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Results for “DIMETHYL SULFOXIDE”

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At least 19 recordsLinked to original sources

PubMed1987

Physicochemical study of percutaneous absorption enhancement by dimethyl sulfoxide: dimethyl sulfoxide mediation of vidarabine (ara-A) permeation of hairless mouse skin.

Dimethyl sulfoxide's (DMSO) concentration-dependent influences on its own permeation rate through hairless mouse skin and on the concurrent permeation rates of water and the antiviral drug vidarabine (ara-A) have been studied at 37 degrees C using in vitro diffusion cells. Solubilities of ara-A in DMSO-water mixtures were also determined in order to assess ara-A's relative thermodynamic activity in the binary solvent media used in the mass transfer studies. Solubilities increased exponentially with increasing percentages of DMSO. Activity coefficients decreased accordingly. When the same DMSO medium was placed in each side of diffusion cell (balanced solvent configuration) permeability coefficients for ara-A decreased exactly as ara-A's solubility increased up to a 50% DMSO concentration, indicating the observed decreases in the mass transfer coefficients have thermodynamic origins. When DMSO media were placed in either the donor or receiver side of the cell up to the same 50% concentration point and opposed by a normal saline medium on the other side (asymmetric solvent configurations), the permeability of ara-A did not decrease and at some DMSO levels was substantially increased, behavior in marked departure from thermodynamic control. The behavior disparity between the 2 configurations of the cell suggests that cross-currents of solvents play a role in permeability enhancement. Regardless of solvent configuration, permeability coefficients for ara-A at 90 and 100% DMSO strengths were exaggeratedly large, consistent with severe impairment of the stratum corneum. Similar overall permeability behavior was observed for the 2 solvents, water and DMSO. Possible underlying mechanisms for these effects and the relative importance of the various mechanisms of DMSO enhancement as a function of DMSO's concentration and configuration are discussed.

Animals↗

PubMed1975

Increased virus budding from Friend erythroleukemic cells treated with dimethyl sulfoxide, dimethyl formamide, and/or bromodeoxyuridine in vitro.

Chronically infected Friend leukemia cells (FLC), grown in the presence of dimethyl sulfoxide (DMSO) (2%, v/v), dimethyl formamide (DMF) (1% v/v), or bromodeoxyuridine (BrdU) (3 or 20 mug/ml) for 4 or 7 days, were examined under the electron microscope. It was found that at the 4th day all three compounds induced comparable increases in the number of budding viruses (3 to 5 times that of the control). At the 7th day, the number had remained relatively constant in the BrdU-treated cells in contrast to the cells of the DMSO- or DMF-treated cultures, which showed a further increase of budding viruses. The greatest increase was seen when BrdU was added in combination with either DMSO or DMF, and this was reflected in the apparent increase in the number of extracellular viruses seen in cell pellets. Scanning electron microscopy on whole FLC mounts provided a rapid means of counting budding viruses and a good correlation was obtained between these counts and those made on thin sections by transmission electron microscopy. Attempts to quantitate the number of released viruses in controls and treated cultures after 4 days of growth revealed a 5- to 10-fold increase per cell in the samples treated with a combination of BrdU and either DMSO or DMF. Thymidine failed to prevent the increase of budding viruses induced by BrdU treatment. The number of budding viruses found after treatment with 3 mug/ml BrdU in the presence of 12 mug/ml thymidine was at a level comparable to that found after the individual BrdU treatment Finally, although FLC always contained varying amounts of intracisternal particles, their number, as compared to the paired controls, always decreased after BrdU treatment.

Animals↗

PubMed2004

Vibrational spectroscopic force field studies of dimethyl sulfoxide and hexakis(dimethyl sulfoxide)scandium(III) iodide, and crystal and solution structure of the hexakis(dimethyl sulfoxide)scandium(III) ion.

