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PubMed1985

Ultrastructural evidence of dimethylformamide-induced differentiation of cultured human colon carcinoma cells. Increased expression of desmosomes.

N,N-dimethylformamide (DMF) induces differentiation of human colon carcinoma (DLD-1) cells in culture and reduces their tumorigenicity in nude mice. The current investigation analyzed DLD-1 (clone D) cells for ultrastructural evidence of differentiation. Examination of treated and untreated confluent monolayers by transmission electron microscopy revealed an occasional intracytoplasmic lumen indicative of adenocarcinoma. DMF-treated cells showed no signs of a toxic reaction. Cytoplasmic organelles were essentially unchanged except for an increase in tonofilaments and associated desmosomes. The number of desmosomes per unit length of contiguous cell border increased almost sixfold in treated monolayers. No other type of cell junction was seen. The increased frequency of desmosomes in DMF-treated cultures is significant because of the direct correlation known to exist between the number of desmosomes and degree of differentiation of some human carcinomas. Desmosomes serve as foci of cell adhesion and are reduced in number in some invasive tumors. Whether the supernumerary desmosomes in DMF-treated cells contribute to the reduction in malignant behavior of these cells in vivo remains to be determined.

Acetylation↗
PubMed2002

Electrophoretic mobilities of large organic ions in nonaqueous solvents: determination by capillary electrophoresis in propylene carbonate, N,N-dimethylformamide, N,N,-dimethylacetamide, acetonitrile and methanol.

The mobilities of the monocharged permanent tertraphenylphosphonium cation and tetraphenylborate anion are determined by capillary zone electrophoresis in different organic solvents as a function of the ionic strength, I, of the background electrolyte. The nonaqueous solvents are propylene carbonate (PC), N,N-dimethylformamide (DMF), N,N,-dimethylacetamide (DMA), acetonitrile (MeCN) and methanol (MeOH). The ionic strength is between 5 and 50 mmol/L. The mobility as a function of I is in good agreement with the theory of Debye, Hückel and Onsager (DHO), extended by the ion size parameter as introduced by Falkenhagen and Pitts. The values of the limiting DHO slopes of the mobility vs. I curves (the slopes express the influence of the solvent on the reduction of the mobility with increase of I) decrease in the order MeCN > MeOH > DMF > DMA > PC. Absolute mobilities (obtained by extrapolation to I = 0) of a particular ion differ by a factor of about 7 between the solvents. However, constancy within 10% is observed for their Walden products (the absolute mobility multiplied with the solvent's macroviscosity). The role of dielectric friction on the mobility of the present monocharged, large analyte ions is discussed according to the theory of Hubbard and Onsager. Based on the radii of the ions, the static permittivity of the solvent and its permittivity at infinite frequency, and the relaxation time of polarization, an equal contribution of dielectric and hydrodynamic friction is predicted in MeOH as solvent. Experimental data are in contrast to this prediction, indicating the overestimation of dielectric friction, and the dominance of hydrodynamic friction on the migration of the analyte ions in all solvents under consideration.

Acetamides↗
PubMedDate not supplied

High sensitive fluorophotometric determination of nucleic acids with Pyronine G sensitized by N,N-dimethylformamide.

In Tris-HCl buffer (pH 8.0), the fluorescence of Pyronine G emitted at 552 nm was quenched by nucleic acids when excited at 525 nm. Adding N, N-dimethylformamide (DMF) as a sensitive media can enhance the sensitivity greatly. Based on the fluorescence reactions sensitive fluorimetric methods for nucleic acids at nanogram levels were proposed. Under the optimum conditions, the calibration curves were linear in the range of 0.0032 - 2.5 microg mL(-1) for ct DNA and 0.0024 - 2.5 microg mL(-1) for hs DNA. The limits of determination were 3.2 ng mL(-1) and 2.4 ng mL(-1) respectively. This method has good selectivity and high sensitivity. It has been applied to the determination of DNA in the synthetic samples and real samples with satisfactory results.

Animals↗
PubMed1987

Replacement of aromatic fluorine by a methoxy group during reaction with methyl iodide in N,N-dimethylformamide solvent.

