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PubMed1990

Triple combination of retinoic acid plus actinomycin D plus dimethylformamide induces differentiation of human acute myeloid leukaemic blasts in primary culture.

Differentiation induction therapy provides an alternative for treatment of acute myeloid leukaemia (AML) patients who are either unsuitable for or unresponsive to conventional cytotoxic chemotherapy. The effect of a triple combination of retinoic acid (RA) + actinomycin D (Act-D) + dimethylformamide (DMF) on differentiation of blasts from 24 AML patients was studied. Non-adherent mononuclear cells were seeded at a concentration of 5 x 10(5) cells/ml in 24-well tissue-culture plates containing RPMI 1640 culture medium with 20% fetal calf serum, 10% autologous serum and 10% 5637-conditioned medium and incubated with 10(-6) M retinoic acid, 5 nM actinomycin D and/or 100 mM dimethylformamide alone and in combination with each other for 6 days at 37 degrees C in a humidified incubator and an atmosphere containing 5% CO2. The triple combination of 10(-6) M retinoic acid + 5 nM actinomycin D + 100 mM dimethylformamide induced 90% of the blasts from 22 of the 24 AML patients to differentiate. The combination of N-methylformamide (a compound similar to dimethylformamide) with cyclophosphamide significantly increased the in vivo activity with no concomitant increase in its reversible hepatotoxicity. Since several polar compounds related to dimethyl-formamide, e.g. hexamethylene bisacetamide and N-methylformamide, are currently undergoing phase II clinical trials, it may be feasible to combine one of these with retinoic acid and/or actinomycin D in the treatment of AML patients.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1986

Identification by proton NMR of N-(hydroxymethyl)-N-methylformamide as the major urinary metabolite of N,N-dimethylformamide in mice.

Urine samples from mice which had received N,N-dimethylformamide were investigated by high field 1H-NMR spectroscopy. The most prominent signals in the N-CH3 region had chemical shifts identical with those of N,N-dimethylformamide (delta 2.85, 3.01) and N-(hydroxymethyl)-N-methylformamide (delta 2.91, 3.05). Resonances downfield of delta 7.5 (from formyl protons) also coincided with those of the reference formamides. When [14C]methyl-labelled N,N-dimethylformamide was injected and urine samples investigated by radio thin layer chromatography, the major area of radioactivity corresponded to the Rf of N-(hydroxymethyl)-N-methylformamide. Dimethylamine and methylamine were found to be minor metabolites of N,N-dimethylformamide.

Animals↗
PubMed1985

Mercapturates in the urine of persons exposed to N,N-dimethylformamide.

N,N-dimethylformamide, a nucleophilic aprotic dipolar solvent, has multipurpose uses, especially in the manufacture of plastics. Its acute toxicity for mammals is low; it is hepatotoxic. Vapors are absorbed by the lungs, in the liquid form it causes cutaneous maceration and is rapidly absorbed through the skin. In the organism it is primarily metabolized to N-monomethylformamide, to a lesser extent to formamide. Urine of individuals exposed to N,N-dimethylformamide was newly found to have higher levels of thioethers, most likely mercapturates, as yet of unknown chemical structure. The correlation between the urinary concentrations of mercapturates (y) and N-monomethylformamide (x) can be expressed by equation y = 4.93 + 0.58 x, with the coefficient of correlation r = 0.90. Part of N,N-dimethylformamide metabolites is likely to react with biopolymers, part of it is excreted as metabolic end products, i.e. carbon dioxide, water and urea. Breakdown to mercapturates may implicate N,N-dimethylformamide as being a potential carcinogen.

Acetylcysteine↗
PubMed1988

The effects of dimethylformamide on the interaction of the estrogen receptor with estradiol.

