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This is a knowledge network extract, and will likely be somewhat hard to understand


  • Ingestion is probably unadvisable since the membrane permeability increased would probably cause issues with leaky gut
  • Use should be limited based on glutahione and insulin receptor interaction
  • Use around the skull is probably even less advisable considering interaction with astrocytes


  • Inhibition of insulin receptor binding by dimethyl sulfoxide

On Reactions

  • Turns glutathione into a gel
    • This would be problematic internally
  • Turns methylene blue clear


  • Application of over 6 inches sq to skin tends to cause headache within 12hr. I estimate this to be a consequence of decreased insulin receptor binding (less available energy for the brain) combined with glutathione binding (this plays an important role in insulin metabolism)
  • Application with honokiol damaged skin
  • Application with bromelain dyed skin. Took 45 days to return to normal.
  • Appliation with melatonin on scalp did not appear to be an effective delivery of melatonin
  • Application with noopept did not increase effect of noopept
  • Initial application of DMSO solution, to point of burning, following by application of saturated fat, appeared to improve skin


Unexpected low-dose toxicity of the universal solvent DMSO.
Galvao J1, Davis B, Tilley M, Normando E, Duchen MR, Cordeiro MF.
Author information
Dimethyl sulfoxide (DMSO) is an important aprotic solvent that can solubilize a wide variety of otherwise poorly soluble polar and nonpolar molecules. This, coupled with its apparent low toxicity at concentrations <10%, has led to its ubiquitous use and widespread application. Here, we demonstrate that DMSO induces retinal apoptosis in vivo at low concentrations (5 μl intravitreally dosed DMSO in rat from a stock concentration of 1, 2, 4, and 8% v/v). Toxicity was confirmed in vitro in a retinal neuronal cell line, at DMSO concentrations >1% (v/v), using annexin V, terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL), 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), and AlamarBlue cell viability assays. DMSO concentrations >10% (v/v) have recently been reported to cause cellular toxicity through plasma membrane pore formation. Here, we show the mechanism by which low concentrations (2-4% DMSO) induce caspase-3 independent neuronal death that involves apoptosis-inducing factor (AIF) translocation from mitochondria to the nucleus and poly-(ADP-ribose)-polymerase (PARP) activation. These results highlight safety concerns of using low concentrations of DMSO as a solvent for in vivo administration and in biological assays. We recommend that methods other than DMSO are employed for solubilizing drugs but, where no alternative exists, researchers compute absolute DMSO final concentrations and include an untreated control group in addition to DMSO vehicle control to check for solvent toxicity.

AIF; DARC; neuronal apoptosis; retina; toxicity

PMID: 24327606 DOI: 10.1096/fj.13-235440
  • Toxicity was confirmed in vitro in a retinal neuronal cell line,
    • but does DMSO even get to the brain?
The concentrations of DMSO in growth medium above 0.1-0.5% often decrease the proliferation of cultured cells. This may be in some cases associated with a reversible cell cycle arrest (CHO cells, 1-2% DMSO, 96 hrs), and in other cases with cell differentiation to other lineages (HL-60 cells, 1.3% DMSO, 96 hrs) or cell death at even higher concentrations of DMSO (Caco-2 cells, >10% DMSO, the release of  LDH).
However, lower concentrations of DMSO may not always be safe in cell proliferation assays either. There are reports suggesting that DMSO at low concentrations actually stimulates the proliferation of some cell types; for example at 100 uM (0.00078% m/V) DMSO increased proliferation of OVCAR-3, SK-OV-3 and Caov-3 ovarian cancer cell lines (PMID: 12713137). Likewise, at 0.05-0.2% DMSO significantly increased the proliferation of RPMI-8226 myeloma cells relative to medium only control [ref]. Even using DMSO in control treatments may not solve the problem, since the combined effects of evaluated drugs and DMSO may not be additive.

Dimethyl Sulfoxide Damages Mitochondrial Integrity and Membrane Potential in Cultured Astrocytes
Chan Yuan, Junying Gao, Jichao Guo, Lei Bai, Charles Marshall, Zhiyou Cai, Linmei Wang, Ming Xiao

Dimethyl sulfoxide (DMSO) is a polar organic solvent that is used to dissolve neuroprotective or neurotoxic agents in neuroscience research. However, DMSO itself also has pharmacological and pathological effects on the nervous system. Astrocytes play a central role in maintaining brain homeostasis, but the effect and mechanism of DMSO on astrocytes has not been studied. The present study showed that exposure of astrocyte cultures to 1% DMSO for 24 h did not significantly affect cell survival, but decreased cell viability and glial glutamate transporter expression, and caused mitochondrial swelling, membrane potential impairment and reactive oxygen species production, and subsequent cytochrome c release and caspase-3 activation. DMSO at concentrations of 5% significantly inhibited cell variability and promoted apoptosis of astrocytes, accompanied with more severe mitochondrial damage. These results suggest that mitochondrial impairment is a primary event in DMSO-induced astrocyte toxicity. The potential cytotoxic effects on astrocytes need to be carefully considered during investigating neuroprotective or neurotoxic effects of hydrophobic agents dissolved by DMSO.
  • if you apply DMSO solution directly to astrocytes, at certain concentration, they dont’ proliferate as much . Does DMSO even cross the blood brain barrier?
  • DMSO at concentrations of 5% significantly inhibited cell variability and promoted apoptosis of astrocytes, accompanied with more severe mitochondrial damage. These results suggest that mitochondrial impairment is a primary event in DMSO-induced astrocyte toxicity.
  • The present study showed that exposure of astrocyte cultures to 1% DMSO for 24 h did not significantly affect cell survival, but decreased cell viability and glial glutamate transporter expression,



  • slightly destabilized cell membranes (recovers within 24hr) (7458406)
  • promotes herpes, epstein bar, viruses
  • anti inflammatory
  • anti leukemia
  • ok to apply to skin
    • don’t apply to scalp: not good when applied to the brain (28644892)
  • seemingly anti-tumor for some sorts


DMSO inhibits NO generation by endothelial cells through modulation of CAT-1 activity
DMSO Represses Inflammatory Cytokine Production from Human Blood Cells and Reduces Autoimmune Arthritis

DMSO efficiently down regulates pluripotency genes in human embryonic stem cells during definitive endoderm derivation and increases the proficiency of hepatic differentiation
inhibited LPS-mediating IL-1s transcription. Taken together, DMSO shows anti-inflammatory characteristics, attenuates NLRP3 inflammasome activation, and mediates inhibition of IL-1s transcription.

