming efficiency in soft agar. A twofold increase in doubling time was obtained with RA (1 microM), but cell replication ceased with NaBu (1 mM), forskolin (50 microM), DMF (1%), HMBA (5 mM), and TPA (8 nM). Total growth arrest induced by these last compounds was preceded by an accumulation of cells in G0/G1 phase observed at 24 h by flow cytometry and accompanied by a change in cell morphology as seen by light and electronic microscopy. An increase in cell volume and the presence of lipid droplets was noted in treated cells that were spread out, as compared with controls. The acquisition of a more mature phenotype was confirmed by an increased expression of EMA monitored by flow cytometry. A specific reduction in the number of ER without any constant dissociation (Kd) modification was also observed after treatment with the 5 DIAs. No modification of morphological or biochemical characteristics, including EMA expression and ER binding, were observed for RA (1 microM)-treated cells. All these results suggest that induction of a more differentiated phenotype is associated with a block in G1 cell cycle phase, resulting in total growth arrest. Apparently, RA (1 microM)-treated cells did not fulfill these criteria, since only a slight accumulation in G1 and a slowed growth rate were evaluated.

Acetamides↗

PubMed1990

Simultaneous flow cytometric measurements of cytoplasmic Ca++ and membrane potential changes upon FMLP exposure as HL-60 cells mature into granulocytes: using [Ca++]in as an indicator of granulocyte maturity.

Treatment of human leukemic HL-60 cells with N,N-dimethylformamide (DMF) induces them to mature until they reach granulocytoid morphology 3-6 d later. We have reported a maturation-dependent ability of these cells to respond to phorbol myristate acetate (PMA), as evaluated by membrane depolarization and by oxidative burst product formation (Newburger et al.: J. Biol. Chem. 259,3771, 1984). More recently we have attempted to develop techniques for simultaneous evaluation of these parameters during HL-60 cell maturation. Here, we compare the cytoplasmic [Ca++] and membrane potential changes elicited by the chemotactic peptide fMLP via simultaneous measurement of individual cells in a fluorescence-activated cell sorter (FACS), as done previously for mature granulocytes (Lazzari et al.: J. Biol. Chem. 261,9710, 1986). The stimulus-induced [Ca++]in changes are detected with the fluorescent probe Indo-1 and reproducibly increase in magnitude for a subpopulation of cells as the cells mature into granulocytes. Ca++ responsiveness to formyl peptide is restricted to a subpopulation of HL-60 granulocytes which expresses receptors for chemotactic peptide and consistently increases in magnitude (in response to the same concentration of agonist) with maturation. In contrast, there is less consistency in the direction or magnitude of membrane potential changes elicited under the same circumstances from the same maturing HL-60 cells.

Calcium↗

PubMed1981

Steroid transformation with immobilized microorganisms. VI. The reverse reaction of steroid-1-dehydrogenases from different micoorganisms in immobilized state.

Whole cells of Nocardia erythropolis, N. opaca and Mycobacterium phlei containing 4-en-3-oxosteroid: (acceptor)-1-en-oxidoreductase activities were immobilized by adsorption on DEAE-cellulose and silica and by entrapment in polyacrylamide gel. The obtained biocatalysts were used in an anaerobic continuous column process to transform 1,4-dien-3-oxo-steroids into 4-en-3-oxo- steroids. The half life of steroid-1(2)-reductase activity of the N. erythropolis was found to be up to 15 days. The DEAE-cellulose-adsorbed cells showed a slightly higher relative activity than free cells. The influence of substrate concentration and the action of dimethylformamide were also investigated.

Cholesterol↗

PubMed1975

Behavior of erythrocytes in ternary solvent systems.

The effect of ternary solvent systems on erythrocytes was investigated. Hemolysis experiments were run at 37degree in solutions containing various amounts of water, two nonaqueous solvents, and 0.9% sodium chloride. The nonaqueous solvents were propylene glycol, polyethylene glycol 400, dimethyl sulfoxide, dimethylformamide, and tetramethylurea. Ternary diagrams based on the critical hemolytic compositions of the various ternary systems are presented.

Adult↗

PubMed1983

Gas chromatographic-mass spectrometric quantitation of theophylline and its metabolites in biological fluids.

