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At least 19 recordsLinked to original sources
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↗
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↗
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

Dimethyl sulfoxide in central nervous system trauma.

Dimethyl sulfoxide has been tested in various experimental injuries of the central nervous system in relation to other therapies. It appears to be a useful drug in acute extradural mass-forming lesions, middle cerebral artery occlusion, respiratory anoxia, and spinal cord injuries, in rhesus and squirrel monkeys, dogs, and rats. The data from these studies suggest that in the experimental models used, DMSO is clearly superior to no treatment, and appears to be more generally effective than other comparable treatments. No satisfactory answer has yet been found to explain the beneficial effects of DMSO, but several hypothetical suggestions are offered; their validation hinges primarily on further confirmatory evidence. Further experiments with our present models and alternative research lines are discussed.

Animals↗
PubMed1979

Inhibition of insulin receptor binding by dimethyl sulfoxide.

Little is known of the effects of the solvent on hormone-receptor interactions. In the present study the effect of the polar solvent dimethyl sulfoxide on the binding of insulin to its surface receptors on cultured human lymphocytes of the IM-9 line was investigated. At concentrations exceeding 0.1% (v/v), dimethyl sulfoxide produced a dose-related inhibition of 125-I-labeled insulin binding. Insulin binding was totally abolished in 20% dimethyl sulfoxide. This inhibition was immediately present and was totally reversible. Analysis of the data of binding at steady state indicated that the decrease in binding of 125I-labeled insulin was due to a reduced affinity of the insulin receptor without noticeable change in the concentration of receptor sites. Kinetic studies showed that the decreased affinity could largely be accounted for by a decreased association rate constant; effects on dissociation and negative cooperativity of the insulin receptor was affected to a much lesser extent.

Depression, Chemical↗
PubMed1976

Effect of nonionic surfactants on percutaneous absorption of salicylic acid and sodium salicylate in the presence of dimethyl sulfoxide.

Fifteen nonionic surfactants, 10% (w/w), were each incorporated into white petrolatum USP ointment base containing 10% (w/w) salicylic acid or 11.6% (w/w) sodium salicylate with 10% (w/w) dimethyl sulfoxide. Percutaneous absorption was determined from blood salicylate levels in New Zealand white rabbits at regular intervals for 8 hr following application of the ointment. Percutaneous absorption of salicylic acid was increased significantly when sorbitan monopalmitate, sorbitan trioleate, poloxamer 231, poloxamer 182, polyoxyethylene 4 lauryl ether, polyoxyethylene 2 oleyl ether, or polyoxyl 8 stearate was added to the ointment containing dimethyl sulfoxide, salicylic acid, and white petrolatum. Percutaneous absorption of sodium salicylate was increased significantly when sorbitan monolaurate, sorbitan monopalmitate, or poloxamer 182 was added to the ointment containing dimethyl sulfoxide, sodium salicylate, and white petrolatum.

Animals↗
PubMed1976

Role of hydroxyl radical scavengers dimethyl sulfoxide, alcohols and methional in the inhibition of prostaglandin biosynthesis.

Prostaglandin biosynthesis from eicosa-8, 11, 14-trienoic acid in microsomes from bovine seminal vesicles is inhibited by relatively high concentrations of hydroxyl radical scavengers: dimethyl sulfoxide, n- and t-butanol, and methional. Methional is a more effective scavenger than t-butanol and dimethyl sulfoxide, two compounds which are more miscible with water than methional. The synthesis of both PGE and PGF is inhibited with incubation systems that promote PGE formation and with incubation systems that promote PGF formation. Furthermore, dimethyl sulfoxide and methional inhibit arachidonic acid-induced platelet aggregation, a reaction involving endoperoxide biosynthesis. The water soluble alcohol, ethanol, stimulates PGF biosynthesis when it is added in the same concentration range as t-butanol. Thus hydroxyl radical scavengers inhibit biosynthesis when their effective concentrations are high and stimulate biosynthesis when their effective concentrations are low. The results of this study and other studies where low concentrations of hydroxyl radical scavengers stimulate both prostaglandin biosynthesis and lipid peroxidation are consistent with a mechanism involving the hydroxyl radical both in the generation of singlet oxygen and the elimination of hydrogen peroxide.