  • high concentrations of DMSO inhibit the non-selective cation channels in human erythrocytes and thus protect the cells against Na+ and Ca2+ overload
    DMSO, a kind of chemical chaperone, activated autophagy by suppressing ATF4 expression and might play a protective role in the development of fatty acid-induced hepatosteatosis.
  • DMSO may be an important stimulator of the tumor suppressor protein HLJ1 through AP-1 activation
  • Oral administration of DMSO is an effective treatment for amyloid A amyloidosis, especially for gastrointestinal involvement and the early stage of renal dysfunction.

Dimethyl sulfoxide potentiates death receptor-mediated apoptosis in the human myeloid leukemia U937 cell line through enhancement of mitochondrial membrane depolarization. [15998540]
Anti-angiogenic effects of dimethyl sulfoxide on endothelial cells. [12951474]
Intermittent use of topical dimethyl sulfoxide in macular and papular amyloidosis. [9888342]
– this seems to validate the idea DMSO is used as a solvent that clears cells and makes way for recovery

reduced affinity of the insulin receptor

The use of dimethylsulfoxide as a solvent in enzyme inhibition studies: the case of aldose reductase. [28856935]
Aldose reductase (AR) is an enzyme devoted to cell detoxification and at the same time is strongly involved in the aetiology of secondary diabetic complications and the amplification of inflammatory phenomena. AR is subjected to intense inhibition studies and dimethyl sulfoxide (DMSO) is often present in the assay mixture to keep the inhibitors in solution. DMSO was revealed to act as a weak but well detectable AR differential inhibitor, acting as a competitive inhibitor of the L-idose reduction, as a mixed type of non-competitive inhibitor of HNE reduction and being inactive towards 3-glutathionyl-4-hydroxynonanal transformation. A kinetic model of DMSO action with respect to differently acting inhibitors was analysed. Three AR inhibitors, namely the flavonoids neohesperidin dihydrochalcone, rutin and phloretin, were used to evaluate the effects of DMSO on the inhibition studies on the reduction of L-idose and HNE.
Mesh:Aldehyde Reductase,Dimethyl Sulfoxide,Dose-Response Relationship, Drug,Enzyme Inhibitors,Humans,Recombinant Proteins,Solvents,Structure-Activity Relationship
Keywords:Dimethyl sulfoxide,aldose reductase,aldose reductase differential inhibitors

R-Modafinil exerts weak effects on spatial memory acquisition and dentate gyrus synaptic plasticity. [28644892]
Modafinil is a wake promoting drug approved for clinical use and also has cognitive enhancing properties. Its enantiomer R-Modafinil (R-MO) is not well studied in regard to cognitive enhancing properties. Hence we studied its effect in a spatial memory paradigm and its possible effects on dentate gyrus long-term potentiation (DG-LTP). Clinically relevant doses of R-MO, vehicle dimethyl sulfoxide (DMSO) or saline were administered for three days during the hole-board test and in in vivo DG-LTP. Synaptic levels of dopamine receptors D1R, D2R, dopamine transporter (DAT), and its phosphorylated form (ph-DAT) in DG tissue 4 h after LTP induction were quantified by western blot analysis. Monoamine reuptake and release assays were performed by using transfected HEK-293 cells. Possible neurotoxic side effects on general behaviour were also studied. R-MO at both doses significantly enhanced spatial reference memory during the last training session and during memory retrieval compared to DMSO vehicle but not when compared to saline treated rats. Similarly, R-MO rescues DG-LTP from impairing effects of DMSO. DMSO reduced memory performance and LTP magnitude when compared to saline treated groups. The synaptic DR1 levels in R-MO groups were significantly decreased compared to DMSO group but were comparable with saline treated animals. We found no effect of R-MO in neurotoxicity tests. Thus, our results support the notion that LTP-like synaptic plasticity processes could be one of the factors contributing to the cognitive enhancing effects of spatial memory traces. D1R may play an important regulatory role in these processes.
Mesh:Animals,Benzhydryl Compounds,Dentate Gyrus,Dimethyl Sulfoxide,Dopamine,Dopamine Plasma Membrane Transport Proteins,Drug Evaluation, Preclinical,Excitatory Postsynaptic Potentials,HEK293 Cells,Humans,Learning,Long-Term Potentiation,Male,Nootropic Agents,Rats, Sprague-Dawley,Receptors, Dopamine,Spatial Memory
  • DMSO impairs DG-LTP (dentate gyrus long-term potentiation)
  • DMSO reduced memory performance and LTP magnitude when compared to saline treated groups

