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PubMed1991

Column liquid chromatographic determination of carbadox and olaquindox in feeds.

A column liquid chromatographic method for simultaneous determination of carbadox and olaquindox in swine feeds is described. The drugs were extracted from feeds with carbon tetrachloride-dimethylformamide (80:20) at 60 degrees C for 30 min. The extract was mixed with water (25:45). After centrifugation the aqueous layer was chromatographed on a reversed-phase column using gradient elution and ultraviolet detection at wavelengths of 305 and 262 nm. Recoveries from samples fortified at levels of 20-50 ppm were 92 +/- 9% for carbadox and 93 +/- 6% for olaquindox (means +/- standard deviations, n = 71).

Animal Feed↗

PubMed1996

Induction or suppression of SV40 amplification by genotoxic carcinogens, non-genotoxic carcinogens or tumor promoters.

Carcinogens are generally classified into two groups: genotoxic and non-genotoxic. As the final product of genotoxic and non-genotoxic carcinogens is the same, i.e., a clone of genetically altered cells, it could be possible that non-genotoxic carcinogens may yield genotoxic events as a secondary result of cell toxicity having led to mitogenesis/cellular proliferation, or that genetic alterations are induced that are normally neglected in genotoxicity tests. A genetic effect with possible relevance for the ultimate mechanism of carcinogenicity is the amplification of oncogenes. In the present experiments, amplification of SV40-virus DNA in transformed CO631-cells has been measured. In this system, two genotoxic carcinogens (positive control), two non-carcinogens (negative control), and eight non-genotoxic carcinogens have been tested. With the exception of testosterone and BVDU, all substances were tested when given alone. Testosterone and BVDU were tested in combination with either MTX or AMP in the presence or absence of S9-mix. The genotoxic carcinogens TEM and 4-NQO as well as the tumor promoters TPA, coumarin, mezerein and chrysarobin were able to induce SV40 amplification when given alone. The same was for acetamide and thioacetamide. The non-carcinogens acetone and dimethylformamide were ineffective. In case of testosterone, a co-amplification effect was seen in the absence of S9-mix, and an anti-amplification effect in presence of S9-mix. The anti-recombinogen BVDU reduced the SV40 amplification effect of AMP in experiments without addition of S9-mix. In the presence of activating S9-mix, this substance was effective at lower concentrations than without S9-mix, and showed an enhanced anti-amplification effect. Similar effects of testosterone and BVDU had been observed before in respect to stimulation or suppression of recombination. These results can be used as supportive evidence for the assumption that gene amplification is mechanistically related to recombination.

Acetamides↗

PubMed1991

Potential bile acid metabolites. 17. Synthesis of 2 beta-hydroxylated bile acids.

The 2 beta-hydroxylated derivatives of lithocholic, chenodeoxycholic, deoxycholic, and cholic acids were synthesized from the respective parent bile acids by established procedures. The principal reactions involved were (1) bromination of 3-oxo formylated bile acids in N,N-dimethylformamide, (2) rearrangement and substitution of the resulting 4 beta-bromo-3-oxo derivatives to the 2 beta-acetoxy-3-oxo compounds with potassium acetate, and (3) reduction to the 2 beta-acetoxy-3 alpha-hydroxy compounds with tert-butylamine-borane complex. As for the prepared 2 beta-hydroxylated bile acids with a diequatorial trans-glycol structure, proton and carbon-13 nuclear magnetic resonance spectroscopic and gas-liquid chromatographic/mass spectrometric properties are discussed.

Acetates↗

PubMed1995

Homogeneous catalytic dehalodimerization of 17-iodo-delta 16 steroids.

17-Iodo-delta 16 steroids undergo selective dimerization and carbonylative dimerization in the presence of palladium catalysts in dimethylformamide which result in 16-17'-coupled dienes and 17-carboxylic anhydrides, respectively. Moderate to good yields have been obtained for both types of dimers.

Androstenes↗

PubMed1989

Effects of altered platelet number on pulmonary hypertension and platelet sequestration in monocrotaline pyrrole-treated rats.