The DNA base uracil was derivatized with pentafluorobenzoyl chloride, followed by methylation with methyl iodide in the presence of N,N-dimethylformamide (DMF). In addition to a 3-pentafluorobenzoyl-1-methyl derivative of uracil, GC/MS analysis of the reaction mixture revealed the formation of an unusual product, whose molecular weight was 12 U higher than that of the prior derivative. This unexpected product has been identified as the 3-(para-methoxytetrafluorobenzoyl)-1-methyl derivative of uracil. Isotopic labeling and related experiments have revealed that the DMF solvent contributes the oxygen atom of the methoxy group that replaces the para fluorine atom. This work allowed a single derivative to be obtained for the methylation reaction by changing the solvent to acetonitrile.

Acylation↗
PubMed2005

Capillary electrophoresis in N,N-dimethylformamide.

N,N-Dimethylformamide (DMF) is a dipolar protophilic solvent with physicochemical properties that makes it suitable as solvent for capillary electrophoresis (CE). It is prerequisite for the proper application of CE to adjust and to change the pH of the background electrolyte (BGE) in a defined manner. This was done in the present work using benzoic acid-benzoate by selecting different concentration ratios of acid and salt, and calculating the theoretical pH from the activity-corrected Henderson-Hasselbalch equation. The mobilities of the analytes (chloro- and nitro-substituted phenolates) were found to follow reasonably well the typical sigmoid mobility versus pH curve as predicted by theory. The actual mobilities and pK(a) values (at 25 degrees C) of the analytes were derived from these curves. pK(a) values were in the range of 11.1-11.7, being thus 3-4.4 units higher than in water. This pK(a) shift is caused by the destabilization of the analyte anion and the better stability (solubility) of the molecular analyte acid in DMF, which overcome the higher basicity of DMF compared to water. Absolute mobilities were calculated from the actual mobilities; they were between 32x10(-9) and 42x10(-9) m(2)/Vxs. Slight deviations of the measured mobilities from the theoretical mobility versus pH curve were discussed on the bases of ion pairing and heteroconjugation and homoconjugation of either buffer components or buffer components and analytes. Heteroconjugation was used as a mechanism for the electrically driven separation of neutral analyte molecules in a BGE where salicylate acted as complex forming ion. Rough estimation of the complexation constants for the phenolic analytes gave values in the range of 100-200 L/mol. Addition of water to the solvent decreased the effect of heteroconjugation, but it was still present up to the surprisingly high concentration of 20% water. Electrophoretically relevant parameters like ionic mobilities and pK(a) values, and conjugation and ion pairing are dependent on the water content of the solvent. The water uptake of DMF was measured when exposed to humidity of ambient air. The resulted behavior of the water uptake was found rather similar to that for acetonitrile and methanol.

Dimethylformamide↗
PubMed1989

Anti-tumor and differentiation-inducing activity of N,N-dimethylformamide (DMF) in head-and-neck cancer xenografts.

The anti-tumor activity of the putative differentiation-inducing agent dimethylformamide (DMF) was assessed in 7 head-and-neck xenograft (HNX) lines transplanted into nude mice. The drug was administered intra-peritoneally at the maximum tolerated dose. A significant growth-inhibitory effect was observed in 3 out of 7 tumor lines tested. When compared with 5 conventional drugs active in patients with squamous-cell carcinoma of the head and neck (HNSCC), DMF was as effective as the most active drugs (cisplatin and bleomycin). The most sensitive xenograft line, the poorly differentiated tumor HNX-14C, was used to test the hypothesis that differentiation induction might play a role in the anti-tumor activity of DMF. Light microscopic examination did not show clear-cut alteration of differentiation characteristics such as keratin and keratin pearl formation. Furthermore, we used a monoclonal antibody to study the expression of cytokeratin 10 which is useful as a differentiation marker of human HNSCC tumors. Keratin 10, not present in HNX-14C tumors grown under control conditions, became expressed in some cells upon DMF treatment. Further evidence for a differentiation-inducing activity of DMF was found in electron-microscopic studies. In treated HNX-14C tumors, in addition to cells with normal ultrastructural features, better-differentiated cells were observed, as manifested by an increase in the number of tonofilaments and desmosomes. The results show that DMF has a potential value for the treatment of patients with head-and-neck cancer, and that differentiation induction might play a role in the anti-tumor action of the drug.