Effect of dimethyl sulfoxide on dentin collagen. [28610709]
Infiltration of adhesive on dentin matrix depends on interaction of surface and adhesive. Interaction depends on dentin wettability, which can be enhanced either by increasing dentin surface energy or lowering the surface energy of adhesive. The objective was to examine the effect of dimethyl sulfoxide (DMSO) on demineralized dentin wettability and dentin organic matrix expansion.
– Acid-etched human dentin was used for sessile drop contact angle measurement to test surface wetting on 1-5% DMSO-treated demineralized dentin surface, and linear variable differential transformer (LVDT) to measure expansion/shrinkage of dentinal matrix. DMSO-water binary liquids were examined for surface tension changes through concentrations from 0 to 100% DMSO. Kruskal-Wallis and Mann-Whitney tests were used to test the differences in dentin wettability, expansion and shrinkage, and Spearman test to test the correlation between DMSO concentration and water surface tension. The level of significance was p<0.05.
– Pretreatment with 1-5% DMSO caused statistically significant concentration-dependent increase in wetting: the immediate contact angles decreased by 11.8% and 46.6% and 60s contact angles by 9.5% and 47.4% with 1% and 5% DMSO, respectively. DMSO-water mixtures concentration-dependently expanded demineralized dentin samples less than pure water, except with high (≥80%) DMSO concentrations which expanded demineralized dentin more than water. Drying times of LVDT samples increased significantly with the use of DMSO.
– Increased dentin wettability may explain the previously demonstrated increase in adhesive penetration with DMSO-treated dentin, and together with the expansion of collagen matrix after drying may also explain previously observed increase in dentin adhesive bonding.
Mesh:Collagen,Dental Bonding,Dental Cements,Dentin,Dentin-Bonding Agents,Dimethyl Sulfoxide,Humans,Surface Properties
Keywords:Adhesion,Collagen expansion,Collagen shrinkage,Contact angle,DMSO,Wettability
– increase dentin binding

Neurotoxicity Associated With Dimethyl Sulfoxide Used in Allogeneic Stem Cell Transplantation. [28121745]
Dimethyl sulfoxide (DMSO) is a cryoprotective agent used in storage of frozen stem cells in stem cell transplantation. Central nervous system side effects of DMSO such as epileptic seizures, stroke, transient global amnesia, and temporary leucoencephalopathy are rarely seen. Here, we report a pediatric patient who developed seizures after DMSO-cryopreserved stem cell infusion and whose magnetic resonance imaging of the brain demonstrated parietal and occipital focal cortical T2-signal intensity increase. DMSO toxicity should be kept in mind in patients who received cryopreserved stem cell infusion and magnetic resonance imaging may be helpful in differential diagnosis of central nervous system involvement.
Mesh:Adolescent,Allografts,Cryopreservation,Cryoprotective Agents,Diagnosis, Differential,Dimethyl Sulfoxide,Female,Humans,Neurotoxicity Syndromes,Stem Cell Transplantation

Dimethyl sulfoxide attenuates nitric oxide generation via modulation of cationic amino acid transporter-1 in human umbilical vein endothelial cells. [27426075]
Dimethyl sulfoxide (DMSO) is a solvent that is commonly used in medicine. Conflicting data exist as to its effects on endothelial function. Endothelial cell dysfunction (ECD) is characterized by decreased endothelial nitric oxide synthase (eNOS) activity. Cationic amino acid transporter-1 (CAT-1), the specific arginine transporter for eNOS, has been shown to modulate eNOS activity. We hypothesize that DMSO inhibits eNOS activity through modulation of its selective arginine supplier CAT-1. We studied the effect of DMSO on arginine transport, NO2/NO3 generation as an index of NO production, as well as CAT-1 and Protein Kinase C alpha (PKC-α) (CAT-1 inhibitor) protein expression in human umbilical vein endothelial cell cultures (HUVECs). DMSO 2.5% and 3.5% (v/v) significantly attenuated arginine transport, a phenomenon which was prevented by co-incubation with l-arginine (1 mM). The aforementioned findings were accompanied by a decrease in NO2/NO3 generation. DMSO significantly increased the abundance of phosphorylated CAT-1 (the inactive form) and phosphorylated PKC-α protein, an effect that was attenuated by l-arginine. GO 6976 (PKC-α antagonist) prevented the decrease in arginine transport caused by DMSO. DMSO also induced profound transient morphological changes in HUVECs’ structure but these were not related to its effect on arginine transport. In conclusion, DMSO inhibits NO generation by endothelial cells through modulation of CAT-1 activity.
Mesh:Cationic Amino Acid Transporter 1,Cells, Cultured,Dimethyl Sulfoxide,Human Umbilical Vein Endothelial Cells,Humans,Nitric Oxide,Nitric Oxide Synthase Type III
Keywords:Arginine transport,CAT-1,Cytoskeleton,DMSO,Endothelial function,HUVEC,Nitric oxide,PKC-α
DMSO inhibits NO generation by endothelial cells through modulation of CAT-1 activity
significantly attenuated arginine transport
induced profound transient morphological changes in HUVECs [human umbilical vein endothelial cell cultures]

DMSO Represses Inflammatory Cytokine Production from Human Blood Cells and Reduces Autoimmune Arthritis. [27031833]
Dimethyl sulfoxide (DMSO) is currently used as an alternative treatment for various inflammatory conditions as well as for cancer. Despite its widespread use, there is a paucity of data regarding its safety and efficacy as well as its mechanism of action in human cells. Herein, we demonstrate that DMSO has ex-vivo anti-inflammatory activity using Escherichia coli- (E. coli) and herpes simplex virus-1 (HSV-1)-stimulated whole human blood. Specifically, we found that between 0.5%-2%, DMSO significantly suppressed the expression of many pro-inflammatory cytokines/chemokines and prostaglandin E2 (PGE2). However, a significant reduction in monocyte viability was also observed at 2% DMSO, suggesting a narrow window of efficacy. Anti-inflammatory concentrations of DMSO suppressed E. coli-induced ERK1/2, p38, JNK and Akt phosphorylation, suggesting DMSO acts on these signaling pathways to suppress inflammatory cytokine/chemokine production. Although DMSO induces the differentiation of B16/F10 melanoma cells in vitro, topical administration of DMSO to mice subcutaneously implanted with B16 melanoma cells was ineffective at reducing tumor growth, DMSO was also found to block mouse macrophages from polarizing to either an M1- or an M2-phenotype, which may contribute to its inability to slow tumor growth. Topical administration of DMSO, however, significantly mitigated K/BxN serum-induced arthritis in mice, and this was associated with reduced levels of pro-inflammatory cytokines in the joints and white blood cell levels in the blood. Thus, while we cannot confirm the efficacy of DMSO as an anti-cancer agent, the use of DMSO in arthritis warrants further investigation to ascertain its therapeutic potential.
Mesh:Animals,Arthritis,Blood Cells,Cell Differentiation,Cell Line, Tumor,Cell Survival,Chemokines,Cytokines,Dimethyl Sulfoxide,Dinoprostone,Escherichia coli,Female,Herpesvirus 1, Human,Humans,Macrophages,Male,Melanoma,Mice,Mice, Inbred C57BL,Mitogen-Activated Protein Kinase 1,Mitogen-Activated Protein Kinase 3,Signal Transduction