To study the role of platelets in monocrotaline pyrrole (MCTP)-induced pulmonary hypertension, pulmonary sequestration of 111In-labeled platelets in rats treated with MCTP and anti-rat platelet serum (PAS) was examined. Lung injury from a single, intravenous injection of MCTP (3.5 mg/kg) at Day 8 was evident as elevated lung weight and lavage fluid protein and lactate dehydrogenase activity. Additionally, right ventricular hypertrophy and elevated pulmonary arterial pressures (PAP) occurred. Treatment with PAS on Days 6-8 did not affect the lung injury but resulted in an attenuation of the pulmonary hypertensive response. Pulmonary platelet sequestration was also decreased in PAS-treated rats, yet the sequestration in the lungs of MCTP-treated rats that received PAS was significantly higher than that in the lungs of N,N-dimethylformamide (DMF) controls. MCTP-treated rats receiving control serum (CS) tended to sequester more 111In-labeled platelets than respective DMF controls, but this was not statistically significant. Blood platelet half-life was unaltered in rats receiving CS. When rats were treated similarly with MCTP and PAS and were killed at 18 days, the attenuation of the pulmonary hypertensive response previously described was not observed, and lung injury was more extensive than when CS was given. Apparently, platelet depletion delayed the development of the pulmonary hypertensive response. Supranormal platelet numbers produced by splenectomy did not affect MCTP-induced lung injury or the elevation in PAP. These results support the hypothesis that the development of MCTP-induced pulmonary hypertension is mediated in part by platelets.

Animals↗

PubMed1994

Studies on a new radiopaque polymeric biomaterial.

A new radiopaque polymeric biomaterial has been synthesized. The material, which actually represents an entire family of analogous radiopaque materials, is composed of 2-(p-iodobenzoyl)-ethyl methacrylate (compound 1, 21 mol%), methyl methacrylate (MMA, 60 mol%), and 2-hydroxyethyl methacrylate (HEMA, 19 mol%). The terpolymer was synthesized in a radical polymerization reaction at elevated temperature in N,N-dimethylformamide (DMF). The product was subjected to a set of physicochemical characterization techniques (gel permeation chromatography, 500 MHz 1H NMR in deuterated dimethylsulphoxide (d6-DMSO) solution, differential scanning calorimetry, dynamic water contact angle measurements), as well as to an in vitro thrombogenicity assay. Furthermore, scanning electron microscopy was used to study interactions of the material with blood platelets. The most important findings are: (a) the material is a genuine polymer with excellent X-ray visibility, even in the form of thin (0.4 mm) drawn fibres. This was established under realistic conditions. (b) The material exhibits low in vitro thrombogenicity, i.e. comparable to polyvinyl chloride, which is known as a passive material. These observations lead us to the suggestion that this type of radiopaque polymer holds promise with respect to application as a construction material for a new type of endovascular stent. This could be relevant in particular to stents to be used in conjunction with percutaneous transluminal coronary angioplasty (PTCA), also known as Dottering. Currently there is a clear trend away from metallic stents towards all-polymeric stents, since the latter have superior biocompatibility.(ABSTRACT TRUNCATED AT 250 WORDS)

Biocompatible Materials↗

PubMed1985

Potentiation between intracellular cyclic-AMP-elevating agents and inducers of leukemic cell differentiation.

Acute leukemia is the result of a defect in the process of normal cellular differentiation. Human leukemia cell lines (HL60, RDFD-2) have been established which can be induced to differentiate into phenotypically mature cells by a variety of agents. Recent evidence suggests that cyclic adenosine 3'-5'-monophosphate (cAMP) and the cAMP dependent protein kinase (cAMP-dPK) may be intimately involved in myeloid differentiation. The addition of low levels of a wide variety of inducers of a diverse chemical nature, dimethylformamide (DMF), retinoic acid (RA), actinomycin D (ACT-D) or hypoxanthine (HPX) prior to the addition of 8-bromo-cyclic adenosine 3'-5' monophosphate (8-Br-cAMP), cholera toxin (CT) or the phosphodiesterase inhibitor isobutylmethylxanthine (IBMX) results in marked potentiation of differentiation of both HL60 and RDFD cells as manifested by the acquisition of the antigen OKM-1, the ability to reduce nitroblue tetrazolium or expression of the chemotactic receptor. Potentiation of differentiation is also observed when 8-Br-cAMP, CT or IBMX is added prior to the addition of either RA, DMF, ACT-D or HPX. These results suggest a role for cAMP in myeloid differentiation.