Animals↗
PubMed1992

Response of FR3T3 cells transformed by Ha-ras oncogene and epidermal growth factor gene to differentiation induction by N,N-dimethylformamide.

Treatment of chemically transformed fibroblasts with N,N-dimethylformamide (DMF) results in the restoration of a nontransformed phenotype. In an attempt to identify more precisely the mechanisms by which DMF reverses the transformed phenotype, the effects of DMF on fibroblasts which were transformed by a single gene--specifically a synthetic epidermal growth factor (EGF) gene or the Ha-ras oncogene--were examined. The constitutive expression of either the Ha-ras oncogene or the EGF gene in FR3T3 fibroblasts resulted in cellular transformation. The effect of the differentiation-inducing agent DMF on several properties of these transformed cell lines was examined. The EGF-transfected cells were much more responsive to DMF than the ras-transfected cells. DMF treatment of the EGF-transfected cells resulted in the inhibition of anchorage-independent growth, the restoration of a normal cellular morphology and growth rate in monolayer culture, and the down-regulation of the proliferation-associated nucleolar protein B23. DMF treatment had a much slighter effect on growth of the ras-transfected cells in monolayer culture or under anchorage-independent growth conditions. The high proliferation rate of the ras-3 cells was associated with elevated expression of protein B23. The 19-3 cells, but not the ras-3 cells, expressed cell-surface fibronectin. Treatment of the ras-3 cells with DMF did not restore fibronectin expression. The binding of EGF was increased 3-fold in the EGF-transfected cells and decreased 20-fold in ras-transfected cells, but in neither case did DMF alter EGF binding. DMF treatment increased the secretion of EGF in the 2 transfected lines as well as in control cells. These results suggest that the aberrant-growth control in the EGF-transfected cells, but not in the ras-transfected cells, could be modulated by DMF and that the aberrant-growth control mechanisms were different in these 2 cell types.

Animals↗
PubMed1993

Induction of the fundic mucosa-specific glycolipid with dimethylformamide in gastric-cancer cell lines.

We have previously reported that a glycolipid GalNAc beta 1-4[NeuAc alpha 2-3]Gal beta 1-4GlcNAc beta 1-3Gal beta 1-4Glc-Cer named NGM-1 is present specifically in the human gastric fundic mucosa, but not in other organs. In gastric-cancer tissue and cancer cell lines, this glycolipid completely disappears. These findings imply that NGM-1 is expressed only in well-differentiated fundic mucosa. The purpose of this study is to examine the expression of NGM-1 as a differentiation-related molecule. A gastric cell line AZ521 was cultured in the medium with various reagents which had been reported to induce differentiation in cancer cells. The growth of AZ521 was suppressed by the addition of 0.8% dimethylformamide (DMF) to the medium, but not by addition of dimethylsulfoxide (DMSO), retinoic acid or butyric acid. In the ganglioside fraction of the cells cultured with DMF, a glycolipid regarded as NGM-1 which had not been present before treatment was detected using a monoclonal antibody. Suppression of the proliferation of AZ521 by eliminating the serum from the medium could not induce the expression of NGM-1. A colonic cell line treated with DMF also failed to express the glycolipid. The synthase activity of NGM-1 was elevated in the AZ521 cells treated with DMF, but not with DMSO. These results demonstrate that the expression of NGM-1 is induced by DMF specifically in gastric-cancer cells, and suggest the possibility that NGM-1 is a differentiation-related molecule.

Butyrates↗
PubMed1990

Embryotoxicity and teratogenicity study in rats dosed epicutaneously with dimethylformamide (DMF).

The reproductive effect of N,N-dimethylformamide (DMF) administered epicutaneously to rats was examined. The rats were dosed on gestation days 6-15 or on gestation days 1-20 at dose levels of up to 2 ml DMF kg-1 body weight. Body weight, weight gain and pregnancy rate were reduced in those rats receiving 2 ml DMF kg-1 body weight per day on days 6-15. A reduction in the number of live fetuses and in fetal weight, as well as an increase in postimplantation loss, were also observed at this dose level. Similar but more pronounced effects were observed in rats dosed on days 1-20 with 2 ml DMF kg-1 body weight. The lowest effect level was 1 ml DMF kg-1 body weight. No other dose-related effects were found in this study.