stem cells
[DMSO Promotes Hematopoietic Differentiation of Human Embryonic Stem Cells in vitro]. [28641611]
To explore the role of dimethyl sulfoxide (DMSO) in the hematopoietic differentiation of human embryonic stem cells (hESCs).
– The role of DMSO in hematopoietic differentiation of hESC was investigated by using a established stepwise hematopoietic differentiation system from hESC, immunofluorescouse assay and flow cytometry. Furthermore, the window phase of DMSO action was explored by adding it to the different stage of hematopoietic differentiation.
– Immunofluorescence and flow cytometry analysis showed that DMSO significantly promoted the generation of CD43 hematopoietic progenitor cells (HPC). The flow cytometry demonstrated that DMSO profoundly promoted the generation of APLNR lateral plate mesoderm cells and CD31CD34 hemogenic endothelium progenitors (HEP). The addition of DMSO in the window phase of lateral plate mesoderm cell generation could markedly improve the generation of hematopoietic progenitor cells.
– DMSO promotes hematopoietic differentiation of hESC through enhancing the generation of APLNR positive lateral plate mesoderm cells. The addition of DMSO in the window phase of lateral plate mesoderm cell generation can significantly improve the generation of hematopoietic progenitor cells.
Mesh:Cell Differentiation,Dimethyl Sulfoxide,Free Radical Scavengers,Hemangioblasts,Hematopoietic Stem Cells,Human Embryonic Stem Cells,Humans

DMSO efficiently down regulates pluripotency genes in human embryonic stem cells during definitive endoderm derivation and increases the proficiency of hepatic differentiation. [25659159]
Definitive endoderm (DE) is one of the three germ layers which during in vivo vertebrate development gives rise to a variety of organs including liver, lungs, thyroid and pancreas; consequently efficient in vitro initiation of stem cell differentiation to DE cells is a prerequisite for successful cellular specification to subsequent DE-derived cell types [1, 2]. In this study we present a novel approach to rapidly and efficiently down regulate pluripotency genes during initiation of differentiation to DE cells by addition of dimethyl sulfoxide (DMSO) to Activin A-based culture medium and report its effects on the downstream differentiation to hepatocyte-like cells.
-   Human embryonic stem cells (hESC) were differentiated to DE using standard methods in medium supplemented with 100ng/ml of Activin A and compared to cultures where DE specification was additionally enhanced with different concentrations of DMSO. DE cells were subsequently primed to generate hepatic-like cells to investigate whether the addition of DMSO during formation of DE improved subsequent expression of hepatic markers. A combination of flow cytometry, real-time quantitative reverse PCR and immunofluorescence was applied throughout the differentiation process to monitor expression of pluripotency (POUF5/OCT4 & NANOG), definitive endoderm (SOX17, CXCR4 & GATA4) and hepatic (AFP & ALB) genes to generate differentiation stage-specific signatures.
-   Addition of DMSO to the Activin A-based medium during DE specification resulted in rapid down regulation of the pluripotency genes OCT4 and NANOG, accompanied by an increase expression of the DE genes SOX17, CXCR4 and GATA4. Importantly, the expression level of ALB in DMSO-treated cells was also higher than in cells which were differentiated to the DE stage via standard Activin A treatment.
Mesh:Antigens, Differentiation,Cell Differentiation,Cryoprotective Agents,Dimethyl Sulfoxide,Down-Regulation,Embryonic Stem Cells,Hepatocytes,Humans,Pluripotent Stem Cells
  • perhaps significant to cancer

The effect of dimethyl sulfoxide on hepatic differentiation of mesenchymal stem cells. [24978442]
Adipose tissue-derived mesenchymal stem cells (AT-MSCs) are suitable choices in autologous stem cell treatment of liver-associated diseases due to their hepatic differentiation potential. Dimethyl sulfoxide (DMSO) is an amphipathic molecule with potential of delivering both lipophilic and hydrophilic agents into cells, also a common cryoprotectant for freezing of the cells. DMSO was used in some protocols for induction of AT-MSCs towards hepatocyte like cells. However, the effect of DMSO on hepatogenic differentiation of AT-MSCs were not surveyed, previously. In the present study, we aimed at evaluation of the effect of DMSO on differentiation of AT-MSCs into hepatic lineage.
– We isolated mesenchymal stem cells (MSCs) from adipose tissue, and then verifies multi-potency and surface markers of AT-MSCs . Isolated AT-MSCs randomly dispensed in four groups including Group 1: HGF treated, 2: HGF+ DMSO treated, 3: HGF+ DMSO+ OSM treated, and group control for a period of 3 weeks in the expansion medium without serum; EGF and bFGF were also included in the first days of inductions. The morphologic changes during induction period was observed with microscopy. The secretion of albumin (ALB) of the differentiating MSCs was investigated using ELISA, and urea production was evaluated using colorimetric assay. The qRT-PCR was performed for quantitation of hepatocyte marker genes including AFP, ALB, CK18, HNF4a, and HNF6. The glycogen storage of differentiated cells was visualized by periodic-acid Schiff‘s staining.
– The results demonstrate that DMSO speeds up hepatic differentiation of AT-MSCs characterized by rapid changes in morphology; higher expression of hepatic marker gene (ALB) in both mRNA and protein level (P < 0.05); also increased transcriptional levels of other liver genes including CK18, HNF4a, and HNF6 (P < 0.01); and moreover, greater percentage of glycogen storage(p < 0.05) in DMSO-treated groups.
– DMSO catalyzes hepatic differentiation; therefore, using DMSO for acceleration of the hepatogenic protocols of AT-MSCs appears advantageous.
Mesh:Adipose Tissue,Biomarkers,Cell Differentiation,Cell Line,Cell Survival,Dimethyl Sulfoxide,Fibroblast Growth Factors,Gene Expression,Glycogen,Hepatocyte Nuclear Factor 4,Hepatocyte Nuclear Factor 6,Hepatocytes,Humans,Immunophenotyping,Keratin-18,Liver,Mesenchymal Stromal Cells,Primary Cell Culture,alpha-Fetoproteins
Keywords:AFP,Adipose tissue–derived mesenchymal stem cells,CK18,DMSO,HNF4a,HNF6,glycogen storage,hepatic differentiation

