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PubMed1986

Role of glutathione depletion in the mechanism of action of N-methylformamide and N,N-dimethylformamide in a cultured human colon carcinoma cell line.

The mechanism of the antitumor action of N-methylformamide (NMF), an agent currently undergoing clinical trials, and its congener, N,N-dimethylformamide (DMF), was examined in the DLD-1 Clone A human colon carcinoma cell line in vitro. The primary action of NMF and DMF on these cells is a depletion of cellular reduced glutathione levels which results in cytostasis. Evidence to support this hypothesis include (a) the extent of growth inhibition produced by NMF and DMF is directly proportional to the extent of depletion they effect on cellular reduced glutathione levels; (b) removal of NMF (170 mM) or DMF (103 mM) from the culture medium results in a parallel restoration of cell growth and cellular glutathione levels; (c) coaddition of the glutathione precursor, L-cysteine (0.5 mM), or certain precursors for this amino acid, significantly reverses NMF- and DMF-induced glutathione depletion and cytostasis; and (d) the specific glutathione-depleting agent, buthionine sulfoximine (7.5 mM) mimics the ability of NMF and DMF to induce cytostasis. In addition, NMF- and DMF-mediated reduced glutathione depletion accounts for the previously reported ability of these agents at high concentrations (less than 100 mM) to induce a more benign phenotype in DLD-1 Clone A human colon carcinoma cells. This is evidenced by the findings that (a) L-cysteine (0.5 mM) reverses NMF- and DMF-mediated (170 and 103 mM, respectively) increases in doubling time, decreases in saturation density, and decreases in clonogenicity; (b) buthionine sulfoximine (7.5 mM) mimics these actions of NMF and DMF; and (c) the tumorigenicity of DLD-1 Clone A cells in nude mice, which is completely eliminated by the in vitro treatment of these cells for 4 passages with 170 mM NMF prior to inoculation, is fully restored if the cells are passaged in the presence of 170 mM NMF and 0.5 mM L-cysteine. Thus, NMF- and DMF-induced depletion of cellular reduced glutathione is responsible for not only the cytostatic effect of these agents on human colon carcinoma cells but also for their ability to induce more benign characteristics in these cells.

Buthionine Sulfoximine↗

PubMed1985

In vitro effects of N,N-dimethylformamide on sublethal and potentially lethal damage recovery processes after X-irradiation in heterogeneous human colon tumor cells.

The responses of unfed plateau-phase cultures of two clonal subpopulations of cells (clones A and D) from a human colon adenocarcinoma (DLD-1) to X-irradiation were examined in detail either as control cultures or after growth in medium containing the differentiating agent N,N-dimethylformamide (DMF, 0.8%, three passages). Specifically, the cultures were studied with regard to their ability to express both potentially lethal and sublethal damage recovery (PLDR and SLDR, respectively). In PLDR studies on control cells, clone D expressed more PLDR than clone A, although recovery half-times were the same. DMF treatment increased the expression of PLDR in both cell lines and decreased the half-times for recovery. When recovery from sublethal radiation injury was assessed, the rate and extent of SLDR in non-DMF-treated clone A and D cells were identical. In contrast to the PLDR results, DMF treatment had no significant effect on SLDR in either cell line. These studies show that, while DMF treatment of human colon tumor cells increases cell killing in the clinically relevant, low-dose ("shoulder") region of the X-ray survival curve, this increase in cytotoxicity is not due to an inhibition of the repair of sublethal damage.

Cell Line↗

PubMed1984

Enzymatic activity of activated sludge in biological treatment of wastewater containing dimethylamine, dimethylformamide and methylethylketone.

Activated sludge treating synthetic wastewater carrying dimethylamine (DMA), dimethylformamide (DMF) and methylethylketone (MEK) was examined. The compounds in question were found to affect the enzymatic activity of the activated sludge. Dehydrogenase activity was higher than in control activated sludge and stabilization of this activity was achieved on the twelfth day of the run. Alkaline phosphatase activity was lower than in the control sludge. No correlation between activity of the studied enzymes and biodegradation of DMA, DMF and MEK was observed.