1-Methyl-3-isobutylxanthine↗

PubMed1983

Temperature dependence of the electronic spin-lattice relaxation time in a 2-iron-2-sulphur model complex.

The complex [Fe2S2(S2-o-xylyl)2]2- in DMF (dimethylformamide), DMSO (dimethylsulphoxide) or a 1:1 DMF/DMSO mixture, a model for the chromophore in the 2Fe-2S proteins (ferredoxins), has been reduced and studied by conventional EPR over a temperature range. The low-field feature of the spectrum, Hz, has been computer simulated in order to analyse the lineshape in terms of a convolution product of Lorentzian and Gaussian distributions. The Gaussian contribution to the linewidth and a fixed part of the Lorentzian contribution, which is a function of the solvent and the way it freezes, were measured at a low temperature (less than or equal to 100 K) and subtracted from the linewidths in the higher-temperature range (130-200 K). The variable Lorentzian contribution thus obtained was related to spin-lattice relaxation times. The spin-lattice relaxation times of the sample having 1:1 DMSO/DMF solvent were measured in the range 6 to 11 K by the saturating pulse technique and in the range 10 to 65 K by continuous saturation methods. Up to 65 K the results follow the law 1/T1 alpha T4.5, a relationship which is not readily interpreted in terms of a simple Debye model. At higher temperatures the results may be interpreted in terms either of a dominant Orbach mechanism involving excited states at approx. 900 +/- 50 cm-1 (DMSO, DMF) or 770 +/- 50 cm-1 (1:1 DMSO/DMF), or of a Raman process in which 1/T1 alpha T7.5. The former is compatible with the two-phonon process already described in some ferredoxins, especially those with little anisotropy (gy - gx approximately 0.0) which have characteristically high [J] values.

Dimethyl Sulfoxide↗

PubMed1975

Skin deposition and penetration of trichlorocarbanilide.

Studies are reported on the localization and quantitative distribution of 3,4,4'-trichloro[14C]carbanilide([14C]TCC) in guinea-pig and human skin, and on the percutaneous absorption of TCC following topical application to guinea pigs. [14C]TCC was applied to guinea-pig skin in various vehicles (conventional, superfatted, 10 percent non-soap detergent (NSD) and 30 percent NSD soap suspensions or in N,N-dimethylformamide [DMF]) and under various conditions (e.g. freshly prepared or equilibrated suspensions; single or multiple washes). Most of the amount of TCC remaining in the skin after rinsing was deposited on the skin surface and only relatively minute amounts actually penetrated through the epidermis into the dermis. Whereas conventional soap facilitated a greater deposition of TCC on the skin surface than NSD, the latter caused greater amounts of TCC to be deposited in the pilosebaceous system and lower dermis than conventional soap. The absence of TCC in the blood and tissues of guinea pigs given topical applications of TCC lends further support to the very low order of percutaneous absorption of TCC. The localisation of TCC followed a similar pattern in human skin as in guinea-pig skin, but the amount deposited was less and the rate of disappearance was more for human than for guinea-pig skin.

Animals↗

PubMed1987

Alkylformamides as inducers of tumour cell differentiation--a mini-review.

The induction of terminal differentiation in tumour cells represents a possible therapeutic strategy for treating cancer. The alkylformamides are 1 group of experimental compounds which have been shown to induce terminal differentiation in human HL-60 leukemia and murine Friend erythroleukemia cells in vitro. Their mechanism of action is unknown. Dimethylformamide has been used as a model inducer in carcinoma and fibroblastic models. Analysis of the relationship between structure and inducing activity of the alkylformamides in vitro reveals that no specificity of structure exists and that their properties as inducers of terminal differentiation extend to related compounds, e.g. the alkylacetamides and alkylureas. This is in contrast to the marked specificity of N-methylformamide (NMF) as an in vivo antitumour agent. The potency of these compounds as inducers of differentiation is predictable and correlated with their molecular weight. High concentrations of NMF are required to induce differentiation in vitro and these concentrations are not achievable in vivo. However, while NMF is unlikely to be a useful inducer in vivo many of its higher MW analogues are very much more potent as inducers in vitro and yet no more toxic (to the host) in vivo. Some of these (e.g. tetramethylurea or 1,3-dimethylurea) may be capable of achieving inducing concentrations in vivo.