Dimethyl sulfoxide inhibits NLRP3 inflammasome activation. [24380723]
Dimethyl sulfoxide (DMSO) is an amphipathic molecule that is commonly/widely used as a solvent for biological compounds. In addition, DMSO has been studied as a medication for the treatment of inflammation, cystitis, and arthritis. Based on the anti-inflammatory characteristics of DMSO, we elucidated the effects of DMSO on activation of inflammasomes, which are cytoplasmic multi-protein complexes that mediate the maturation of interleukin (IL)-1β by activating caspase-1 (Casp1). In the present study, we prove that DMSO attenuated IL-1β maturation, Casp1 activity, and ASC pyroptosome formation via NLRP3 inflammasome activators. Further, NLRC4 and AIM2 inflammasome activity were not affected, suggesting that DMSO is a selective inhibitor of the NLRP3 inflammasomes. The anti-inflammatory effect of DMSO was further confirmed in animal, LPS-endotoxin sepsis and inflammatory bowel disease models. In addition, DMSO inhibited LPS-mediating IL-1s transcription. Taken together, DMSO shows anti-inflammatory characteristics, attenuates NLRP3 inflammasome activation, and mediates inhibition of IL-1s transcription.
Mesh:Animals,Anti-Inflammatory Agents,CARD Signaling Adaptor Proteins,Calcium-Binding Proteins,Carrier Proteins,Caspase 1,Cells, Cultured,DNA-Binding Proteins,Dimethyl Sulfoxide,Disease Models, Animal,Humans,Inflammasomes,Inflammatory Bowel Diseases,Interleukin-1beta,Lipopolysaccharides,Macrophages,Mice,Mice, Inbred C57BL,NLR Family, Pyrin Domain-Containing 3 Protein,Sepsis

