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Results for “Dimethyl Sulfoxide”

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At least 19 recordsLinked to original sources
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↗
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↗
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↗
PubMed1978

Alteration of myoblast phenotype by dimethyl sulfoxide.

Application of dimethyl sulfoxide to proliferating L8 myoblasts (an established cell line of rat skeletal muscle) for 72 hr completely prevented fusion and induction of creatine phosphokinase (EC 2.7.3.2) activity (an indicator of muscle differentiation). The growth pattern changed from the usual sheets of randomly oriented cells to flattened, whorled monolayers of elongated fibroblast-like cells. By electron microscopy, rough endoplasmic reticulum increased and extracellular material appeared that had the morphologic and staining characteristics of collagen. After 120 hr in dimethyl sulfoxide-containing medium, the cells secreted about 6 times more collagen than untreated controls. Dimethyl sulfoxide was ineffective when applied to L8 cells just prior to fusion, and effects of dimethyl sulfoxide were not readily reversible unless treated cells were subcultured at low density.

Animals↗
PubMed1992

Inhibition of the human erythrocyte calcium pump by dimethyl sulfoxide.

The action of dimethyl sulfoxide on the human red cell Ca2+ pump was studied in inside-out vesicles. In a high-K+ medium at pH 7.6, the organic solvent inhibited both Ca2+ transport and ATP hydrolysis. Half-maximal effect was obtained with about 2% (v/v). At or below 10% dimethyl sulfoxide, the inhibition was overcome by adding inorganic phosphate or oxalate. In the absence of organic solvent, Ca2+ efflux from Ca(2+)-loaded vesicles consisted of a slow and a fast component whilst in its presence, there appears additionally a leakage component. The size of the latter depended markedly on dimethyl sulfoxide concentration, being about 3% at that level where Ca2+ uptake was half-maximally inhibited. ATP hydrolysis was more sensitive to dimethyl sulfoxide (10%) when free Ca2+ was increased within the millimolar level than when it was raised within the micromolar range. On the other hand, raising Ca2+ with organic solvent greatly stimulated ATP synthesis through ATP-Pi exchange, without reaching saturation. The results suggest that dimethyl sulfoxide blocks the red cell Ca2+ pump by increasing the affinity of the Ca2+ translocating site at the releasing step. They also show that at high concentrations, this solvent increases Ca2+ permeability.

Adenosine Triphosphate↗
PubMed1975

The safe use of dimethyl sulfoxide in the laboratory.

Dimethyl sulfoxide is being increasingly utilized in medical laboratories and in experimental clinical situations. The drug must be considered dangerous since there has been one reported case of fatal allergic reaction and numerous reports of liver damage following exposure to dimethyl sulfoxide. Caution must be exercised in the handling of the drug as it can aid the entry of other drugs into the human body. Although dimethyl sulfoxide is not highly flammable, normal safety precautions used with any flammable solvent are the minimal requirements for safe use of this drug.

Accident Prevention↗
PubMed1976

Dissociation of alpha beta DNA polymerase of avian myeloblastosis virus by dimethyl sulfoxide.

The alpha beta DNA polymerase of avian myeloblastosis virus was treated with dimethyl sulfoxide to dissociate the enzyme subunits. The dimethyl sulfoxide treated enzymes were passed over phosphocellulose to purify and characterize the dissociated subunits as well as to remove the dimethyl sulfoxide. RNA-directed DNA polymerase, RNase H, and nucleic acid-binding activity were monitored, as well as the subunit structure (on sodium dodecyl sulfate-polyacrylamide gels) of the various enzyme species obtained. With 30% dimethyl sulfoxide, the majority of DNA polymerase and RNase H activities as well as the alpha subunit were displaced from the alpha beta DNA polymerase position on phosphocellulose (0.23 M potassium phosphate) to the alpha DNA polymerase position (0.1 M). The association of DNA polymerase and RNase H activities with the alpha subunit suggests that alpha is the enzymatically active subunit in alpha beta. In addition to alpha DNA polymerase, a minor polymerase species eluted from phosphocellulose at 0.4 M potassium phosphate. The dissociated beta subunit eluted from phosphocellulose at a wide range of salt concentrations (0.28 to 0.5 M potassium phosphate). The dissociated beta subunit bound 3H-labeled murine leukemia virus RNA and [3H]poly(dT)-poly(dA) approximately 20-fold more avidly than alpha DNA polymerase alone. In contrast to the results with the alpha subunit, there was no correlation between DNA polymerase and RNase H activity profiles and the elution profile of the beta subunit from phosphocellulose. These observations suggest the beta subunit is either enzymatically inactive or possesses limited DNA polymerase and RNase H activity when compared with the alpha subunit.

Avian Leukosis Virus↗
PubMed1975

Biological effects of the metabolites of dimethyl sulfoxide.