Alkylation↗

PubMed1985

Modulation of cellular phosphoprotein profiles in transformation and redifferentiation of murine AKR embryonic fibroblastic cells.

Cellular phosphoprotein profiles from normal mouse embryonic fibroblast AKR-2B cells were compared to those of their permanently, chemically transformed malignant counterparts AKR-MCA cells, and AKR-2B cells reversibly transformed by transforming growth factor (AKR-TGF). Similar 32P-phosphorylation profiles were observed for both the AKR-TGF and AKR-MCA cells which were distinct from that of the normal AKR-2B cells. Dimethylformamide (DMF)-induced differentiation of the AKR-MCA cells resulted in a restoration of the normal AKR-2B phosphorylation profile to the malignant AKR-MCA cells.

Animals↗

PubMed1989

Effect of polar-planar compounds on the differentiation of normal human myeloid immature marrow cells.

Polar-planar compounds which are potent differentiating agents, have been reported to enhance the response of friend erythroleukaemic cells and other malignant cell lines to mitomycin C, cis-platinum and radiation. With the upcoming of phase II clinical trials of these polar compounds alone and in combination with cytotoxic agents, the effect of 3 polar compounds: dimethylsulphoxide, dimethylformamide and hexamethylene bisacetamide on the differentiation of normal human myeloid immature marrow cells was studied. The results showed that a long-term exposure to these polar compounds may lead to a premature senescence of these marrow progenitors.

Acetamides↗

PubMed1993

Transforming growth factor-beta 2 is an autocrine growth inhibitory factor for the MOSER human colon carcinoma cell line.

The MOSER human colon carcinoma cell line is significantly growth inhibited by exogenous transforming growth factor-beta (TGF-beta). The secretion of TGF-beta by these cells was examined to determine if endogenous TGF-beta might also regulate MOSER cell growth. MOSER cells secreted 11 ng TGF-beta/10(6) cells, 24% of which was in the active form. Blocking antibodies specific for TGF-beta 2 stimulated growth 1.4-fold, while TGF-beta 1 specific antibodies were without effect. Treatment of MOSER cells with the differentiation agent, N,N-dimethylformamide (DMF), inhibited cell growth and resulted in an 8-fold increase in secreted TGF-beta (20% active). Only antibodies specific for TGF-beta 2 were able to reverse the growth inhibitory effect of DMF on these cells. Therefore, TGF-beta 2 acted as a negative autocrine inhibitory factor for MOSER cells and the growth inhibitory effects of DMF were mediated by the increased secretion of active TGF-beta 2.

Antibodies↗

PubMed1979

Early changes in ornithine decarboxylase activity during Friend leukemia cell differentiation.

Agents such as dimethylsulfoxide, N,N'-dimethylformamide and bisacetyldiaminopentane that induce erythroid differentiation of Friend leukemia cells, cause a rapid increase in ornithine decarboxylase (EC 4.1.1.17) activity in intact cells during the 'latent' period preceding the accumulation of hemoglobin-containing cells. Blockage of erythroid differentiation with 5-bromo-2'-deoxyuridine did not prevent these alterations in enzyme activity. Addition of each chemical inducer in the extracts of these cells stimulate the basal levels of ornithine decarboxylase activity. These data indicate that the chemical inducers of differentiation modify the normal pattern of ornithine decarboxylase activity in this system.

Animals↗

PubMed1984

One- and two-electron reduction of hydroxy-1,4-naphthoquinones and hydroxy-9,10-anthraquinones. The role of internal hydrogen bonding and its bearing on the redox chemistry of the anthracycline antitumour quinones.

First and second half-wave reduction potentials of 11 1,4-naphthoquinones and 42 9,10-anthraquinones have been measured for solutions in dimethylformamide. The presence of hydroxy groups at the 5- and 8-positions of the 1,4-naphthoquinone nucleus, and at the 1-, 4-, 5- and 8-positions of the 9,10-anthraquinone (the alpha-positions) markedly raises both reduction potentials. Measurements on the corresponding methoxy- and acetoxyquinones indicate that internal hydrogen bonding in the alpha-hydroxyquinones makes a major contribution to stabilisation of the semiquinone, probably as a result of increased delocalisation due to exchange of the hydroxy hydrogen between the two neighbouring oxygen atoms. The bearing of this phenomenon on the mechanism of action of anthracycline antitumour quinones is discussed, and the stabilising effect on the semiquinone of hydroxy groups at the 1- and 5-positions of the 9,10-anthraquinone nucleus is highlighted.