Characterization of damaged skin by impedance spectroscopy: chemical damage by dimethyl sulfoxide. [23820866]
To relate changes in the electrochemical impedance spectra to the progression and mechanism of skin damage arising from exposure to dimethyl sulfoxide (DMSO).
-   Electrochemical impedance spectra measured before and after human cadaver skin was treated with neat DMSO or phosphate buffered saline (control) for 1 h or less were compared with electrical circuit models representing two contrasting theories describing the progression of DMSO damage. Flux of a model lipophilic compound (p-chloronitrobenzene) was also measured.
-   The impedance spectra collected before and after 1 h treatment with DMSO were consistent with a single circuit model; whereas, the spectra collected after DMSO exposure for 0.25 h were consistent with the model circuits observed before and after DMSO treatment for 1 h combined in series. DMSO treatments did not significantly change the flux of p-chloronitrobenzene compared to control.
-   Impedance measurements of human skin exposed to DMSO for less than about 0.5 h were consistent with the presence of two layers: one damaged irreversibly and one unchanged. The thickness of the damaged layer increased proportional to the square-root of treatment time until about 0.5 h, when DMSO affected the entire stratum corneum. Irreversible DMSO damage altered the lipophilic permeation pathway minimally.
Mesh:Aged,Cadaver,Dielectric Spectroscopy,Diffusion Chambers, Culture,Dimethyl Sulfoxide,Electric Impedance,Humans,Male,Models, Biological,Nitrobenzenes,Permeability,Phenols,Skin,Solvents
  • skin damage on normal people (not cadavers) though?
Dimethyl sulfoxide at high concentrations inhibits non-selective cation channels in human erythrocytes. [23531832]
Dimethyl sulfoxide (DMSO), a by-product of the pulping industry, is widely used in biological research, cryobiology and medicine. On cellular level DMSO was shown to suppress NMDA-AMPA channels activation, blocks Na+ channel activation and attenuates Ca2+ influx (Lu and Mattson 2001). In the present study we explored the whole-cell patch-clamp to examine the acute effect of high concentrations of DMSO (0.1-2 mol/l) on cation channels activity in human erythrocytes. Acute application of DMSO (0.1-2 mol/l) dissolved in Cl--containing saline buffer solution significantly inhibited cation conductance in human erythrocytes. Inhibition was concentration-dependent and had an exponential decay profile. DMSO (2 mol/l) induced cation inhibition in Cl-- containing saline solutions of: 40.3 ± 3.9% for K+, 35.4 ± 3.1% for Ca2+ and 47.4 ± 1.9% for NMDG+. Substitution of Cl- with gluconate- increased the inhibitory effect of DMSO on the Na+ current. Inhibitory effect of DMSO was neither due to high permeability of erythrocytes to DMSO nor to an increased tonicity of the bath media since no effect was observed in 2 mol/l glycerol solution. In conclusion, we have shown that high concentrations of DMSO inhibit the non-selective cation channels in human erythrocytes and thus protect the cells against Na+ and Ca2+ overload. Possible mechanisms of DMSO effect on cation conductance are discussed.
Mesh:Calcium,Cations,Chloride Channels,Dimethyl Sulfoxide,Dose-Response Relationship, Drug,Electrophysiology,Erythrocytes,Gluconates,Humans,Ion Channels,Membrane Potentials,Patch-Clamp Techniques,Time Factors
  • high concentrations of DMSO inhibit the non-selective cation channels in human erythrocytes and thus protect the cells against Na+ and Ca2+ overload
Dimethyl sulfoxide reduces hepatocellular lipid accumulation through autophagy induction. [22722716]
Induction of autophagy is known not only to regulate cellular homeostasis but also to decrease triglyceride accumulation in hepatocytes. The aim of this study is to investigate whether DMSO (dimethyl sulfoxide) has a beneficial role in free fatty acid-induced hepatic fat accumulation.   In HepG2 cells, treatment with 0.5 mM palmitate for six hours significantly increased lipid and triglyceride (TG) accumulation, assessed by Oil-red O staining and TG quantification assay. Treatment with 0.01% DMSO for 16 h statistically reduced palmitate-induced TG contents. Pretreatment of 10 mM 3-methyladenine (3MA) for 2 h restored hepatocellular lipid contents, which were attenuated by treatment with DMSO. DMSO increased LC3-II conversion and decreased SQSTM1/p62 expression in a time and dose-dependent manner. In addition, the number of autophagosomes and autolysosomes, as seen under an electron microscopy, as well as the percentage of RFP-LAMP1 colocalized with GFP-LC3 dots in cells transfected with both GFP-LC3 and RFP-LAMP1, as seen under a fluorescent microscopy, also increased in DMSO-treated HepG2 cells. DMSO also suppressed p-eIF2α/p-EIF2S1, ATF4, p-AKT1, p-MTOR and p-p70s6k/p-RPS6KB2 expression as assessed by western blotting. Knockdown of ATF4 expression using siRNA suppressed ATF4 expression and phosphorylation of AKT1, MTOR and RPS6KB2, but increased LC3-II conversion. DMSO reduced not only soluble but also insoluble mtHTT (mutant huntingtin aggregates) expressions, which were masked in the presence of autophagy inhibitor. DMSO, a kind of chemical chaperone, activated autophagy by suppressing ATF4 expression and might play a protective role in the development of fatty acid-induced hepatosteatosis.
Mesh:Activating Transcription Factor 4,Autophagy,Biomarkers,Cell Proliferation,Dimethyl Sulfoxide,Down-Regulation,Endoplasmic Reticulum Stress,Hep G2 Cells,Hepatocytes,Humans,Lipid Metabolism,Palmitic Acid,Peptides,Phosphorylation,Protein Structure, Quaternary,Proto-Oncogene Proteins c-akt
Keywords:ATF4,autophagy,dimethyl sulfoxide,hepatosteatosis

DMSO, a kind of chemical chaperone, activated autophagy by suppressing ATF4 expression and might play a protective role in the development of fatty acid-induced hepatosteatosis.

Dimethyl sulfoxide promotes the multiple functions of the tumor suppressor HLJ1 through activator protein-1 activation in NSCLC cells. [22529897]
Dimethyl sulfoxide (DMSO) is an amphipathic molecule that displays a diversity of antitumor activities. Previous studies have demonstrated that DMSO can modulate AP-1 activity and lead to cell cycle arrest at the G1 phase. HLJ1 is a newly identified tumor and invasion suppressor that inhibits tumorigenesis and cancer metastasis. Its transcriptional activity is regulated by the transcription factor AP-1. However, the effects of DMSO on HLJ1 are still unknown. In the present study, we investigate the antitumor effects of DMSO through HLJ1 induction and demonstrate the mechanisms involved.
-   Low-HLJ1-expressing highly invasive CL1-5 lung adenocarcinoma cells were treated with various concentrations of DMSO. We found that DMSO can significantly inhibit cancer cell invasion, migration, proliferation, and colony formation capabilities through upregulation of HLJ1 in a concentration-dependent manner, whereas ethanol has no effect. In addition, the HLJ1 promoter and enhancer reporter assay revealed that DMSO transcriptionally upregulates HLJ1 expression through an AP-1 site within the HLJ1 enhancer. The AP-1 subfamily members JunD and JunB were significantly upregulated by DMSO in a concentration-dependent manner. Furthermore, pretreatment with DMSO led to a significant increase in the percentage of UV-induced apoptotic cells.
-   Our results suggest that DMSO may be an important stimulator of the tumor suppressor protein HLJ1 through AP-1 activation in highly invasive lung adenocarcinoma cells. Targeted induction of HLJ1 represents a promising approach for cancer therapy, which also implied that DMSO may serve as a potential lead compound or coordinated ligand for the development of novel anticancer drugs.
Mesh:Apoptosis,Carcinoma, Non-Small-Cell Lung,Cell Line, Tumor,Cell Movement,Cell Proliferation,Cell Survival,Dimethyl Sulfoxide,Enhancer Elements, Genetic,Gene Expression,Gene Expression Regulation, Neoplastic,HSP40 Heat-Shock Proteins,Humans,Lung Neoplasms,Transcription Factor AP-1,Transcriptional Activation,Tumor Suppressor Proteins
  • DMSO may be an important stimulator of the tumor suppressor protein HLJ1 through AP-1 activation