The study of the mechanism of interaction of antiestrogens with the estrogen receptor is complicated by the limited solubility of these compounds and their nonspecific, hydrophobic interactions with proteins in estrogen receptor preparations and with the glass or plastic wall of the test tube. The organic solvent dimethylformamide increases the solubility of these compounds in aqueous solution and interferes with hydrophobic interactions with solid phases and thereby reduces their loss from the solution. For these reasons some investigators use dimethylformamide in the antiestrogen-estrogen receptor binding assay. In this study we report that dimethylformamide interferes with the estrogen receptor's binding kinetics and the estradiol-induced activation of the estrogen receptors, and inactivates the receptor.

Allosteric Regulation↗
PubMed1984

Reversal by L-cysteine of the growth inhibitory and glutathione-depleting effects of N-methylformamide and N,N-dimethylformamide.

N-Methylformamide and N,N-dimethylformamide, which can induce differentiation in selected malignant cell lines, are known to increase doubling times, inhibit clonigenicity in agar, and to effect responses against particular human colon carcinomas in vivo. At concentrations which inhibit growth and clonigenicity, N-methylformamide (170 mM) and N,N-dimethylformamide (103 mM) deplete total intracellular glutathione levels of DLD-1 Clone A human colon carcinoma cells in a dose and time dependent manner. In the presence of 0.5 mM 1-cysteine, both the growth and glutathione levels of polar-solvent treated DLD-1 Clone A cells are restored. 1-Cysteine also reverses the inhibition of clonigenicity mediated by NMF. The mechanism of action of N-methylformamide and N,N-dimethylformamide against this cell line, at least in vitro, is therefore related to its effects on cysteine/glutathione metabolism. Furthermore, this evidence suggests that glutathione plays a key role in regulating the growth of these cells.

Antineoplastic Agents↗
PubMed1992

Induction of myogenic differentiation in human rhabdomyosarcoma cells by ionising radiation, N,N-dimethylformamide and their combination.

Differentiation-inducing ability of gamma-radiation, N,N-dimethylformamide and their combination has been tested on human rhabdomyosarcoma RMZ-RC2 clone cells. Ionising radiation at 2-5 Gy doses induced a more differentiated morphology, with the appearance of an increased proportion of multinuclear myotube-like cells, and a significant increase in myosin-positive and multinuclear cells. Radiation appeared to act by inducing de novo differentiated elements. N,N-dimethylformamide was able to induce an increased myosin expression, but did not affect multinuclear cell proportion. The combined treatment (ionising radiation and N,N-dimethylformamide) resulted in an additive increase in the proportion of myosin-positive cells, approaching 25-35%, but de novo differentiated elements were not increased above the levels obtained with irradiation alone.

Cell Differentiation↗
PubMed2005

Comparative solubilisation of potassium carbonate, sodium bicarbonate and sodium carbonate in hot dimethylformamide: application of cylindrical particle surface-controlled dissolution theory.

A surface-controlled dissolution of cylindrical solid particles model is applied to potassium carbonate, sodium bicarbonate and sodium carbonate in dimethylformamide at elevated temperatures. Previously published data for the dissolution of potassium carbonate is interpreted assuming a cylindrical rather than a spherical shape of the particles, the former representing a closer approximation to the true shape of the particles as revealed by scanning electron microscopy. The dissolution kinetics of sodium carbonate and sodium bicarbonate in dimethylformamide at 100 degrees C were investigated via monitoring of the deprotonation of 2-cyanophenol with dissolved solid to form the 2-cyanophenolate anion that was detected with UV-visible spectroscopy. From fitting of experimental results to theory, the dissolution rate constant, k, for the dissolutions of potassium carbonate, sodium bicarbonate and sodium carbonate in dimethylformamide at 100 degrees C were found to have the values of (1.0 +/- 0.1) x 10(-7) mol cm(-2) s(-1), (5.5 +/- 0.3) x 10(-9) mol cm(-2) s(-1) and (9.7 +/- 0.8) x 10(-9) mol cm(-2) s(-1), respectively.