Anthraquinones↗

PubMed1984

Polar solvent modification of X ray induced potentially lethal damage in heterogeneous human colon tumor cells in vitro.

Two subpopulations of tumor cells (clones A and D) obtained from a human colon adenocarcinoma were examined for their sensitivities to x-irradiation as unfed, early plateau phase cultures. Both the single dose survival curves and the kinetics of potentially lethal damage recovery (PLDR) were determined for the two tumor lines. Also, possible modification of PLDR by N,N-dimethylformamide (DMF), which has previously been shown to enhance the radiosensitivity of exponentially growing tumor cells, was investigated by adding DMF (0.8% v/v) to plateau phase cultures immediately after irradiation, and determining effects on the extent of PLDR. For non-DMF treated cells, the survival curve parameters of the diploid (clone D) and aneuploid (clone A) lines were very similar. The single-hit, multitarget values for n, Do (Gy), and Dq (Gy) were: 7.9, 0.82, and 1.70 for clone D; and 10.6, 0.83, and 1.96 for clone A. Using initial survival levels of 3.5% (clone D) or 5.5% (clone A) to investigate PLDR, it was found that the increase in survival (surviving fraction ratio or SFR) for clone D was 2.2, while the SFR for clone A was 1.6. DMF did not change either the kinetics or extent of PLDR in these two tumor lines when added to cultures immediately after irradiation. Our results indicate that significant heterogeneity in PLDR exists between these closely related tumor subpopulations.

Adenocarcinoma↗

PubMed1992

High-performance liquid chromatographic determination of N-methylformamide and N-methyl-N-(hydroxymethyl)-formamide in human urine.

A reliable high-performance liquid chromatographic (HPLC) method which allows the determination in human urine of two important metabolites of N,N-dimethylformamide (DMF), namely N-methylformamide (MMF) and N-methyl-N-(hydroxymethyl)formamide (DMFOH), is reported. A single-step rapid purification of urine was performed on a C18 solid-phase extraction column and the eluate was injected directly on to the HPLC column. HPLC was carried out isocratically on Aminex Ion Exclusion HPX-87H column using 7.5.10(-4) M sulphuric acid as the mobile phase with ultraviolet detection at 196 nm. The method is specific, accurate, precise and sufficiently sensitive to be applied to the biological monitoring of MMF and DMFOH in workers exposed to DMF.

Chromatography, High Pressure Liquid↗

PubMed1993

Quantification of methylmalonic acid in serum measured by capillary gas chromatography-mass spectrometry as tert.-butyldimethylsilyl derivatives.

Quantification of methylmalonic acid in serum is considered one of the most sensitive parameters for diagnosis of cobalamin deficiency. Methylmalonic acid was measured as tert.-butyldimethylsilyl derivatives formed in the presence of dimethylformamide. Under these conditions the derivative was quantified using gas chromatography-mass spectrometry with selected-ion monitoring at 403 and 406 for methylmalonic acid and methyl-d3-malonic acid, respectively. The characteristics of the method were: linearity from 0.04 to 1.7 mumol/l with linear regression equation y = -0.0199 + 0.727 x (r = 0.999); recovery 95.5 +/- 6.8%; detection threshold 17 fmol injected; within-day variation coefficient ranging from 3.10% to 5.6% according to sample concentration; and day-to-day coefficient of variation of 6.8% and 5.3% for methylmalonic acid concentrations of 0.103 mumol/l and 0.360 mumol/l, respectively. The normal range after log transformation was estimated at 0.03-0.26 mumol/l, 0.06-0.33 mumol/l and 0.02-0.40 mumol/l in children of 4-14 years (n = 39), in healthy subjects at 20-40 years (n = 70) and in healthy elderly persons older than 60 years (n = 14), respectively. The normal range in children was significantly lower than that in adults and, in contrast, normal values in the elderly were significantly higher.

Adolescent↗