Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Dimethylformamide”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 55 records · Page 3Linked to original sources
PubMed1996

Effects of dimethylformamide on in vivo fatigue and metabolism in rat skeletal muscle measured by 31P-NMR.

Dimethylformamide (DMF) is widely used as an industrial solvent in spite of well-established hepatotoxicity and adverse effects on in vitro muscle contractility. The doses used in the studies describing these effects were higher than the doses required to solubilize drugs to be injected at very low levels and the potential effects of DMF at very low levels has not yet been explored. The goal of this work was to study the effects of an acute, low dose of DMF (3 mu/100 g body weight, administered i.p.) on mechanical parameters and energy metabolism of contracting rat skeletal muscle. Metabolic changes were followed by 31P nuclear magnetic resonance spectroscopy. Tension was significantly lower during the fatigue test in DMF-treated rats than in controls. Phosphomonoesters and inorganic phosphorus level were lower, and intracellular pH was higher in DMF-treated rats than in controls, showing that energy metabolism was activated to a lesser degree, in relation with the lower mechanical performance, after DMF. Skeletal muscle is a target organ for dimethylformamide which has a major effect on muscle contractility by decreasing the tension developed. The effects of DMF suggest that it is unsuitable for use as a drug vehicle for in vivo injections, even at a very low nonhepatotoxic doses.

Animals↗
PubMed2005

Reactions at the solid-liquid interface: surface-controlled dissolution of solid particles. The dissolution of potassium bicarbonate in dimethylformamide.

We present a mathematical model for the surface-controlled dissolution of solid particles. This is applied to the dissolution of a solid having different particle size distribution functions: those of a monodispersed solid containing particles of all one size, a two-size-particle distribution, and a Gaussian distribution of the particle sizes. The dissolution of potassium bicarbonate in dimethylformamide is experimentally studied indirectly at elevated temperatures. We monitor the dissolution via the homogeneous deprotonation of 2-cyanophenol by dissolved KHCO3. The loss of 2-cyanophenol was detected electrochemically at a platinum microdisk electrode, and separately, the formation of the 2-cyanophenolate anion was monitored via UV-visible spectroscopic analysis. The results presented show that the kinetics of the loss of 2-cyanophenol behaves on one hand as a homogeneous chemical process and on the other hand as a dissolution-rate-controlled process. Initially, predissolved KHCO3 in solution deprotonates the 2-cyanophenol and homogeneous reaction dominates the observed kinetics, and at longer times, the observed kinetics is controlled by the rate of KHCO3 dissolution. Modeling of the experimental results for the surface-controlled dissolution of KHCO3 in dimethylformamide (DMF) yielded a mean value for the dissolution rate constant, k, at elevated temperatures; k was found to have a value of (1.1 +/- 0.3) x 10(-8) mol cm(-2) s(-1) at 100 degrees C, and the activation energy for the dissolution was 34.4 +/- 0.4 kJ mol(-1) over the temperature range 60-100 degrees C.

Bicarbonates↗
PubMed2005

Heterogeneous kinetics of the dissolution of an inorganic salt, potassium carbonate, in an organic solvent, dimethylformamide.

Understanding the mechanisms of solid-liquid systems is fundamental to the development and operation of processes for the production of agrochemicals and pharmaceuticals. The use of a strong inorganic base in an organic solvent, typically, potassium carbonate in dimethylformamide, is often used to facilitate the formation of a required anionic organic nucleophile. In this paper, the dissolution kinetics of potassium carbonate in dimethylformamide at elevated temperatures is studied in the presence of ultrasound, as revealed via monitoring of the deprotonation of 2-cyanophenol by dissolved K2CO3. Two independent experimental methods were employed; the loss of 2-cyanophenol was detected electrochemically at a platinum microdisk working electrode, and the formation of the 2-cyanophenolate anion was monitored via UV/visible spectroscopic analysis. The results were modeled by fitting the experimental data to a theoretical model for the surface-controlled dissolution of solid particles. The dissolution rate constant, k, for the dissolution of K2CO3 in DMF was found to have a value of (1.3 +/- 0.2) x 10(-7) mol cm(-2) s(-1) at 100 degrees C, and the activation energy for the dissolution was 44.2 +/- 0.4 kJ mol(-1) over the temperature range of 70-100 degrees C studied.

Carbonates↗
PubMed1993

Tuning the activity of an enzyme for unusual environments: sequential random mutagenesis of subtilisin E for catalysis in dimethylformamide.