Rapamycin enhances dimethyl sulfoxide-mediated growth arrest in human myelogenous leukemia cells. [22497230]
Rapamycin and its derivatives have been proposed in the treatment of leukemia based on their cytostatic effects, but their possible role in differentiation therapy is less explored. The aim of the present study was to investigate the possible beneficial effects of the combination of rapamycin and dimethyl sulfoxide (DMSO) on growth arrest and differentiation of acute myelogenous leukemia (AML) cells. In myeloblastic HL-60, promyelocytic NB4, monocytic U937, immature KG-1 and erythro-megakaryocytic K562 cell lines, rapamycin alone had modest inhibitory effects, DMSO inhibited proliferation in a dose-dependent manner, and the combination of rapamycin and DMSO reduced the number of viable cells significantly more than either agent alone. In NB4 cells, rapamycin had no statistically significant effects on the DMSO-mediated increase in expression of CD11b, but increased apoptosis. These results demonstrate that rapamycin enhances DMSO-mediated growth arrest, and suggest that mTOR (mammalian target of rapamycin) inhibitors may have beneficial effects in differentiation therapy of AML.
Mesh:Cell Proliferation,Dimethyl Sulfoxide,Drug Synergism,HL-60 Cells,Humans,Leukemia, Myeloid, Acute,Ribosomal Protein S6 Kinases, 70-kDa,Sirolimus,TOR Serine-Threonine Kinases

Dimethyl sulfoxide enhances effectiveness of skin antiseptics and reduces contamination rates of blood cultures. [22378911]
Effective skin antisepsis is of central importance in the prevention of wound infections, colonization of medical devices, and nosocomial transmission of microorganisms. Current antiseptics have a suboptimal efficacy resulting in substantial infectious morbidity, mortality, and increased health care costs. Here, we introduce an in vitro method for antiseptic testing and a novel alcohol-based antiseptic containing 4 to 5% of the polar aprotic solvent dimethyl sulfoxide (DMSO). The DMSO-containing antiseptic resulted in a 1- to 2-log enhanced killing of Staphylococcus epidermidis and other microbes in vitro compared to the same antiseptic without DMSO. In a prospective clinical validation, blood culture contamination rates were reduced from 3.04% for 70% isopropanol-1% iodine (control antiseptic) to 1.04% for 70% isopropanol-1% iodine-5% DMSO (P < 0.01). Our results predict that improved skin antisepsis is possible using new formulations of antiseptics containing strongly polarized but nonionizing (polar aprotic) solvents.
Mesh:2-Propanol,Adult,Anti-Infective Agents, Local,Bacterial Load,Blood,Dimethyl Sulfoxide,Drug Synergism,Female,Humans,Iodine,Male,Microbial Viability,Middle Aged,Skin,Staphylococcus epidermidis

[Efficacy of a topical treatment protocol with dimethyl sulfoxide 50% in type 1 complex regional pain syndrome]. [22266201]
Evaluate the efficacy of a topical treatment protocol with DMSO 50% to alleviate inflammatory processes in type 1 complex regional pain syndrome (CRPS) with a course of less than 1 year.
– Retrospective study performed in a traumatology hospital on patients with type 1 CRPS for whom a standard treatment algorithm was prescribed with stepwise administration of oral drugs and interventional techniques. Patients also received topical DMSO 50% cream as a magistral formula. The follow-up period, lasting until patient discharge, or during 1 year for persistent cases, included 6 visits: baseline, 15 days, 1 month, 3 months, 6 months, and 1 year. The evaluation was performed using a visual analogue scale (VAS) as the main efficacy variable. Secondary variables were the Likert scale for quality of life and the limb capacity variable (range of motion, strength, overall limb function). A questionnaire designed for the study was also given.
– Overall decrease in VAS score in the 29 patients was 3.09 points. The Likert scale score increased by 1.36 points. The scores measuring limb capacity increased to 12.03 for range of motion and to 3 in strength with overall function rated «moderate».
– Topical application of DMSO 50% associated with a treatment algorithm decreased pain intensity according to the VAS score with results approaching absence of pain, and led to higher scores on the quality of life questionnaire. Topical DMSO 50% is an additional tool for use in treating CRPS I. Its side effects are scarce and it provides an overall sense of relief and lessens rigidity.
Mesh:Adult,Algorithms,Anti-Infective Agents, Local,Complex Regional Pain Syndromes,Dimethyl Sulfoxide,Female,Humans,Male,Middle Aged,Pain Management,Pain Measurement,Quality of Life,Retrospective Studies,Treatment Outcome,Young Adult

Dimethyl sulfoxide: an effective penetration enhancer for topical administration of NSAIDs. [22030943]
Dimethyl sulfoxide (DMSO) is a molecule with a long history in pharmaceutics and is now well established as a penetration enhancer in topical pharmaceutical formulations. It is currently used for this purpose in diclofenac sodium topical solution (approved in the United States to treat signs and symptoms of osteoarthritis) and idoxuridine topical solution (approved in Europe for the treatment of herpes zoster). This article reviews the mechanism of action of DMSO as a pharmaceutical penetration enhancer, the characteristics of the molecule that facilitate transdermal drug delivery, and studies of efficacy and safety. The clinical use of pharmaceutical-grade DMSO as a penetration enhancer is supported by the robust data that have accumulated over the past 3 decades demonstrating the favorable safety and tolerability profile. Dimethyl sulfoxide is a safe and effective mechanism for facilitating the transdermal delivery of both hydrophilic and lipophilic medications to provide localized drug delivery.
Mesh:Administration, Topical,Anti-Inflammatory Agents, Non-Steroidal,Dimethyl Sulfoxide,Drug Delivery Systems,Drug Synergism,Herpes Zoster,Humans,Osteoarthritis,Skin Absorption,Solvents