Adsorption↗
PubMed1983

Penetration enhancers for human skin: mode of action of 2-pyrrolidone and dimethylformamide on partition and diffusion of model compounds water, n-alcohols, and caffeine.

Penetration-enhancing solvents may modify diffusional routes through the stratum corneum and the partitioning of drugs into these pathways. To investigate the mechanisms of action of enhancers, steady-state fluxes were measured in vitro for polar methanol, nonpolar octanol, and an intermediate compound, caffeine, selected as model penetrants; human stratum corneum conditioned on both sides with water or accelerants (2-pyrrolidone or dimethylformamide solutions) was used. We determined partition, permeability, and apparent diffusion coefficients, and derived the standard free energy of transfer of the methylene group from water to stratum corneum (-423 cal mol-1); less negative values were obtained for transfer from 2-pyrrolidone solutions. We conclude that for these model compounds, and taking a fully hydrated membrane as a standard: (a) 2-pyrrolidone enhances permeation through the polar route of the skin by increasing the diffusivity, and reduces passage through the nonpolar route by decreasing diffusivity and partitioning, (b) dimethylformamide promotes polar route absorption by raising diffusivity and partitioning and reduces nonpolar absorption by decreasing both parameters, and (c) for caffeine, the markedly increased absorption (15-fold) caused by dimethylformamide is associated with damage to the membrane.

Aged↗
PubMed1976

Molecular weight of an extremely hydrophobic protein, zein, in dimethylformamide and in formamide.

Both alpha zein purified from a commericial preparation and beta zein prepared fresh from corn are soluble in the nonaqueous solvents formamide and dimethylformamide; in this regard zein resembles water soluble proteins such as insulin, ribonuclease, and lysozyme. On the basis of osmotic pressure measurements made in both formamide and dimethylformamide, alpha zein has a number average moleular weight of 21000-24000 daltons and shows no tendency to aggregate or dissociate. Beta zein exists in an aggregated state (dimer and higher forms) in dimethylformamide. Formamide dissociates the beta zein dimer into monomer units but aggregation to higher species occurs with increasing protein concentration.

Binding Sites↗
PubMed1985

Elevated growth factor levels in transformed mouse embryo cells treated with N,N-dimethylformamide.

The transformed mouse embryo fibroblast cell line AKR-MCA, produces several transforming growth factor (TGF) activities which can be identified in cell extracts and serum-free conditioned medium. Treatment of these transformed cells with 1% N,N-dimethylformamide resulted in a more normal phenotype and an increased level of TGFs in cell extracts and conditioned medium. In addition, an 11-fold increase in an epidermal growth factor receptor-competing activity was observed in cell extracts and conditioned medium compared to control untreated cells. Fractionation of the conditioned medium on Bio-Gel P-100 showed that the same size classes of TGFs were present in N,N-dimethylformamide-treated as well as untreated cells. The increased EGF-receptor-competing activity was eluted in two peaks at Mr 6500 and Mr 4000. The Mr 6500 peak did not coelute with a TGF peak in the N,N-dimethylformamide-treated cells.

Animals↗
PubMed1979

N,N-dimethylformamide-induced alteration of cell culture characteristics and loss of tumorigenicity in cultured human colon carcinoma cells.

Human colon carcinoma cell lines established in this laboratory were treated in vitro with N,N-dimethylformamide. This polar solvent caused morphological changes in the cells as well as alterations in their growth properties. Untreated cells had cloning efficiencies of up to 77% in soft agar; treatment with N,N-dimethylformamide resulted in a complete loss of clonogenicity in semisolid medium. Growth in the presence of the polar solvent also effected a marked reduction in the tumorigenicity of the cells. Ten of ten nude mice that received a s.c. inoculum of 1 X 10(6) untreated cells developed tumors histologically similar to colonic adenocarcinomas in 10 to 14 days, whereas nine of ten nude mice inoculated with 1 X 10(6) treated cells have shown no sign of tumor 3 to 6 months postinjection. Removal of the polar solvent from the culture medium was accompanied by the reappearance of tumorigenicity and the original cell culture characteristics. Therefore, it appears that N,N-dimethylformamide can reversibly effect the reversion of cultured human colon carcinoma cells to less malignant cell types.