Random mutagenesis has been used to engineer the protease subtilisin E to function in a highly nonnatural environment--high concentrations of a polar organic solvent. Sequential rounds of mutagenesis and screening have yielded a variant (PC3) that hydrolyzes a peptide substrate 256 times more efficiently than wild-type subtilisin in 60% dimethylformamide. PC3 subtilisin E and other variants containing different combinations of amino acid substitutions are effective catalysts for transesterification and peptide synthesis in dimethylformamide and other organic media. Starting with a variant containing four effective amino acid substitutions (D60N, D97G, Q103R, and N218S; where, for example, D60N represents Asp-60-->Asn), six additional mutations (G131D, E156G, N181S, S182G, S188P, and T255A) were generated during three sequential rounds of mutagenesis and screening. The 10 substitutions are clustered on one face of the enzyme, near the active site and substrate binding pocket, and all are located in loops that connect core secondary structure elements and exhibit considerable sequence variability in subtilisins from different sources. These variable surface loops are effective handles for "tuning" the activity of subtilisin. Seven of the 10 amino acid substitutions in PC3 are found in other natural subtilisins. Great variability is exhibited among naturally occurring sequences that code for similar three-dimensional structures--it is possible to make use of this sequence flexibility to engineer enzymes to exhibit features not previously developed (or required) for function in vivo.

Amino Acid Sequence↗
PubMed1996

[Toxic hepatitis due to dimethylformamide: case reports and literature review].

We report two patients with toxic hepatitis due to the solvent dimethylformamide (DMF). Other causes of hepatitis such as viral, drug induced or alcoholic hepatitis, could be excluded or were considered to be unlikely. Hepatotoxicity due to professional exposure to solvents e.g. dimethylformamide should be considered in any patient with unexplained hepatitis. The fast improvement of the clinical symptoms and the progressive normalisation of the liver function tests once the exposure to the product has been stopped, supports the diagnosis. Yet, non-drug induced toxic hepatitis remains an exclusion diagnosis. Therapy consists of avoiding every contact with the causative agent. Table 3 (Addendum) gives an overview of some industrial agents able to cause hepatitis.

Adolescent↗
PubMed1990

Liver injury in workers exposed to dimethylformamide.

An apparent epidemic cluster of toxic liver disease was reexamined among workers exposed to the solvent dimethylformamide. A demographically similar but unexposed group from a preemployment population was used for comparison. Analysis, after data transformation of the liver transaminases, revealed significant differences between the two populations with respect to the serum glutamic pyruvic transaminase and the ratio of serum glutaminic oxaloacetic transaminase to serum glutamic pyruvic transaminase. Thus a value of the ratio of serum glutamic oxaloacetic transaminase to serum glutamic pyruvic transaminase. Thus a value of the ratio less than 1 may be suggestive of toxic liver disease. Medical surveillance of the working population for 14 months revealed no further cases of toxic liver disease. Dimethylformamide was almost certainly the causative agent of the original epidemic. The use of preemployment populations as a source of unexposed subjects in the analysis of occupational clusters is recommended, especially in the scenario of relatively acute, and highly prevalent, occupational diseases.

Adult↗
PubMed1988

Liver disease associated with occupational exposure to the solvent dimethylformamide.

STUDY OBJECTIVE: to characterize an outbreak of liver disease among workers in a fabric coating factory; and to determine the outbreak's cause and natural history and strategies for clinical recognition, treatment, and prevention. DESIGN: clinical-epidemiological investigation. SETTING: academic medical center, Occupational Medicine Clinic, and worksite. PATIENTS: fifty-eight of sixty-six workers participated in the study. All had standard liver function tests at least once. Forty-six workers completed a questionnaire; 27 had more extensive clinical evaluation for recognized liver abnormalities. RESULTS: a plant-wide outbreak of liver disease was recognized after a new employee presented with signs and symptoms of hepatitis. Evaluation of the worksite showed that dimethylformamide, a widely used industrial solvent and known hepatotoxin, was being used to coat fabric in poorly ventilated areas without appropriate skin protection. No other major hepatotoxic exposure was identified. Overall, 36 of 58 (62%) workers tested had elevations of either aspartate aminotransferase (AST) or alanine aminotransferase (ALT) levels. Enzyme abnormalities occurred almost exclusively in production workers (35 of 46 were abnormal), whereas only 1 of 12 nonproduction workers showed any elevations in enzyme levels (P less than 0.0001). Serologic tests excluded known infectious causes of hepatitis in all but 2 workers and changes characteristic of toxic liver injury were confirmed by histologic examinations of biopsy specimens from 4 workers. The ratio of AST to ALT levels was one or less in all but 1 worker. After modification of work practices and removal of workers most severely affected from exposure, improvement in liver enzyme abnormalities and symptoms in most patients were seen, although some patients showed persistent elevations of enzyme levels. CONCLUSIONS: an outbreak of toxic liver disease has been associated with exposure to dimethylformamide in the workplace. The diagnosis of toxic liver disease was established by the clinical histories, negative viral serologies, an enzyme pattern of ALT levels being greater than AST levels, epidemiologic data on coworkers, and liver biopsy specimens. The high prevalence of unsuspected liver enzyme abnormalities in these workers suggests that occupational liver disease may occur more frequently than is generally recognized.