Hexakis(dimethyl sulfoxide)scandium(III) iodide, [Sc(OS(CH(3))(2))(6)]I(3) contains centrosymmetric hexasolvated scandium(III) ions with an Sc-O bond distance of 2.069(3) angstroms. EXAFS spectra yield a mean Sc-O bond distance of 2.09(1) angstroms for solvated scandium(III) ions in dimethyl sulfoxide solution, consistent with six-coordination. Raman and infrared absorption spectra have been recorded, also of the deuterated compound, and analysed by means of normal coordinate methods, together with spectra of dimethyl sulfoxide. The effects on the vibrational spectra of the weak intermolecular C-H...O interactions and of the dipole-dipole interactions in liquid dimethyl sulfoxide have been evaluated, in particular for the S-O stretching mode. The strong Raman band at 1043.6 cm(-1) and the intense IR absorption at 1062.6 cm(-1) have been assigned as the S-O stretching frequencies of the dominating species in liquid dimethyl sulfoxide, evaluated as centrosymmetric dimers with antiparallel polar S-O groups. The shifts of vibrational frequencies and force constants for coordinated dimethyl sulfoxide ligands in hexasolvated trivalent metal ion complexes are discussed. Hexasolvated scandium(iii) ions are found in dimethyl sulfoxide solution and in [Sc(OSMe(2))(6)]I(3). The iodide ion-dipole attraction shifts the methyl group C-H stretching frequency for (S-)C-H...I(-) more than for the intermolecular (S-)C-H...O interactions in liquid dimethyl sulfoxide.

Journal Article↗

PubMed1983

The catalytic activity and physical properties of bovine thrombin in the presence of dimethyl sulfoxide.

Dimethyl sulfoxide produces an opposite effect on the esterase and amidase activities of bovine thrombin. The esterase activity is increased by two fold but the amidase activity is decreased to 9% of the initial activity in 20% dimethyl sulfoxide. The stimulation of the esterase activity is due to the change in Vmax rather than Km for the substrate p-Tosyl-L-Arginine methyl ester. The inhibition of the esterase activity of thrombin by NaCl is not affected due to the addition of dimethyl sulfoxide. Ki for NaCl, 0.03 M, is the same for both in the absence and in the presence of 10% dimethyl sulfoxide. The catalytic activity of thrombin is inhibited by heparin. This effect is significantly decreased by dimethyl sulfoxide. The dissociation constant of heparin-thrombin complex, measured in the absence and in the presence of 10% dimethyl sulfoxide are 4 nM and 28 nM respectively. Thermal stability of thrombin, determined by monitoring catalytic activity, is increased in the presence of dimethyl sulfoxide. The enhancement of the fluorescence intensity of thrombin in the presence of dimethyl sulfoxide reflects the contribution of more exposed tryptophanyl residues. The alteration of the conformation of the enzyme structure due to the perturbation of the aqueous medium by dimethyl sulfoxide, has been attributed to these observed effects.

Animals↗

PubMed1977

Treatment of experimental murine amyloidosis with dimethyl sulfoxide.

Dimethyl sulfoxide was administered intravenously for 60 days to twenty mice with casein-induced amyloidosis. Partial or total disappearance of amyloid deposits occurred in all treated animals. The urine of these animals contained a substance from which amyloid fibrils could be synthesized. A control group of mice with casein-induced amyloidosis given saline injections showed massive amyloid deposition in the liver and in the spleen at the end of the experiment. Neither the urine of these mice nor the urine of normal control mice treated with dimethyl sulfoxide contained substances from which amyloid fibrils could be synthesized. It is our assumption that dimethyl sulfoxide treatment of mice with amyloidosis resulted in a break up of amyloid fibres into small subunits which were excreted in the urine.

Amyloid↗

PubMed2002

Formation of methane sulfinic acid in the gas-phase OH-radical initiated oxidation of dimethyl sulfoxide.

