Disease relevance of dimethyl sulfoxide

• The stability of globin mRNA in murine erythroleukemia cells (Friend cells) before and during DMSO-induced differentiation was investigated [1].
• Factors affecting recovery of functional reactivity were related to toxicity of DMSO for the cells, the osmotic stress placed upon the cells as the DMSO was being removed after thawing, the handling temperature of the freshly thawed cells, and the susceptibility of cells to mechanical damage immediately after thawing [2].
• To determine whether alterations in the lipid composition and fluidity of rat colonic brush border membranes existed before the development of DMH-induced colon cancer, rats were injected s.c. with this agent (20 mg/kg body weight per wk) or diluent for 5, 10, and 15 wk [3].
• Thus DMSO can induce H-2 expression and alter the sensitivity of murine lymphoma cells to different effector cells [4].
• The effects of HIV infection on U937 cells strikingly resemble the effects of differentiation-inducing agents, such as PMA and DMSO, on the U937 phenotype [5].

Psychiatry related information on dimethyl sulfoxide

• The relationship between drug dose and loss of PE is much steeper for DMSO than for RA, suggesting that these two drugs affect different stages of the differentiation decision-making apparatus [6].
• The highest yields of tertiary amine products were seen when DMSO was used as reaction solvent in conjunction with a reaction time of 18 h at room temperature [7].
• Role of AMPA receptor desensitization and the side effects of a DMSO vehicle on reticulospinal EPSPs and locomotor activity [8].
• RESULT(S): At time 1, MMP and MMPI activities were similar in all rats; however, PA and PAI activities were less in rats pretreated with GnRH-a than with diluent [9].
• At sub-toxic concentrations, DMSO decreases planarian exploratory behavior in a concentration-dependent manner [10].

High impact information on dimethyl sulfoxide

• Its role in differentiation has now been investigated using Friend erythroleukemia cells, which can be induced to differentiate along the erythroid pathway by dimethylsulfoxide and certain other agents [11].
• Human beta-globin genes introduced into mouse erythroleukemia (MEL) cells by DNA cotransformation are correctly regulated when erythroid cell differentiation is induced by dimethylsulfoxide (DMSO) [12].
• The effect of DMSO on MEL cell mitochondria is mimicked by FCCP, a proton ionophore that dissipates mitochondrial membrane potential [13].
• It appears that cells exposed to DMSO are locked indefinitely in a proliferative myoblast stage of development and are unable to enter the Go phase of the cell cycle necessary for initiation of differentiation [14].
• Dimethylsulfoxide (DMSO) prevents the terminal differentiation of L8 myoblasts in vitro, and its effect is reversible [14].

Chemical compound and disease context of dimethyl sulfoxide

• Treatment of controls, a lymphoma cell line and mouse erythrocytes, with DMSO or butyric acid had no effect [15].
• In contrast, both allopurinol and dimethylsulfoxide reduced peripancreatic edema formation, suggesting that edema, but not the other features that characterize this model of pancreatitis, may result from generation of oxygen-derived free radicals [16].
• Murine-virus-infected erythroleukemia cells cultured in a medium with dimethylsulfoxide or N,N-dimethylformamide are induced to differentiate to erythroid cells [17].
• Purine metabolism was studied in murine virus-induced erythroleukemia cells stimulated to differentiate in vitro in the presence of dimethylsulfoxide [18].
• The results indicate that the free radical scavengers SOD, catalase, SOD-catalase, and DMSO inhibit (but do not prevent) vascular hyperpermeability and cellular damage during acute, angiotensin II--induced hypertension [19].

Biological context of dimethyl sulfoxide

• This suppressive action of dexamethasone is more effective with DMSO as the inducer of globin gene expression than with hemin as the inducer [20].
• The kinetics of globin mRNA induction in hemin as compared to DMSO are very different: globin message accumulation begins 4 hr after hemin addition, but not until 30--40 hr after DMSO addition [21].
• Manipulation of myogenesis in vitro: reversible inhibition by DMSO [14].
• The cells resemble proerythroblasts and, when exposed to dimethyl sulphoxide (DMSO) or a variety of other chemicals, can be induced to undergo a programme of differentiation which closely resembles the final stages of normal erythropoiesis [22].
• Induction by HMBA and DMSO of genes introduced into mouse erythroleukemia and other cell lines by transient transfection [23].