In premature infants, theophylline is converted to caffeine, and the biological half-life is prolonged. To assess the metabolic alterations of theophylline during development of premature infants, a sensitive and simple method was developed which quantitated all theophylline metabolites in plasma, urine, and red blood cells. Theophylline and its metabolites in the sample were converted to the N-propyl derivative using n-propyl iodide in dimethylformamide with potassium carbonate catalysis and were analyzed under isothermal conditions on a gas chromatograph-mass spectrometer with a 3% methylsilicone-phenylsilicone column. Deuterated caffeine (caffeine-d3) was used as the internal standard. A selected ion-monitoring technique, together with 70-eV electron impact ionization mode, was used. The ion current ratios between caffeine-d3 (m/z 197) and caffeine (m/z 194), theophylline (m/z 222), 3-methylxanthine (m/z 250), 1,3-dimethyluric acid (m/z 280), and 1-methyluric acid (m/z 308) were monitored. The total analysis time was 12 min with a detection limit ranging from 500 pg to 10 ng, depending on the metabolites. With this sensitivity, sample sizes of 50-100 microliters of plasma and 0.5 ml of urine were sufficient for the analysis of all theophylline metabolites. The coefficient of variation of this method was less than 5% for the analysis of biological samples.

Body Fluids↗

PubMed1983

Embryotoxicity and teratogenicity of thalidomide in rats.

The teratogenicity of thalidomide in Wistar rats was investigated after a single maternal intravenous injection during the organogenetic period. Thalidomide was administered at 45 mg/kg in 0.5 ml dimethylformamide (DMF) on day 10, 11, or 12 of the pregnancy. Thalidomide induced skeletal deformities of thoracic ribs and of the spinal column in 33 and 56 percent of the fetuses upon maternal administration of the drug on day 11 or 12, respectively. As compared to the solvent (DMF) control, thalidomide caused two- to three-fold higher skeletally malformed fetuses. Deformities of the eyeball in fetuses (ophthalmorrhexis and microphthalmia) were induced by the maternal administration of the drug on day 10 and 12. The solvent (DMF) failed to induce organ deformities. Thalidomide induced embryotoxicity (as measured by percent dead and resorbed fetuses), at a rate three to eight times higher than the DMF control and represented 11 to 24 percent of dead and resorbed fetuses in thalidomide treated groups as compared to three percent in the DMF control group. Mean fetal weight was significantly reduced after maternal administration of thalidomide on day 11 of pregnancy, as compared to the DMF control. These studies conclude that thalidomide is teratogenic and embryotoxic in rats, when administered intravenously at 45 mg/kg bw.

Abnormalities, Drug-Induced↗

PubMed1993

Cryogenic solvents inhibit the binding of the Escherichia coli heat-stable enterotoxin to intestinal brush border membranes.

The cryogenic solvents ethylene glycol, glycerol, dimethyl sulfoxide (Me2SO) and dimethylformamide (Me2FM), with increasing potency, produced concentration-dependent inhibition of the binding of the Escherichia coli heat-stable enterotoxin (STa) to pig intestinal brush border membranes. Inhibition increased with time, and both Me2SO and Me2FM appeared to decrease both the affinity of the STa receptor and the effective receptor number. Both solvents stimulated the release of previously bound 125I-STa (Me2FM > Me2SO), 3 M Me2FM inducing 93% release by 120 min. These effects were reversible, and preincubation of membranes with up to 3 M Me2SO or Me2FM at 37 degrees C for 30 min, followed by washing, did not alter subsequent 125I-STa binding. Also, 125I-STa released from membranes by 3 M Me2FM was shown to rebind to the membranes after 10-fold dilution of Me2FM. Since pretreating membranes with the thiol reagent p-chloromercuribenzenesulfonate had no effect on the release of bound 125I-STa by Me2SO or Me2FM, and since neither of these can reduce disulfide bonds, the formation of mixed disulfides between STa and receptor is unlikely. Me2SO inhibition of 125I-STa binding was greater with membranes than with a partially purified receptor preparation, which may result from the substitution of detergent for the phospholipid normally associated with the receptor(s).

4-Chloromercuribenzenesulfonate↗