Animals↗
PubMedDate not supplied

Monitoring of industrial exposure to dimethylformamide by analysis of alveolar air.

The occupational exposure to Dimethylformamide was studied by testing the environmental and alveolar air of 8 workers, at hourly intervals, during the workshift. The correlations between alveolar and environmental concentrations of Dimethylformamide turned out to be statistically significant at all the intervals studied, except at the 4th hour when the correlation was not significant. In six out of the eight workers studied, the correlation between alveolar and environmental concentrations was statistically significant. Only in two workers was the correlation not significant. On the basis of the slope of the regression line between all the data, the alveolar concentration of Dimethylformamide turned out to correspond to 27,8% of the environmental concentration.

Air Pollutants, Occupational↗
PubMed1981

Dose-dependent effects of peroral dimethylformamide administration on rat brain.

Three-month-old Wistar rats were given dimethylformamide in their drinking water at three concentrations. Succinate dehydrogenase activity decreased at the two higher doses in brain after 2 or 7 weeks. Decreased glutathione concentration occurred at the highest dose. Cerebral azoreductase activity was below the control range after 7 weeks at all doses. Glial cell succinate dehydrogenase activity was below the control range in all animals. No qualitative changes in the spinal cord axon protein composition were detected. It is postulated that formic acid generated in the dimethylformamide metabolism might have led to a significant derangement of cerebral energy metabolism.

Animals↗
PubMed2003

The effects of co-exposure to methyl ethyl ketone on the biological monitoring of occupational exposure to N,N-dimethylformamide.

OBJECTIVES: (1) To assess whether urinary N,N-dimethylformamide (U-DMF) is suitable as a biomarker when co-exposure to methyl ethyl ketone (MEK) exists, and to evaluate whether it is suitable as an exposure biomarker of DMF. (2) To examine whether the co-exposure to MEK affects the characteristics of U-NMF and U-DMF. (3) To investigate if the difference in creatinine-adjusted and non-adjusted measurements of urinary biomarkers of DMF exposure is substantial. METHODS: Personal exposure monitoring of N,N-dimethylformamide (DMF) and MEK on 11 synthetic-leather workers was performed for 5 consecutive days. Daily post-shift urine for each individual was collected and was analyzed for urinary N-methylformamide (U-NMF) and U-DMF levels on both non-adjusted and creatinine-adjusted bases. RESULTS: Both U-NMF and U-DMF showed significant associations with airborne DMF. Positive and significant associations between U-NMF and U-DMF on either a non-adjusted basis or a creatinine-adjusted basis were found. Satisfactory linear associations ( P<0.01) between all kinds of urinary biomarkers and DMF exposure were found. The co-exposure to MEK exerted more effect on the relationship of airborne DMF to U-DMF than to U-NMF. CONCLUSIONS: U-DMF is detectable when occupational DMF exposure is near or below the occupational exposure limit of 10 ppm. In view of the performance of sensitivity, specificity, and positive predictive value, U-NMF, in general, is superior to U-DMF. However, on a par with other findings in this and previous studies, U-DMF might be considered as a complimentary biomarker of exposure to DMF in addition to U-NMF. No distinction between creatinine-adjustment or non-adjustment for urine specimens was found in the biological monitoring of DMF exposure. Further exploration of the influence of co-exposure to MEK at higher exposure is warranted.

Butanones↗
PubMed1976

Affinity chromatography of 3 alpha-hydroxysteroid dehydrogenase from Pseudomonas testosteroni. Use of N,N-dimethylformamide to prevent hydrophobic interactions between the enzyme and the ligand.