Anatomical context of dimethyl sulfoxide

• These cell lines have previously been shown to differentiate in vitro in response to dimethylsulfoxide (DMSO) and a number of other polar solvents [24].
• In cells cultured with dimethylsulfoxide (Me2SO), hexamethylene bisacetamide (HMBA) or butyric acid, accumulation of alpha-globin mRNA is detectable after 16, 12 and 8 hr of culture, respectively [25].
• Hybrid cells formed by the fusion of murine teratocarcinoma and Friend erythroleukemia cells synthesize hemoglobin in the presence of chemical inducers such as dimethylsulfoxide (DMSO) [26].
• Protein synthetic patterns of DMSO-inhibited cells are almost indistinguishable from those of untreated myoblasts and distinct from differentiated myotubes [14].
• We report here that many of the compounds that induce erythroid differentiation in FL cells are similar to DMSO in selectively suppressing PMA-induced lymphocyte mitogenesis [27].

Associations of dimethyl sulfoxide with other chemical compounds

• The size of the total RNA synthesized, determined by sedimentation on sucrose density gradients containing dimethylsulfoxide, ranged from less than 5S to 45S, and the size of the affinity-labeled sequences ranged from less than 5S to 28S [28].
• MGI+D+ clones were also induced to synthesize and secrete lysozyme by dexamethasone, prednisolone, cytosine arabinoside, or thymidine and in one of four clones by dimethylsulfoxide but not by sodium butyrate [29].
• The modulation of globin gene expression by steroid hormones is achieved in DMSO-treated cells without altering the growth and morphological changes which characteristically attend the differentiation of these cells [20].
• The net result is continued c-myc expression following DMSO or Hyp induction and a complete or partial inhibition of F-MEL differentiation [30].
• To tackle this problem, the c-fes protooncogene expression has been inhibited in HL60 cells, and fresh leukemic promyelocytes of acute promyelocytic leukemia have been induced to differentiate with retinoic acid (RA) and dimethylsulfoxide (DMSO) [31].

Gene context of dimethyl sulfoxide

• DMSO was found to directly inhibit IL-8 expression at the level of transcription [32].
• Fluorescence-activated cell sorter analysis revealed induction of H-2Kk and beta 2m 3 days after culture of YAC-1 with DMSO, whereas optimal H-2Dd induction required more than 1 week [4].
• The E-boxes at the hTERT proximal promoter were occupied in vivo by c-Myc in exponentially proliferating HL60 cells but not in cells induced to differentiate by DMSO [33].
• In this work, P19 cells were allowed to aggregate from day 0 to day 4 in the presence of 0.5% DMSO, 10(-7) M OT and/or 10(-7) M OT antagonist (OTA), and then cultured in the absence of these factors until day 14 [34].
• During the first 12 h of treatment with DMSO, MEL cells undergo a temporary decrease in the level of c-myc mRNA, followed by a temporary withdrawal from the cell cycle [35].

Analytical, diagnostic and therapeutic context of dimethyl sulfoxide

• In the double-blind study, none of the 12 lesions in the six patients injected with diluent had responses, as compared with 10 of the 12 lesions in the six patients injected with hCG (P=0.015) [36].
• In a double-blind trial, 12 additional patients were randomly assigned to receive intralesional injections of 2000 IU of hCG or diluent alone (6 patients each; two lesions per patient) [36].
• The process of erythroid differentiation in mouse Friend leukemia virus transformed cells (T3-C1-2) was examined by following changes in several enzyme activities of the heme biosynthetic pathway and in heme concentration while the cells were undergoing erythroid differentiation after treatment with dimethylsulfoxide [37].
• A final experiment on rats with established bladder tumors compared the cytoreductive effect of continuous intravesical infusion of DOX in 50% DMSO with that of DOX alone and with that in a sham-treated control group; there were 20 rats in each group [38].
• The use of DMSO as a drug carrier merits further evaluation as a way of enhancing the efficacy of regional chemotherapy regimens [38].

References