Adolescent↗
PubMedDate not supplied

[Measurement of N-methylformamide in occupational exposure to N,N-dimethylformamide].

N,N-dimethylformamide (DMF) is a solvent that is widely used in industry. The major occupational sources of exposure results from production of synthetic leather. The main metabolite formed in both man and animals is N-hydroxymethyl-N-methylformamide. Demethylation leads to N-methylformamide (NMF) and formamide and also to a small extent to hydroxy-methylformamide. All the metabolites are excreted in urine, as are very small amounts of the unchanged substance. N-acetyl-S-(N-methyl-carbamoyl)-cysteine can be determined in urine as a further metabolite. We conducted this biomonitoring study with the aim of evaluating the correlation between the excretion of N-methylformamide (mainly from N-hydroxymethylformamide) and levels of exposure to N,N-dimethylformamide among occupationally exposed people. The mean time-weighted average (TWA) exposure was about half (13.5 mg/m3) of the current threshold limit value, the range of the values varying from 0.4 to 75.2 mg/m3. A linear equation existed between urinary NMF concentration and DMF concentration in the environment. The findings show that the urinary NMF concentration can be used as an appropriate biological exposure index. The authors suggest for occupationally exposed subjects, a urinary NMF concentration corresponding to the time-weighted average of the threshold limit value of 39.9 mg/l (37.2 mg/g creatinine) and a 95% lower confidence limit (biological threshold) of 23.4 mg/l (22.2 mg/g creatinine).

Adult↗
PubMed1977

N,N-Dimethylformamide-induced morphological differentiation and reduction of tumorigenicity in cultured mouse rhabdomyosarcoma cells.

N,N-Dimethylformamide treatment of cell cultures established from a transplantable murine rhabdomyosarcoma-induced morphological differentiation and a marked reduction in the tumorigenicity of the sarcoma cells. Fourteen of 17 CE/J mice receiving injections of inducer-treated cells did not develop tumors after 6 months, whereas all 21 mice receiving inocula of untreated sarcoma cells died of disease between 11 and 31 days. The drug-treated cells did not grow in soft agar; untreated tumor cells grew in the semisolid medium. The untreated tumor cells showed a reduced serum requirement and had a higher saturation density compared to drug-treated cells. Thus the reduction in tumorigenicity of N,N-dimethylformamide-treated cells correlated with certain in vitro growth properties that are more characteristic of normal, mesenchymally derived cells than of sarcoma cells.

Animals↗
PubMed1989

Dimethylformamide-induced changes in the radiation survival of low- and high-passage intestinal epithelial cells (IEC-17) in vitro.

The effects of dimethylformamide (DMF) on the radiation response of low- and high-passage intestinal epithelial cells (IEC-17) were examined. The IEC-17 cell line, a rat intestinal epithelial cell line, exhibited a bimodal response to X radiation. The sensitive fraction, which was attributed to a stem cell-like component, had a D0 of 0.90 Gy. The resistant fraction, thought to be the expression of a more mature component, exhibited a D0 of 2.00 Gy. Treatment using a putative cell differentiating agent, N,N-dimethylformamide, increased the resistant fraction of the population from 35 to 80%, suggesting that DMF treatment (100 mM) increased the proportion of mature cells in the IEC-17 cell population. In addition, extended age in culture (greater than 100 passages) resulted in altered morphology, decreased doubling time, increased chromosome number, and loss of anchorage dependence, all features characterizing spontaneously transformed high-passage IEC-17 cells. These high-passage cells also exhibited a bimodal response to X radiation; the sensitive fraction had a D0 of 0.80 Gy while the resistant fraction D0 was 1.50 Gy. DMF increased the resistant fraction from 35 to 55% of the population. Results suggested that the different radiosensitivities of the subpopulations remained throughout the spontaneous transformation of high-passage IEC-17 cells.

Animals↗
PubMedDate not supplied

Triple combination of retinoic acid+aclacinomycin A+ dimethylformamide induces differentiation of human acute myeloid leukaemic blasts in primary culture.