Dimethyl sulfoxide (CH3S(O)CH3: DMSO) is an important product of dimethyl sulfide (CH3SCH3: DMS) photooxidation. The mechanism of the OH-radical initiated oxidation of DMSO is still highly uncertain and a major aim of recent studies has been to establish if methane sulfinic acid (CH3S(O)OH: MSIA) is a major reaction product In the present work the products of the OH-radical gas-phase oxidation of dimethyl sulfoxide have been investigated in the absence and presence of NOx All experiments were performed in a 1,080 L reaction chamber in 1,000 mbar synthetic air at 284 +/- 2 K using long-path FT-IR spectroscopy and ion chromatography to monitor and quantify reactants and reaction products. Formation of methane sulfinic acid in high yield (80-99%) was observed in both in the absence and presence of NOx, and the results support that it is the major primary reaction product Other products observed included dimethyl sulfone (CH3S(O)2CH3: DMSO2), sulfur dioxide (SO2), methane sulfonic acid (CH3S(O)2OH: MSA), and methane sulfonyl peroxynitrate (CH3S(O)2OONO2: MSPN). The formation behavior of these products is in line with their source being mainly secondary production via oxidation of a primary product, i.e. MSIA.

Dimethyl Sulfoxide↗

PubMed1972

Activation of viruses in human tumors by 5-iododeoxyuridine and dimethyl sulfoxide.

Dimethyl sulfoxide added to cultures first treated with 5-iododeoxyuridine increased C-type virus production approximately tenfold in a human rhabdomyosarcoma cell line. 5-Iododeoxyuridine followed by dimethyl sulfoxide also activated a similar C-type virus in a metastatic tumor from a bronchial node taken from a 52-year-old male.

Adenocarcinoma↗

PubMed1998

Asymmetric reduction of racemic sulfoxides by dimethyl sulfoxide reductases from Rhodobacter capsulatus, Escherichia coli and Proteus species.

The enantioselective reduction of racemic sulfoxides by dimethyl sulfoxide reductases from Rhodobacter capsulatus, Escherichia coli, Proteus mirabilis and Proteus vulgaris was investigated. Purified dimethyl sulfoxide reductase from Rhodobacter capsulatus catalysed the selective removal of (S)-methyl p-tolyl sulfoxide from a racemic mixture of methyl p-tolyl sulfoxide and resulted in an 88% recovery of enantiomerically pure (R)-methyl p-tolyl sulfoxide. Rhodobacter capsulatus was shown to be able to grow photoheterotrophically in the presence of certain chiral sulfoxides under conditions where a sulfoxide is needed as an electron sink. Whole cells of Rhodobacter capsulatus were shown to catalyse the enantioselective reduction of methyl p-tolyl sulfoxide, ethyl 2-pyridyl sulfoxide, methylthiomethyl methyl sulfoxide and methoxymethyl phenyl sulfoxide. Similarly, whole cells of Escherichia coli, Proteus mirabilis and Proteus vulgaris reduced these sulfoxides but with opposite enantioselectivity.

Anaerobiosis↗

PubMed1977

The prevention of alloxan-induced diabetes in mice by dimethyl sulfoxide.

Dimethyl sulfoxide (DMSO, 7.3 g/kg) administered to mice prior to alloxan completely protected against the diabetogenic actions of 50 mg/kg alloxan. The same dose of DMSO provided a partial protection against 75 mg/kg alloxan. This protection against alloxan-induced diabetes is consistent with the scavenging of the hydroxyl radical by DMSO.

Animals↗

PubMed1974

Plaque formation with simian virus 40: enhancement by dimethyl sulfoxide.

Dimethyl sulfoxide (DMSO) added to agar overlays during plaque assays of simian virus 40 (SV40) in CV1 monkey cells increases the plaque size and number and enables plaques to be read several days earlier than usual. DMSO appears to act during development of plaques, perhaps by causing cell lysis at smaller burst sizes in the presence of near-lethal DMSO concentrations. It does not act synergistically in determining virus inactivation with UV light and is equally effective on wild type and a late mutant of SV40.

Animals↗

PubMed1988

Regulation of heme synthesis in HepG2 human hepatoma cells by dimethyl sulfoxide.

Dimethyl sulfoxide (DMSO) treatment of human HepG2 hepatoma cells increases the activity and the concentration of delta-aminolevulinic acid dehydratase (ALAD) to a comparable degree. Results of experiments with transcriptional inhibitors suggest that the increase in ALAD reflects de novo synthesis of the enzyme resulting from transcriptional activation. Commitment to increased ALAD activity in HepG2 cells is seen after 18 hr and complete by 48 hr. In contrast to the effects on ALAD, DMSO decreases the activities of porphobilinogen deaminase and uroporphyrinogen decarboxylase.