Administration, Topical↗
PubMed1983

Nuclear protein changes following N,N-dimethylformamide (DMF)-induced maturation.

A human colonic carcinoma cell line was exposed to a nontoxic concentration of N,N-dimethylformamide (DMF) for 2 wk. Nuclear proteins were isolated from control and treated cells and compared by sodium dodecyl sulfate (SDS) electrophoresis. Qualitative and quantitative differences were observed. Metabolic labeling with tritiated leucine demonstrated qualitative variation between control and treated cells.

Cell Division↗
PubMed1989

Effects of N,N-dimethylformamide and extracellular matrix on transforming growth factor-beta binding to a human colon carcinoma cell line.

Alterations in the binding of transforming growth factor-beta (TGF-beta) to the MOSER human colon carcinoma cell line caused by N,N-dimethylformamide (DMF) or extracellular matrix (ECM) were examined. DMF induced a more differentiated phenotype in the MOSER cells and resulted in a twofold increase in TGF-beta binding to the cells. This was due to an increase in receptor number with no significant alteration in the KD. The extent of increased TGF-beta binding was dependent on the dose and time of exposure to DMF. Upon removal of DMF, the receptor level returned to that of untreated cells within 6 hr. The binding of TGF-beta 1 and TGF-beta 2 to the cells was increased equally. Despite this increase in TGF-beta binding in the presence of DMF, the sensitivity of the MOSER cells to the growth inhibitory effects of TGF-beta was unaltered. Growth of the MOSER cells on ECM derived from a well-differentiated colon cell line increased the TGF-beta receptor number twofold without altering the KD. No change was observed if the MOSER cells were grown on ECM derived from a poorly differentiated cell line. While no alteration in sensitivity to TGF-beta was observed on cells grown in the presence of DMF, MOSER cells grown on the ECM derived from well-differentiated colon carcinoma cell lines were twofold more sensitive to the growth inhibitory effects of TGF-beta. These results indicated that growth conditions which resulted in a more differentiated phenotype resulted in an increase in the cellular receptors for TGF-beta.

Carcinoma↗
PubMed1992

The differential effects of N,N-dimethylformamide and transforming growth factor-beta 1 on a human ovarian cancer cell line (HOC-7).

We have compared the effects of N,N-dimethylformamide (DMF) and transforming growth factor (TGF)-beta 1 on the growth and phenotype of HOC-7 ovarian cancer cells. Previous density gradient fractionation of untreated HOC-7 cells suggested that rapidly growing small polygonal medium density cells revert spontaneously into less malignant flattened low density cells. Here we demonstrate that DMF and TGF-beta 1 induce similar flattened cell phenotypes. Both agents induce qualitatively similar alterations in the cells. DMF, however, exerted stronger effects than TGF-beta 1. The cells become flattened, develop cytoplasmic extensions, and reduce DNA-synthesis as well as anchorage-dependent and -independent growth. These effects are reversible after removal of the inducers, indicating that the cells have not become terminally differentiated. Electron microscopy demonstrates prominent filament bundles in treated cells. Immunofluorescence further shows that these cells contain large amounts of cytokeratin. Immunocytochemistry and ELISA demonstrate 1- to 5-fold higher amounts of desmoplakin and fibronectin after DMF- or TGF-beta 1-exposure. The described differentiation-like responses of HOC-7 cells can be used for recognition of pharmacologically induced maturation of ovarian cancer cells.

Cell Division↗
PubMed1993

Modulation of the immunophenotype of ovarian cancer cells by N,N-dimethylformamide and transforming growth factor-beta 1.