Differentiation induction therapy provides unalternative 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)+aclacinomycin A (ACM)+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 RPM11640 culture medium with 20% fetal calf serum and 10% 5637-conditioned medium and incubated with 10(-6) M retinoic acid, 80nM aclacinomycin A and/or 100mM dimethylformamide alone and in combinations with each other for six days at 37 degrees C in a humidified incubator under 5% CO2. Morphological, cytochemical and functional differentiation into mature cells were induced in blasts from 22 out of the 24 AML patients after exposure to the triple combination of 10(-6)M RA+80nM ACM+100mM DMF for 6 days in primary culture. These highly effective results justify a clinical trial of this triple combination for AML patients who are either unsuitable for or unresponsive to conventional cytotoxic chemotherapy.

Aclarubicin↗
PubMed1979

Electrochemical properties of polycyclic compounds studied by the polarographic method in anhydrous systems. VII. Polarographic oxidation of carcinogenic hydrocarbons in dimethylformamide.

The electrooxidation of polycyclic carcinogenic hydrocarbons in dimethylformamide solutions was studied by polarography. The results generally have confirmed that a correlation exists between oxidation potentials and carcinogenic activity of the studied polycyclic aromatic hydrocarbons. The half-wave potentials of the polarographic curves have been found to be directly related to the root xn of the Hückel secular equation for the highest bonding orbital and to the reduction potentials measured in dimethylformamide.

Carcinogens↗
PubMed1993

Up-regulation of transforming growth factor alpha expression by transforming growth factor beta 1, epidermal growth factor, and N,N-dimethylformamide in human colon carcinoma cells.

This report examines the effects of inhibitors of cell proliferation on transforming growth factor alpha (TGF-alpha) expression in low-density cultures of poorly (PD) and well-differentiated (WD) human colon carcinoma cells, continuously maintained in serum-free medium. In contrast to results in certain untransformed cells, growth inhibitors such as transforming growth factor beta 1 (TGF-beta 1) and N,N-dimethylformamide up-regulated TGF-alpha mRNA and protein expression in these human colon carcinoma cells. Treatment of low-density WD cells with TGF-beta 1 (10 ng/ml) resulted in a 1.5-fold increase in TGF-alpha mRNA levels within 4 h of treatment. TGF-alpha mRNA levels increased to 2.7-fold above control values by 48 h after TGF-beta 1 addition. Additionally, over a TGF-beta 1 concentration range of 1-30 ng/ml, TGF-alpha protein levels were increased by 2-10-fold, despite the fact that the growth of the WD cells remained inhibited. Although TGF-beta 1 control of TGF-alpha expression was altered in these WD colon carcinoma cells, relative to that in untransformed cells previously examined, the cells retained the ability to up-regulate TGF-alpha expression in an epidermal growth factor-dependent manner. In similarity to the results with TGF-beta 1 in WD colon carcinoma cells, the differentiation agent N,N-dimethylformamide (0.7%) resulted in an increase of TGF-alpha mRNA of approximately 3.8-fold in PD colon carcinoma cells, as well as a 4.4-fold increase in TGF-alpha protein after 4 days of treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Cell Differentiation↗
PubMed2003

Products of the electrochemical oxidation of cis-L(2)Ru((II))(NCS)(2) in dimethylformamide and acetonitrile determined by LC-UV/Vis-MS.

The bis tetrabutylammonium salt of the solar cell dye, L(2)Ru(NCS)(2), ((Bu(4)N(+))(2) [Ru(dcbpyH)(2)(NCS)(2)](2-)), was oxidized electrochemically in both dimethylformamide and acetonitrile. Four different ruthenium complexes were identified by LC-UV/Vis-MS during the electrochemical oxidation process in dimethylformamide. The formation of the four complexes may be explained by a competition between a solvent-independent route with the formation of the intermediate complex L(2)Ru(NCS)(CN) and the final oxidation product L(2)Ru(CN)(2) and a solvent-dependent route, which proceeds through the intermediate complex L(2)Ru(NCS)(DMF)(+) to the final product L(2)Ru(CN)(DMF)(+). In acetonitrile the solvent-dependent mechanism is dominant and only the oxidation products L(2)Ru(NCS)(ACN)(+) and L(2)Ru(CN)(ACN)(+) were identified.

Journal Article↗
PubMed1985

Extinction coefficients of chlorophyll a and B in n,n-dimethylformamide and 80% acetone.