Alkaline Phosphatase↗

PubMed1982

Electrochemical properties of polycyclic compounds studied by the polarographic method in anhydrous systems. VIII. The influence of proton-donor on reduction of carcinogenic nitrogen compounds in dimethylformamide.

The authors have studied the electrochemical behavior of a series of carcinogenic and inactive heterocyclic compounds in anhydrous medium in the presence of a proton-donor. As anhydrous medium the authors used anhydrous dimethylformamide as proton-donor phenol. In the presence of proton-donor there had occurred on polarographic reduction of the employed carcinogenic heterocyclic compounds changes in the number of polarographic waves. Between the two original waves in these compounds there arose in the presence of phenol a new wave. In non-carcinogenic heterocyclic compounds such an effect of phenol was not noted. In the present paper the authors discuss the possible mechanism of electroreduction of carcinogenic and inactive heterocyclic compounds in anhydrous medium in the presence of a proton-donor.

Aza Compounds↗

PubMedDate not supplied

[Ascorbic acid supply and cytochrome P-450 levels in guinea pig liver after dimethylformamide poisoning].

The universal solvent dimethylformamide (DMFA) administered to guinea-pigs in a dose of 400 mg/kg bw per os for 14 days produced a considerable decrease in the content of total and reduced ascorbic acid (AA) in the liver, in all forms of AA in the adrenals, and lowering of vitamin C excretion with daily urine. The liver showed an increase in the concentration of dehydroascorbic acid and diminution of the concentration of cytochrome P-450 detected in liver homogenates. Additional administration of AA (50 mg/day) recovered the lowered level of the vitamin in the liver and adrenals but did not make the daily excretion of AA with urine return to normal. Additional administration of vitamin C to guinea-pigs recovered the level of cytochrome P-450 in liver homogenates, which was reduced during DMFA poisoning. One of the reasons for the development of vitamin C deficiency during DMFA poisoning is likely to be high oxidation of AA.

Adrenal Glands↗

PubMedDate not supplied

[Effect of dimethylformamide on the microsomal hydroxylation system in the liver of rats fed diets with different fat contents].

The authors studied the effect of the universal aprotonic solvent dimethylformamide (DFA) on liver microsomal hydroxylation of male rats fed diets with different fats (sunflower oil or lard). DMFA given in a dose of 200 mg/kg bw per os for 4 weeks produced a considerable reduction in cytochrome P-450 content in liver homogenates and microsomes and a lowering of the activity of N-demethylation in microsomes with amidopyrine, ethylmorphine and DMFA being used as substrates. The degree of inhibition of the demethylase reactions and liver cytochrome P-450 content was more demonstrable in rats fed the diet containing sunflower oil as compared with animals whose diet contained lard. During DMFA intoxication, the rate of spontaneous formation of malonic dialdehyde in liver homogenates of rats given sunflower oil was considerably higher than in rats fed the diet with lard. Remarkable coproporphyrinuria was revealed during DMFA intoxication which was more pronounced in rats fed the diet containing sunflower oil. It was demonstrated that the lard-containing diet was marked by a higher vitamin E/polyunsaturated fatty acids ratio (mg/100 g) with regard to alpha-tocopherol acetate added to the diet as compared to the sunflower oil-containing diet. The role of antioxidant properties of the diets in modification of the hepatotoxic action of DMFA is discussed.

Animals↗

PubMed1984

[Changes induced by dimethylformamide on platelet function and coagulation activity].

The effect of Dimethylformamide on platelet function and on clotting system has been studied on eight workers exposed to the product, widely used in industry as a solvent of acrylic resins. A significant reduction of the number of the platelets and a drawing out of PTT and PT has been noticed. Such informations has been explained as chronical peripheral use or as modification of phospholipid components induced by DMF instead of synthesis defect, as no significant variation of the fibrinogen and of AT III values, proteins synthetized by liver, has been observed. The platelet aggregation has pointed out, in vivo, a reduction of ADP aggregation in the exposed subjects; in vitro, increasing quantities have determined an increasing reduction of the primary ADP and adrenaline aggregation.

Adult↗

PubMed1984

Restoration of normal growth control and membrane antigen composition in malignant cells by N,N-dimethylformamide.