Exposure of HOC-7 ovarian adenocarcinoma cells to regulators of cell differentiation caused inducer-dependent alterations of the antigenic pattern of the cells. Immunocytochemistry revealed that N,N-dimethylformamide (DMF) elevated the membrane staining for epidermal growth factor (EGF)-receptor and for desmoplakins I and II. DMF also stimulated cytoplasmic and surface labeling for CA 125 and the deposition of fibronectin into the extracellular matrix. Stimulation of fibronectin was also seen after addition of transforming growth factor (TGF)-beta 1. These responses were quantified using a fixed-cell, enzyme-linked immunosorbent assay (ELISA) and revealed that DMF dose-dependently induced expression of EGF-receptor, CA 125, fibronectin, and desmoplakins I and II. TGF-beta 1 stimulated fibronectin and desmoplakins I and II only. Production of EGF and TGF-alpha was not affected by these inducers. Immunocytochemistry, ELISA and Western blotting showed that both inducers caused down-regulation of myc oncoproteins. DMF was more effective in changing the immunophenotype of HOC-7 cells than TGF-beta 1. Desmoplakins I and II demonstrated elevated epithelial differentiation, whereas fibronectin indicated stimulation of extracellular matrix formation. Elevated EGF-receptor could not compensate for the growth inhibition induced by DMF. The expression of myc oncoproteins was inversely related to cell proliferation. CA 125, however, seems to be unrelated to cell growth.

Blotting, Western↗
PubMed1989

Residual ethylene oxide determination in polymethyl methacrylate disks and intraocular lenses by headspace gas analysis and N,N-dimethylformamide extraction.

The residue in an ethylene oxide (EO)-exposed polymethyl methacrylate (PMMA) material [flat disk and intraocular lens (IOL)] was determined using three methods: semiautomatic and manual headspace methods and N,N-dimethylformamide (DMF) solvent extraction. Results from the analysis of three different sample configurations at three different EO concentrations are compared. Results from the DMF extraction of PMMA indicate that the headspace methods at 100 degrees C are not exhaustive with respect to recovery of total residual ethylene oxide. Furthermore, the manual headspace method appears to be slightly more effective than the semiautomatic injection headspace method. Sorption of EO and subsequent extraction is related to the surface area-to-volume ratio of the sample, with higher concentrations observed in samples with the high ratio.

Autoanalysis↗
PubMed2006

Characterization of Klason lignins by reversed-phase high-performance liquid chromatography using wide-pore octadecylsilica and stepwise gradients of dimethylformamide in water.

RP-HPLC using stepwise gradients of N,N-dimethylformamide (DMF) in a phosphate-buffered (pH 3.00) aqueous mobile phase and a wide-pore (30 nm) octadecylsilica column has been applied to the analysis of a variety of lignins--organocell lignin, dioxane lignin, Björkman lignin, and Klason lignins from both softwoods and hardwoods, respectively, in order to demonstrate the usefulness of the approach for their characterization. Tandem combination of spectrophotometric diode array detection and fluorimetric detection was used to acquire more detailed information about the chromatographic behavior of lignins. The results show that a ten-step gradient can reveal distinct features of lignins and humic substances. Combination of good solvating properties of DMF for lignins together with a wide-pore RP sorbent improves surface interactions of the analytes and suppresses the influence of size exclusion effects. Thus it provides reproducibility of characterization profiles and robustness of the method. The calculated repeatability of the retention time of selected peaks was +/- 0.46% RSD. The reproducibility of the data within one week (set of seven data) was +/- 1.1% RSD. These data are also representative of the other well-shaped peaks of analyzed substances.

Buffers↗
PubMed2001

Electrospray mass spectrometry of hydrophobic compounds using dimethyl sulfoxide and dimethylformamide as solvents.

The use of dimethyl sulfoxide (DMSO) and dimethylformamide (DMF) as solvents in electrospray ionization (ESI) is suggested for the analysis of hydrophobic compounds. Its use was shown to overcome solubility problems and resulted in good quality electrospray spectra of protected hydrophobic peptides, sugars and other hydrophobic compounds. Intense protonated and/or sodiated molecules were formed in positive ion mode while negative ion mode resulted in [M + 95](-) ions from DMSO and [M + Cl](-) ions from DMF in cases where no significant molecular ion related peaks could be observed applying commonly used protic solvents such as methanol or acetonitrile. Deuterium labeling (d6-DMSO), high resolution experiments and tandem mass spectrometric measurements showed that the methanesulfonic acid (MSA), present in DMSO as a common impurity, is responsible for the formation of protonated molecules in positive ion mode and for methane sulfonate anion adducts [M + 95](-) in negative ion mode.