We found inconsistencies in the commonly used data for chlorophyll analysis in 80% acetone. Recently developed extinction coefficients for chlorophyll b in N,N-dimethylformamide (DMF) based on values from 80% acetone are low as a result of these inconsistencies. We determined extinction coefficients of chlorophyll a (Chl a) and chlorophyll b (Chl b) in DMF for wavelengths of 618 to 665 nanometers. The simultaneous equations necessary for quantifying Chl a, Chl b, or total Chl in DMF in the absence of other chlorophyllous pigments are: Chl a = 12.70A(664.5) - 2.79A(647); Chl b = 20.70 A(647) - 4.62A(664.5); total Chl = 17.90A(647) + 8.08A(664.5), where A = absorbance in 1.00 centimeter cuvettes and Chl = milligrams per liter.N,N-Dimethylformamide is a very convenient solvent for Chl extraction since it is effective on intact plant parts and Chl is quite stable in DMF. There was no difference in the amount of Chl extracted when plant tissue was stored for 1 or 3 days at three temperatures, with or without solvent added.

Journal Article↗
PubMed1997

Liver function alterations in synthetic leather workers exposed to dimethylformamide.

A cross-sectional study of the prevalence of chronic liver function alterations was performed in 75 workers employed in a synthetic leather factory, exposed to dimethylformamide (DMF) air concentrations below threshold limit values (30 mg/m3). Biological monitoring among workers revealed acceptable urine levels of monomethylformamide (NMF) on average, but the very wide range indicated that occasional overexposure was possible. The worker survey showed a high percentage of disulfiram-like symptoms (50%) and liver function abnormalities (22.7%), compared with a demographically similar group of unexposed workers. Covariance analysis (ANCOVA) revealed that enzyme levels were significantly higher in exposed workers than in controls after data were corrected for age, alcohol consumption, body mass index, and cholesterol levels. The authors conclude that DMF can cause liver diseases even if air TLVs are respected, because accidental contact with liquid DMF can significantly increase DMF uptake. In this situation, air monitoring is no longer sufficient to evaluate worker exposure.

Adult↗
PubMed1998

Follow-up biological and genotoxicological monitoring of acrylonitrile- and dimethylformamide-exposed viscose rayon plant workers.

In order to investigate the genotoxic effects of occupational acrylonitrile (ACN) and dimethylformamide (DMF) exposures, clinical serum and urine parameters and genotoxicological endpoints such as chromosome aberration (CA), sister chromatid exchange (SCE), high frequency SCE (HFC), cell cycle kinetics, and UV-induced unscheduled DNA synthesis (UDS) were followed up three times during a 20-month period in peripheral blood lymphocytes (PBL) of 26 workers (13 maintainers and 13 fiber producers) occupationally exposed to ANC and/or DMF in a viscose rayon plant, 26 matched control subjects, and six industrial controls (all males). Six of the 26 exposed subjects were hospitalized because of liver dysfunction that had developed due to inhalative DMF exposure. The rate of smoking was estimated on the basis of serum thiocyanate (SCN) levels. Average peak air ACN and DMF concentrations were over the maximum concentration limits at the time of both investigations. Urine ACN and monomethyl-formamide (MMF) excretions of the exposed subjects were almost doubled after work shifts. An increase in lymphocyte count (in months 0 and 7), and severe alterations in the liver function were observed in the exposed subjects. In PBLs the proliferative rate index (PRI) was already increased in month 0 compared with the controls. In each study, significant increases in CA and SCE frequencies, as well as increases in UDS were found in PBLs of the exposed subjects. The frequencies of chromatid breaks and acentric fragments further increased in month 7 and remained constantly elevated in month 20. Increased yields of both chromatid and chromosome-type exchange aberrations first appeared in month 20, when HFCs were 2.72 times more frequent in fiber producers than in maintainers. The role of some important biological confounding factors (age, white blood cell count, and hematocrit) and lifestyle confounding factors (smoking and drinking habits) were subjected to an analysis of variance during the second study. Increased CA, SCE, and UDS were found both in control and exposed smokers when current smoking was established on the basis of the serum SCN levels. The cytogenetic data suggest that occupational exposures to ACN and DMF induce considerable genotoxic consequences and may increase the cancer risk in the exposed human populations.

Acrylonitrile↗
PubMedDate not supplied

Hepatotoxicity of N, N-dimethylformamide in rats following intraperitoneal or inhalation routes of administration.

Male Sprague-Dawley rats were administered a single intraperitoneal injection of N, N-dimethylformamide (DMF, 0.01-1.5 g kg-1) or were exposed for 4 h to DMF vapours (75-900 ppm). The serum activities of the enzymes sorbitol deshydrogenase and glutamate deshydrogenase were used as indicators of liver damage, and were determined at 24, 48 or 72 h post-treatment. Following either route of administration DMF caused concentration-dependent elevations in enzyme activities, the maxima of which occurred later after administration of higher concentrations of DMF than after lower concentrations.

Administration, Inhalation↗