The effects of the differentiation agent, N,N-dimethylformamide (DMF), on malignant AKR-MCA cells were studied. The properties of DMF-treated AKR-MCA cells were compared to those of the normal parental AKR-2B mouse embryo fibroblasts. AKR-MCA cells grown in 1% DMF were found to be more similar to their normal counterparts than to untreated AKR-MCA cells by several criteria. These criteria included the loss of the transformed morphology, a 2-fold reduction of doubling time, a 10-fold reduction of saturation density, and the complete loss of the ability to grow with anchorage independence. The expression of high-molecular-weight membrane antigens (Mr 110,000 to 450,000), which was found to be greatly reduced in AKR-MCA cells in comparison to normal AKR-2B cells, was restored by treatment of AKR-MCA cells with DMF. The expression of a low-molecular-weight AKR-MCA cell-associated membrane antigen, on the other hand was found to be suppressed. Studies on the mitogenic response of these cells indicated that AKR-MCA and AKR-2B cells may be regulated by different types of growth control. Growth-arrested AKR-MCA cells did not respond to epidermal growth factor, but responded to nutrient replenishment. AKR-2B cells, on the other hand, responded to epidermal growth factor, but did not respond to nutrient replenishment. Treatment of AKR-MCA cells with DMF restored their ability to respond to epidermal growth factor, while their ability to respond to nutrient replenishment was lost. The results of this study indicated that DMF treatment induced the normalization of malignant AKR-MCA cells with regard to membrane antigen composition and growth control properties.

Animals↗

PubMed1980

N,N-dimethylformamide-induced modulation of organ- and tumor-associated markers in cultured human colon carcinoma cells.

Cultured human colon carcinoma cells were induced by the polar solvent N,N-dimethylformamide (DMF) to express a more differentiated phenotype as indicated by three types of antigen markers. Carcinoembryonic antigen expression in all DMF-induced cell lines was enhanced. Exposure of cells to DMF resulted in a reduction in ability to bind antibody to tumor-derived colon mucoprotein antigen (CMA) with a concomitant gain in binding of antibody to normal CMA. DMF-induced differentiation was further indicated by modulation of blood group antigen expression. DMF treatment decreased the amount of expression of the H-gene determinant. When DMF-treated cells were cultured in the absence of DMF for 14 days, the levels of expression of the antigen markers reverted to those characteristic of their untreated counterparts.

ABO Blood-Group System↗

PubMed1982

Prolongation of barbiturate-induced sleeping time in mice by dimethylformamide (DMF) and other non-polar solvents: absence of an effect on hepatic barbiturate-metabolising enzymes.

Prior administration of non-polar solvents was shown to prolong sleeping time in female mice induced with pentobarbitone sodium (37.5 mg/kg). The doses of solvents to double sleeping time were extrapolated from individual dose-response curves: they were (g/kg i.p.): dimethylformamide (DMF) 1.15: polyethyleneglycol 2.0: glycerol 0.66: dimethylsulphoxide 1.78: and sulpholone 1.26. The prolongation of sleeping time with DMF was not due to inhibition of hepatic microsomal enzymes because mice pretreated with SK & F 525A (40 mg/kg i.p.) did not exhibit a much greater solvent-induced effect than occurred in control (unpretreated) mice. DMF prolonged sleeping time in mice injected with thiopentone sodium (37.5 mg/kg i.v.), a drug known not to have its duration of narcotic effect determined by microsomal enzyme metabolism. It is concluded that prolongation of barbiturate-induced sleeping time in mice by DMF is not due to an inhibitory effect of the solvent on the hepatic microsomal enzymes.

Animals↗

PubMed1982

[An unusual case of "acute abdomen". Dimethylformamide poisoning].

Dimethylformamide, an industrial solvent largely used, causes intoxication both by inhalation and cutaneous adsorption. The Authors report the case of a young worker suffering from abdominal pain and hepatopathy who was heavily exposed to the solvent. A first diagnosis made by the surgery department was that of acute cholecystitis without gallstones. In the three successive years the worker was controlled and did not show relevant consequences of intoxication.