5-Aminolevulinate Synthetase↗

PubMed1985

Stimulation of tyrosine protein kinase activity by dimethyl sulfoxide.

Dimethyl sulfoxide (DMSO) stimulated the activity of a partially purified tyrosine protein kinase from rat lung. The stimulation was concentration dependent with a maximum stimulation (about 2 fold) observed at 10 per cent (V/V) DMSO. On the other hand, acetone (10 percent, V/V), did not exert any stimulatory effect on the enzyme activity. The stimulation was associated with a decrease in the Km for the substrate and an increase in the Vmax. In contrast, the Km for ATP was not affected by DMSO. Under identical assay conditions, DMSO did not significantly alter the activities of phosphorylase kinase, catalytic subunit of cAMP-dependent protein kinase and Ca2+-phospholipid-dependent protein kinase. It may be speculated that stimulation of tyrosine protein kinase may be one of the mechanisms by which DMSO exerts its biological effects.

Animals↗

PubMed1968

Disruption of T-even bacteriophages by dimethyl sulfoxide.

Dimethyl sulfoxide (DMSO) disrupted T-even bacteriophages as well as lambda bacteriophage. The component substructures of T2L, T4B01, or T6, in particular heads, were readily isolated after treatment with 67% DMSO (v/v). In contrast, concentrations of DMSO above 50% not only separated heads from tails of bacteriophage lambda but led to degradation of the lambda heads. Examination of the isolated free heads of T-even bacteriophage indicated that a distinct neck substructure was attached to one apex of the head. On some free tails a similar neck substructure was also found at the proximal end of the sheath. The dimensions of this neck substructure were found to be about 130 by 180 A; by virtue of its size and morphological attachment to the free heads, it was concluded that this was a distinct substructure and not an extension of the tail tube.

Coliphages↗

PubMed1985

Enhanced immune recognition of H-2 antigen-deficient murine lung carcinoma cells following treatment with dimethyl sulfoxide.

Dimethyl sulfoxide (DMSO) has previously been shown to increase the surface expression of H-2K and H-2D antigens on cultured line 1 carcinoma cells. H-2 densities increase from initial levels barely detectable with flow cytometry to those found on normal BALB/c spleen cells. Here we compare the susceptibilities of untreated and DMSO-treated line 1 cells to lysis mediated by H-2d specific monoclonal antibodies and complement, cytotoxic T-cells, and natural killer cells. Induced H-2 antigens appear to function normally in that DMSO-treated cells are highly susceptible to all types of H-2 restricted immune lysis, whereas untreated line 1 cells are not. DMSO does not increase lysis of line 1 cells mediated by natural killer cells. Our results suggest that DMSO could be used to make the growth of major histocompatibility complex antigen-deficient tumors more sensitive to T-cell-mediated immunological resistance.

Animals↗

PubMed2004

Massive intracranial hemorrhage associated with the ingestion of dimethyl sulfoxide.

Dimethyl sulfoxide (DMSO) has been widely used in the treatment of arthritis and certain inflammatory diseases, and is also considered an alternative remedy for cancer even if not supported by concrete evidence. This report illustrates the first case of a fatal complication following the illicit use of this agent. A 55-y-old man who reportedly ingested 500 mg acetaminophen and approximately 1 ml DMSO solution was brought to the emergency department after experiencing 2 tonic-clonic seizures. He had been diagnosed with lung mesotelioma with brain metastases which caused no neurologic deficit. The ingested DMSO was the first dose within the last 3 mo. Examination revealed right-sided hemiplegia. Unenhanced computed tomography of the head showed 3 hemorrhagic areas with blood-cerebrospinal fluid at the left parietal, occipital and frontal regions accompanied by a midline shift. Despite initial resuscitation, 2 units of fresh frozen plasma and antiedema treatment, the patient experienced cardiac arrest that did not respond to resuscitative measures. DMSO can cause massive intrametastatic hemorrhage, and neurologic deterioration can be profound in patients with metastatic brain lesions.