Amino Acid Sequence↗
PubMed1994

Chronic toxicity/oncogenicity of dimethylformamide in rats and mice following inhalation exposure.

The potential chronic toxicity and oncogenicity of dimethyl-formamide (DMF) was evaluated by exposing male and female rats and mice to 0, 25, 100, or 400 ppm DMF for 6 hr/day, 5 days/week for 18 months (mice) or 2 years (rats). Clinical pathology was evaluated at 3, 6, 12, 18, and 24 (rats only) months. An interim euthanasia for rats occurred at 12 months and hepatic cell proliferation in rats and mice was examined at 2 weeks, 3 months, and 12 months. No compound-related effects on clinical observations or survival were observed. Body weights of rats exposed to 100 (males only) and 400 ppm were reduced. Conversely, body weights were increased in 400 ppm mice. No hematologic changes were observed in either species. Serum sorbitol dehydrogenase activity was increased in rats exposed to 100 or 400 ppm. There were no compound-related effects on the estrous cycle of rats or mice at any concentration. Compound-related morphological changes were observed only in the liver. In rats, exposure to 100 and 400 ppm produced increased relative liver weights, centrilobular hepatocellular hypertrophy, lipofuscin/hemosiderin accumulation in Kupffer cells, and centrilobular single cell necrosis (400 ppm only). In mice, increased liver weights (100 ppm males, 400 ppm both sexes), centrilobular hepatocellular hypertrophy, accumulation of lipofuscin/hemosiderin in Kupffer cells, and centrilobular single cell necrosis were observed in all exposure groups. These observations occurred in a dose-response fashion and were minimal at 25 ppm. No increase in hepatic cell proliferation was seen in mice or female rats. Slightly higher proliferation was seen in male rats exposed to 400 ppm at 2 weeks and 3 months but not at 12 months. Dimethylformamide was not oncogenic under these experimental conditions in either the rat or mouse.

Administration, Inhalation↗
PubMed1997

Assessment of the developmental toxicity, metabolism, and placental transfer of N,N-dimethylformamide administered to pregnant rats.

This study evaluates the developmental toxicity and placental and milk transfer of N,N-dimethylformamide (DMF) in rats. Sprague-Dawley rats were given 0, 50, 100, 200, and 300 mg DMF/kg/day, by gavage, on Gestational Days (GD) 6 through 20. Maternal toxicity was indicated by depressions in weight gain and food consumption at doses >/=100 mg/kg. Fetal toxicity was indicated by decreased fetal body weight at doses >/=100 mg/kg, and by increased incidences of two skeletal variations (absent or poorly ossified supraoccipital and sternebrae) at 200 and 300 mg/kg. Thus, the maternal and developmental no-observed-adverse-effect level was 50 mg/kg/day. The time course disposition of [14C]DMF was examined over a 48-hr period in GD12- and GD18-pregnant rats after a single oral dose of 100 mg [14C]DMF/kg. Peak concentrations of radiocarbon occurred within 1 hr after dosing. Embryonic (GD12) and fetal (GD18) tissues accounted for 0.15 and 6% of the administered dose, respectively. Levels of radiocarbon in embryonic and fetal tissues were equal or slightly less than in maternal plasma up to 8 and 24 hr, respectively, and higher thereafter. HPLC analysis performed at intervals from 1 to 8 hr on GD12 and 1-24 hr on GD18 indicated that unchanged DMF and metabolites were readily transferred to the embryonic and fetal tissues, where their levels were generally equal to those in maternal plasma. The parent compound accounted for most of the radioactivity until 4-8 hr and then decreased. N-Hydroxymethyl-N-methylformamide (HMMF) and N-methylformamide (NMF) were the predominent metabolites and increased with time. Much lower concentrations were found for formamide and N-acetyl-S-(N-methylcarbamoyl)cysteine. Transfer of radioactivity into milk was studied in dams given a single oral administration of 100 mg [14C]DMF on Lactation Day 14. DMF, HMMF, and NMF were found in the milk at concentrations equal to those in plasma.

Abnormalities, Drug-Induced↗