Abdomen, Acute↗

PubMed1981

[Comparison between cryoprotective potentials of glycerol, dimethylsulphoxide, dimethylformamide, and ethylene glycol in cryopreservation of human semen (author's transl)].

The cryoprotective effects of dimethylsulphoxide, dimethylformamide, and ethylene glycol in definite concentrations of 3.5, 7.0, and 12.0 per cent were compared with glycol action in cryoprotective preservation of human semen. Motility behaviour in response to laboratory stress (due to incubation at + 40 degrees C) as well as respiratory activation quotients for succinate, digitonin, and 2.4-dinitrophenol were used as criteria of assessment. The cryoprotective effect of glycerol was in no single instance surpassed by any of the other compounds, with the concentrations tested.

Cryoprotective Agents↗

PubMed1980

Hepatotoxicity of dimethylformamide and dimethylsulfoxide at and above the levels used in some aflatoxin studies.

Albino rats were each treated with a single intraperitoneal injection of dimethylformamide (DMF) or dimethysulfoxide (DMSO). The doses of DMF administered were 0.6, 0.9, and 1.2 ml. per kg. and those of DMSO were 1.2, 2.4, 3.6, and 4.8 ml. per kg. The animals were sacrificed at 24, 48, 72, and 120 hours following administration of each dose. The liver was investigated in all cases. Treatment with DMF at 0.6 ml. per kg. indicated some histologic lesions of the liver which became well defined at 0.9 and 1.2 ml. per kg. causing severe central phlebitis with centrilobular coagulative necrosis of the cells associated with a heavy inflammatory infiltrate. Maximal liver lesions occurred at 48 hours and started to regress after 72 hours. However, cellular atypism became a consistent finding after this inflammatory phase. DMSO-treated animals showed minimal histologic lesions of the liver at 1.2 and 2.4 ml. per kg. Higher doses caused fatty infiltration with a predominatly periportal distribution. It tended to produce its maximal effect in 12 hours which then regressed rapidly after 24 hours. The development of histologic lesions in the liver even at 0.6 ml. per kg. suggests that DMF is not a suitable solvent for aflatoxin studies, and hence the results obtained from such studies need cautious interpretation. DMSO appears to be an ideal alternative for toxicologic studies at a much higher dose level compared to DMF.

Aflatoxins↗

PubMedDate not supplied

[Effect of solvent structure on amide reaction with native DNA molecules. I. Aqueous mixtures of N,N-dimethylformamide and urea].

The influence of N,N-dimethylformamid (DMF) and urea (U) on the conformation of the native DNA molecule has been studied by methods of flow birefringence and viscometry. The investigations have been performed over a wide range of amides and supporting electrolyte concentrations. An essentially different influence of small additions of DMF and U on the macromolecule's dimensions was observed. At urea concentrations Cu < 0.03 mol% the DNA intrinsic viscosity [eta] decreases monotonously and the larger, the lower is the ionic strength mu of the solution. At DMF concentration CDMF approximately 1.5 mol% a cooperative decrease in [eta] of DNA, which also depends on mu was revealed. In the range of intermediate and large nonelectrolyte concentrations the influence of DMF on hydrodynamical and optical behaviour of the native DNA molecule resembles that of alcohols. The observed changes of [eta] are conditioned by conformational transitions in the DNA molecule. The constancy of macromolecule's optical anisotropy over a nonelectrolyte concentration range under investigation permits to interpret these transitions as occuring at the level of the tertiary structure of the native DNA molecule. The polyelecrolyte volume effects are considered on the basis of Manning's condensation model, and the structure singularities of water-organic solvents are taken into account. It has been shown that the nonelectrolyte influence on the native DNA molecule conformation may be direct (by means of ion-dipole interactions) or indirect (as result of changes in dielectric properties of solution). It is noted that the solvent structure is a very important factor which determines the interactions between low molecular organic compounds and the native DNA molecule.

Chemical Phenomena↗

PubMed1980

[Effect of dimethylformamide on the health status of workers].