Diagnosis, Differential↗

PubMed2000

The spectrum of inflammatory cell response to dimethyl sulfoxide.

Dimethyl sulfoxide (DMSO), depending upon the concentration and mode of application to the skin, can induce either a non-immunological immediate contact urticaria or an irritant reaction. The dermal cellular infiltrate after open application of varying concentrations of DMSO has been studied in an experimental guinea pig model. The composition of the dermal cellular infiltrate showed a spectrum dependent on the concentration and number of applications of DMSO. The immediate reaction infiltrate 3 h after application of 100% DMSO consisted of 50% granulocytes, basophils being predominant. On the other hand, 12% DMSO applied 3 x daily for 3 days (cumulative insult) caused histologically a cellular reaction in which 80% of the infiltrate consisted of mononuclear cells. The present findings are compared to the microscopic findings in 3 other cutaneous reactions previously studied in this animal model, namely, the Type I immediate hypersensitivity reaction, the Type IV delayed hypersensitivity reaction, and the irritant reaction. Differing cellular infiltrate patterns are discernible at the same time points. The study illustrates the spectrum of inflammatory reactions seen in the skin and provides background information for future clinical studies, for instance, on the role of the basophil granulocyte in immediate contact reactions.

Administration, Topical↗

PubMed1987

Specific reduction of N,N-dimethylnitrosamine mutagenicity in Drosophila melanogaster by dimethyl sulfoxide.

Dimethyl sulfoxide (DMSO) used as a solvent has been observed to complicate mutagenicity screens by interacting with tested chemicals to yield false positives or negatives. We have used DMSO as a solvent in the Drosophila melanogaster recessive sex-linked lethal mutation assay and find that it reduces, but does not abolish, the detectable mutagenicity of N,N-dimethylnitrosamine (DMN). Its use as a solvent with procarbazine, another promutagen, shows no effect on mutagenicity in Drosophila. DMSO does not exhibit a general inhibitory action on microsome activity when ecdysone 20-monooxygenase activity is used as a measure of cytochrome P-450 activity. We were unable to detect the low DMN demethylase activity in the strain used. Hence, the inhibitory effect of DMSO in Drosophila at both the physiological and biological level appears to be limited and not general in action. Because DMN and DMSO are similar in structure, it is possible that DMSO is interacting with a DMN demethylase in Drosophila. This might lead to a reduction in the conversion of DMN to a mutagen. Consequently, from the results of this study and others DMSO should be used cautiously as a solvent in Drosophila mutagen screening.

Animals↗

PubMed2006

Transient osmotic absorption of fluid in microvessels exposed to low concentrations of dimethyl sulfoxide.

Dimethyl Sulfoxide (DMSO) is a common solvent for pharmacological agents. It is a small, lipophilic molecule thought to be relatively highly permeable through the cell membrane. While measuring the effect of low concentrations of DMSO (0.05-0.5% v/v) on capillary hydraulic conductivity as a vehicle control for pharmacological agents, the authors noticed what appeared to be an unusual transient absorption of fluid across the vessel wall. This absorption occurred during occlusion of the vessel, but dissipated quickly (1.7-8.6 s). The transient reabsorption reappeared upon each successive occlusion. To determine the nature of this transient absorption, the authors have measured the effect of increasing the pressure of the perfusing solution, of the concentration and time of perfusion of DMSO, and of superfusing the DMSO. They found that the absorption rate, but not the filtration rate, was concentration dependent, and was significantly correlated with the osmotic pressure of the DMSO. Moreover, the time taken for completion of the transient, i.e., time to reversal of flow, was inversely proportional to the hydraulic conductivity of the vessel. Furthermore, the transient absorption could be reduced and eventually abolished by increasing the hydrostatic pressure. These results strongly suggested that perfusion with low concentrations of DMSO could set up a significant osmotic pressure gradient across the vessel wall. This proposed mechanism for the absorption was confirmed by the measurement of a significant osmotic reflection coefficient of the vessel wall to DMSO (0.11 +/- 0.01). Relatively low concentrations (0.05-0.5%) of DMSO were therefore able to stimulate a significant osmotic transient across the blood vessel walls.

Absorption↗