8,11,14-Eicosatrienoic Acid↗
PubMed1979

Effects of dimethyl sulfoxide and colchicine on the resorption of experimental amyloid.

The induction of amyloid in C3H mice by either casein solution or complete Freund's adjuvant emulsion with Mycobacterium butyricum was confirmed by partial splenectomy. The animals were autopsied after treatment with dimethyl sulfoxide (550 mg/kg, 50 times), colchicine (0.02 mg/kg, 15--37 times), or saline solution as a control. Detailed histological comparisons of biopsy and autopsy spleens provided evidence that dimethyl sulfoxide was significantly effective in the resorption of amyloid, while in the animals treated with colchicine amyloid deposition was increased. The effect of dimethyl sulfoxide was discussed with reference to the modification of amyloid fibrils.

Amyloid↗
PubMed1976

Further experience with intravesical dimethyl sulfoxide in the treatment of interstitial cystitis.

Intravesical dimethyl sylfoxide has given satisfactory symptomatic relief in 75 per cent of patients with interstitial cystitis so treated. The treatment is simple and inexpensive, and can be safely administered as an office procedure. Objective improvement in the endoscopic appearance of the disease, with improvement in bladder capacity, was noted in 80 per cent of the patients in our series. Further work with dimethyl sulfoxide is indicated in the treatment of interstitial cystitis, as well as a variety of other genitourinary disorders.

Adult↗
PubMed1978

Dimethyl sulfoxide in treatment of inflammatory genitourinary disorders.

Intravesical dimethyl sulfoxide (DMSO) has been used in the treatment of 213 patients with various inflammatory conditions involving the lower genitourinary tract, including intractable interstitial cystitis, radiation cystitis, chronic prostatitis, and chronic female trigonitis. Significant symptomatic relief has been achieved in the majority of patients so treated, and no systemic or local toxicity has been noted. Some patients failed to respond entirely, and others relapsed after DMSO treatment periods of several months, ultimately coming to augmentation cystoplasty or urinary diversion. However, because of its simplicity and ease of administration, intravesical DMSO therapy is recommended in all noninfectious or non-neoplastic inflammatory conditions presenting initially with severe symptoms, or that have failed to respond to conventional therapy.

Adult↗
PubMed1978

[Changes in activities of DNA-dependent RNA-polymerases from rat liver under influence of glycerol, dimethyl sulfoxide and polyethylene glycol-400].

Effects of glycerol, dimethyl sulfoxide (DMSO) and polyethylene glycol (PEG) 400 on transcription of isolated nuclei and DNA in rat liver under the action of homologous RNA-polymerases I and II were studied. Addition of these organic compounds to the reaction mixture before initiation altered RNA synthesis on native DNA matrix. Addition of glycerol or DMSO to the synthesising system 1 and 5 minutes after initiation of RNA synthesis had no effect on the rate of transcription. PEG-400 inhibited incorporation of 3H-UTP into newly-synthesized independently of the time of its introduction to the reaction mixture. The data obtained suggest that the compounds under study may impair the formation of initiation complex of RNA polymerase with DNA and alter RNA synthesis in isolated nuclei of rat liver.

Animals↗
PubMed1976

Effect of dimethyl sulfoxide on embryonic survival and subsequent chick performance.

Dimethyl sulfoxide (DMSO) was injected into the yolk of fertile White Leghorn chicken eggs at levels of 0.0, 0.025; 0.05, 0.10 and 0.20 ml./egg. Injection with 0.20 ml. DMSO/egg resulted in 100% mortality of chick embryos within six days of incubation. Injection with 0.10 ml. DMSO/egg resulted in 22.2% embryonic mortality by 14 days of incubation and 51.9% hatchability of fertile eggs compared to 84.6% for control eggs. Chicks hatched from eggs injected with 0.10 ml. DMSO/egg exhibited a decreased growth rate and high mortality. Injection of 0.05 ml. DMSO/egg or less had no effect on embryonic survival, hatchability of chick performance. The embryos from eggs injected with higher levels of DMSO exhibited hemorrhagic areas of the brain and head region and a retarded vitelline and allantoic circulatory system and were characterized by anopthalmia and celosomia. DMSO had no effect on the packed cell volume of chicks from eggs injected with DMSO.

Animals↗