Results are reported of the clinical examination and some laboratory tests performed in a group of workers, employed in the production of polyacrylnitryl fibers "Bulana" at the oil- processing and chemical works in Burgas, who have been exposed for 3 to 5 years to dimethylformamide (DMF). DMF concentrations in the air of the work environment were within the threshold ones, or exceeded them from 3 to 6 times. The most common constitutional symptoms were: fatigue, weakness, numbness of the extremities, eye and throat irritation. The results of physical examination were comparatively scanty. In spite of careful search, liver function and hemopoiesis were normal, neither were significant arterial pressure variations observed. These data will be used as baseline for comparison in a furture study of the technological staff, working in contact with DMF.

Adult↗

PubMed1994

Acute intravenous toxicity of dimethyl sulfoxide, polyethylene glycol 400, dimethylformamide, absolute ethanol, and benzyl alcohol in inbred mouse strains.

Acute intravenous toxicity of some solvents, i.e. dimethyl sulfoxide (DMSO), polyethylene glycol 400 (PEG 400), dimethylformamide (DMF), absolute ethanol (EtOH) and benzyl alcohol (BeOH), was determined in three inbred (CD2F1, B6D2F1 and C57BL/6N) mouse strains used in many preclinical tests, mainly in oncology and toxicology. Haemolytic and precipitation potential tests in vitro were performed to assess the blood compatibility of the investigated solvents and its relationship with the observed symptoms. The single tested solvents did not show any major differences in acute toxicity in the three tested strains with the exclusion of DMSO (less toxic in CD2F1) and BeOH and EtOH (less toxic in B6D2F1). The tested dose ranges in the three strains (in ml/kg) were 1.0-5.66 for DMSO, 2.0-8.0 for PEG 400, 1.0-4.0 for DMF, 0.75-4.24 for EtOH, 0.025-0.4 for BeOH. The lowest tested dose was a safe dose and the highest one was the dose causing mortality in no more than half the animals in each group. The in vitro results suggest avoiding the use of BeOH (which also is more toxic than the other solvents in the in vivo test) and DMSO and using PEG400, EtOH and DMF even though the latter induced a body weight decrease in the B6D2F1 mouse strain. As a general conclusion, dilution of these solvents in water is suggested to ameliorate their blood compatibility and the use of doses not higher than the lowest dose tested in this study is recommended.

Animals↗

PubMed1994

Liver injury and alterations of hepatic microsomal monooxygenase system due to dimethylformamide (DMF) in rats.

The effects of repeated exposure to N, N-dimethylformamide (DMF) on the liver and the hepatic microsomal monooxygenase system were investigated. DMF was administered to Wistar male rats by subcutaneous (s.c.) injection at 0.5 ml/kg body weight daily for 1-17 days. Macroscopically, mild liver swelling was observed and liver weights significantly increased after 3 days of exposure to DMF respectively. Hematological changes were not observed. In exposed rats, glutamic oxaloacetic transaminase and glutamic pyruvic transaminase significantly increased after 3 and 7 days of exposure to DMF. After 17 days of exposure to DMF, transaminases decreased compared to the 7 days. Hepatic microsomal cytochrome P-450 tended to decrease after 3 days of exposure DMF and decreased by 34% after 7 days and 25% after 17 days. Aminopyrine N-demethylase activity depressed significantly while aniline hydroxylase activity showed no change after 3 days of exposure to DMF. These results indicate that DMF alters the hepatic microsomal monooxygenase system. These findings may greatly contribute to the elucidation of the pathogenesis of DMF hepatotoxicity.

Aminopyrine N-Demethylase↗

PubMed1994

[Effects of dimethylformamide on the monocytophagocytic system of rodents].

The effects of Dimethylformamide (DMF) on monocytophagocytic system (MPS) of rodents were studied. The results showed large dose of DMF (1/20 LD50) with oral administration could significantly inhibit the functions of colloidal carbon clearance of MPS in Wistar rats, and of non-specific phagocytosis of sheep red blood cells (SRBC) by peritoneal macrophage in Kunming mice, and could also lowered significantly the levels of Fc and C3b receptors on the surface of peritoneal macrophage in mice. This showed DMF could cause obvious damage to MPS.

Animals↗