1. The 3alpha-hydroxysteroid: NAD+-oxidoreductase (EC 1.1.1.50) from Pseudomonas testosteroni (ATCC 11996) has been purified by affinity chromatography on Sepharose 4B using glycocholic acid as ligand covalently bound through its carboxyl group to the ethylenediamine spacer. 2. The attachment of the enzyme to the substrate-containing matrix is greatly enhanced by the presence of NAD+ suggesting that this enzyme has a compulsory ordered mechanism where NAD+ binds to the enzyme before the steroid. 3. A NAD+-independent interaction between the enzyme and the ligand was also found. This interaction was mainly hydrophobic and interfered with the NAD+-dependent binding. The NAD+-independent interaction was reduced by N,N-dimethylformamide. 4. By using the affinity column in the presence of 10% N,N-dimethylformamide, highly purified enzyme, as judged from polyacrylamide gel electrophoresis, could be obtained in one step from crude bacterial extracts.

Chromatography, Affinity↗
PubMed1990

Clinical and pathological characteristics of hepatotoxicity associated with occupational exposure to dimethylformamide.

The clinical characteristics, laboratory results, and liver biopsy findings of seven workers with toxic liver injury associated with exposure to several solvents, including substantial levels of the widely used solvent dimethylformamide, are presented. Three patients had short exposure (less than 3 months), four long exposure (greater than 1 year). Among those with brief exposure, symptoms included anorexia, abdominal pain, and disulfiram-type reaction. Aminotransferases were markedly elevated with the ratio of alanine aminotransferase to aspartate aminotransferase always greater than 1. Liver biopsy showed focal hepatocellular necrosis and microvesicular steatosis with prominence of smooth endoplasmic reticulum, complex lysosomes, and pleomorphic mitochondria with crystalline inclusions. Among workers with long exposure, symptoms were minimal and enzyme elevations modest. Biopsies showed macrovesicular steatosis, pleomorphic mitochondria without crystalloids, and prominent smooth endoplasmic reticulum, but no evidence of persisting acute injury or fibrosis. Abnormal aminotransferases in both groups may persist for months after removal from exposure, but progression to cirrhosis in continually exposed workers was not observed. We conclude that exposure of these workers to solvents, chiefly dimethylformamide, may result in two variants of toxic liver injury with subtle clinical, laboratory, and morphological features. This may be readily overlooked if occupational history and biopsy histology are not carefully evaluated.

Adult↗
PubMed1993

Simultaneous determination of N,N-dimethylformamide, N-monomethylformamide and N-hydroxymethyl-N-methylformamide in rat plasma by capillary gas chromatography.

A capillary gas chromatographic method with nitrogen-phosphorus detection for the simultaneous quantitative determination of N,N-dimethylformamide, and its two metabolites, N-monomethylformamide and N-hydroxymethyl-N-methylformamide, in rat plasma has been developed. The method involves a single extraction step with ethyl acetate-acetone (4:1, v/v). The extract is injected into a fused-silica capillary column coated with Carbowax 20M. A temperature gradient (65-110 degrees C) is applied, and the three products can be separated within 10 min. The quantitation limits, using 25 microliters of rat plasma, for N,N-dimethylformamide, N-monomethylformamide and N-hydroxymethyl-N-methylformamide are 0.4, 0.4 and 2 micrograms/ml, respectively. This method is suitable for toxicokinetic studies in rats.

Animals↗
PubMed1993

Deuterium NMR spectroscopy of biofluids for the identification of drug metabolites: application to N,N-dimethylformamide.

The metabolism of N,N-dimethylformamide in the Sprague-Dawley rat has been reinvestigated using NMR spectroscopy of urine. In particular, through the use of N,N-dimethylformamide-d7 (DMF-d7) and 2H-NMR spectroscopy, the principal metabolites of this compound have been confirmed in a direct manner. The use of inverse-detected two-dimensional 2H-13C correlation with 13C decoupling aided metabolite identification through the provision of 13C chemical shifts.

Animals↗