In summary, the effects of dimethyl sulfoxide (DMSO) and its metabolites, dimethyl sulfone (DMSO2) and dimethyl sulfide (DMS), were studied in five selected systems in rats and mice. DMSO enhanced the taurine excretion and the lethality produced by such aromatic hydrocarbons as benzene and chlorobenzene in rats. In mice, DMSO decreased the toxicity such cholinesterase inhibitors as paraoxon and octamethyl pyrophosphoramide. DMSO also lowered the body temperture of rats and reduced the motor activity of mice. Although DMSO2, the major metabolite of DMSO, was not effective in increasing the lethality of solvent hydrocarbons, it seemed to be quite as effective with respect to the other effects. DMS, although quite potent with respect to lowering body temperature and reducing motor activity, was relatively ineffective otherwise. Thus each of the metabolites has a spectrum of activity different from the parent compound; DMSO has the widest spectrum and DMS the narrowest. It remains to be determined whether the therapeutic effects of DMSO are related to the experimental effects reported above in animals, and whether DMSO2 and DMS may share any of the therapeutic effects of DMSO.

Animals↗
PubMed1977

Differentiation of a resistant clone of mouse myeloid leukemia cells with dimethyl sulfoxide and ascitic fluid.

Mouse myeloid leukemia line cells, M1, could be induced to differentiate in vitro into macrophages and granulocytes with ascitic fluid of animals bearing various tumors. M1 cells could not be induced to differentiate with dimethyl sulfoxide alone. During the culture of M1 cells, spontaneously appearing cells resistant to factors stimulating differentiation (D-factor) in ascitic fluid were isolated. These resistant cells were more refractile to the toxic action of dimethyl sulfoxide than sensitive cells and grew in culture medium with 1% dimethyl sulfoxide. Although the resistant cells were not induced to differentiate with dimethyl sulfoxide alone, they were sensitized with the aid of dimethyl sulfoxide to undergo differentiation with the D-factor in ascitic fluid.

Animals↗
PubMed1978

Changes in DNA associated with induction of erythroid differentiation by dimethyl sulfoxide in murine erythroleukemia cells.

The Friend virus-infected murine erythroleukemia cell can be induced to differentiate along erythroid cells in culture with various compounds, including dimethyl sulfoxide. DNA from murine erythroleukemia cells cultured with dimethyl sulfoxide shows a decrease in sedimentation rate in alkaline sucrose gradients after alkali lysis of the cells. These changes can be detected as early as 27 hr after the beginning of culture. Similar results are observed with DNA of the cells cultured with other inducers, butyric acid and dimethylacetamide, but not with DNA from a variant cell line resistant to induction with dimethyl sulfoxide. Ultraviolet irradiation, which is known to cause similar changes in the sedimentation rate of DNA in alkaline sucrose gradients, induces differentiation of the murine erythroleukemia cells. These studies suggest that alterations in DNA may be related to events involved in the induction of differentiation of murine erythroleukemia cells by dimethyl sulfoxide.

Alkalies↗
PubMed1977

Failure of dimethyl sulfoxide in the treatment of scleroderma.

Nineteen patients with systemic scleroderma and five with localized scleroderma were treated with topical dimethyl sulfoxide by painting and immersion techniques. Partial control was obtained by using a very low concentration (5%) on one side when involvement was symmetrical. Duration of treatment ranged from 3 to 15 months. Topical dimethyl sulfoxide did not improve the skin induration, range of motion, or Raynaud's phenomenon in the scleroderma patients. No substantial beneficial effect was noted on the healing of ischemic ulcers, and the continuous application of dimethyl sulfoxide did not prevent new ulceratins from developing. Relief of pain was noted in ten of 16 patients, probably due to the local analgesic effect of dimethyl sulfoxide.

Adult↗
PubMed1975

Stabilization of hog cholera virus by dimethyl sulfoxide.

The stability of hog cholera virus through five freeze-thaw cycles in the presence and absence of dimethyl sulfoxide was studied. In the absence of dimethyl sulfoxide the hog cholera virus titer was reduced 52% to 91% following successive freezing and thawing cycles. However, when dimethyl sulfoxide was added to the viral suspension the virus titer appeared to remain the same after the same number of freezing and thawing cycles.

Animals↗
PubMed1992

Effect of dimethyl sulfoxide on phosphoryl transfer catalyzed by yeast hexokinase.

Hexokinase is a phosphotransferase that catalyzes phosphoryl transfer from ATP to glucose much more rapidly than the transfer from ATP to water (i.e., hydrolysis). Dimethyl sulfoxide has opposite effects on these two phosphotransferase activities: it enhances ATP hydrolysis and inhibits glucose phosphorylation. Xylose, a sugar that is non-phosphorylatable by hexokinase, enhances ATPase activity which is additive to activation by dimethyl sulfoxide, indicating that the mechanism of activation by dimethyl sulfoxide is different from that of xylose. These results suggest that it is possible to change the specificity of the enzyme in the presence of dimethyl sulfoxide.

Adenosine Triphosphatases↗