Dimethyl sulfoxide (DMSO) attenuates the inflammatory response in the in vitro intestinal Caco-2 cell model. [21878375]
This study aimed to investigate dose effects of dimethyl sulfoxide (DMSO) (0.05-1%) on the intestinal inflammatory response in confluent- and differentiated-Caco-2 cells stimulated with interleukin (IL)-1β or a pro-inflammatory cocktail for 24 h. Cyclooxygenase-2 (COX-2) activity was assayed by incubating inflamed cells with arachidonic acid and then measuring prostaglandin-E(2) (PGE(2)) produced. Soluble mediators (IL-8, IL-6, macrophage chemoattractant protein-1 (MCP-1), and COX-2-derived PGE(2)) were quantified by enzyme immunoassays and mRNA expression of 33 proteins by high throughput TaqMan Low Density Array. Data showed that DMSO decreased induced IL-6 and MCP-1 secretions in a dose-dependent manner (P<0.05), but not IL-8; these effects were cell development- and stimulus- independent. Moreover, in IL-1β-stimulated confluent-cells, DMSO dose-dependently reduced COX-2-derived PGE(2) (P<0.05). DMSO at 0.5% decreased significantly mRNA levels of 14 proteins involved in the inflammatory response (including IL-6, IL-1α, IL-1β, and COX-2). Thus, DMSO at low concentrations (0.1-0.5%) exhibits anti-inflammatory properties in the in vitro intestinal Caco-2 cell model. This point is important to be taken into account when assessing anti-inflammatory properties of bioactive compounds requiring DMSO as vehicle, such as phenolic compounds, in order to avoid miss-interpretation of the results.
Mesh:Anti-Inflammatory Agents,Caco-2 Cells,Chemokine CCL2,Dimethyl Sulfoxide,Dinoprostone,Dose-Response Relationship, Drug,Humans,Interleukin-1beta,Interleukin-6,NF-kappa B,RNA, Messenger

Dimethyl sulfoxide induces heme oxygenase-1 expression via JNKs and Nrf2 pathways in human umbilical vein endothelial cells. [21533649]
Dimethyl sulfoxide (DMSO) has recently been proposed as an anti-inflammatory and free radical scavenging agent. However, the mechanisms by which DMSO mediates its therapeutic effects are unclear. In this paper, we investigated the capability of DMSO to up-regulate heme oxygenase-1(HO-1) expression, as well as the possible underlying mechanisms in human umbilical vein endothelial cells (HUVECs). DMSO induced HO-1 expression both at the level of mRNA and protein in dose-and time-dependent manners in HUVECs, resulting in increased HO-1 activity. The pharmacological inhibition of cJun-N-terminal kinases (JNKs) blocked the DMSO-induced HO-1 up-regulation, while inhibition of extracellular regulated kinase and p38-MAPK did not block heme oxygenase-1 up-regulation. In addition, the phosphorylation of JNKs was initiated by DMSO, indicating the involvement of this kinase in the observed response. DMSO increased the nuclear translocation of NF-E2-related factor 2 (Nrf2) and enhanced its binding to the anti-oxidant response element. Inhibition of Nrf2 synthesis by small interfering RNA molecules subsequently inhibited HO-1 expression induced by DMSO, indicating DMSO’s role in inducing HO-1 expression via Nrf2 activation. Utilizing these findings, the present study identified DMSO as a novel inducer of HO-1 expression and identified the underlying mechanisms involved in this process.
Mesh:Cell Nucleus,Cells, Cultured,Dimethyl Sulfoxide,Enzyme Assays,Gene Expression,Heme Oxygenase-1,Human Umbilical Vein Endothelial Cells,Humans,MAP Kinase Kinase 4,NF-E2-Related Factor 2,Phosphorylation,Protein Transport,RNA Interference,Signal Transduction

Systematic review of the nutritional supplements dimethyl sulfoxide (DMSO) and methylsulfonylmethane (MSM) in the treatment of osteoarthritis. [18417375]
Conventional treatment of osteoarthritis (OA) with non-steroidal anti-inflammatory drugs is associated with serious gastrointestinal side effects and in view of the recent withdrawal of some cyclo-oxygenase-2 inhibitors, identifying safer alternative treatment options is needed. The objective of this systematic review is to evaluate the existing evidence from randomised controlled trials of two chemically related nutritional supplements, dimethyl sulfoxide (DMSO) and methylsulfonylmethane (MSM) in the treatment of OA to determine their efficacy and safety profile.
– The electronic databases [Cochrane Library, Medline, Embase, Amed, Cinahl and NeLH (1950 to November 2007)] were searched. The search strategy combined terms: osteoarthritis, degenerative joint disorder, dimethyl sulfoxide, DMSO, methylsulfonylmethane, MSM, clinical trial; double-blind, single blind, RCT, placebo, randomized, comparative study, evaluation study, control. Inclusion and exclusion criteria were applied. Data were extracted and quality was assessed using the JADAD scale.
– Six studies were included [evaluating a total of 681 patients with OA of the knee for DMSO (N=297 on active treatment); 168 patients for MSM (N=52 on active treatment)]. Two of the four DMSO trials, and both MSM trials reported significant improvement in pain outcomes in the treatment group compared to comparator treatments, however, methodological issues and concerns over optimal dosage and treatment period, were highlighted.
– No definitive conclusion can currently be drawn for either supplement. The findings from all the DMSO studies need to be viewed with caution because of poor methodology including; possible unblinding, and questionable treatment duration and dose. The data from the more rigorous MSM trials provide positive but not definitive evidence that MSM is superior to placebo in the treatment of mild to moderate OA of the knee. Further studies are now required to identify both the optimum dosage and longer-term safety of MSM and DMSO, and definitive efficacy trials.
Mesh:Anti-Inflammatory Agents,Dietary Supplements,Dimethyl Sulfoxide,Free Radical Scavengers,Humans,Osteoarthritis,Randomized Controlled Trials as Topic,Sulfones

Dimethyl sulfoxide inhibits tissue factor expression, thrombus formation, and vascular smooth muscle cell activation: a potential treatment strategy for drug-eluting stents. [17000906]
Subacute stent thrombosis is a major clinical concern, and the search for new molecules to cover stents remains important. Dimethyl sulfoxide (DMSO) is used for preservation of hematopoietic progenitor cells and is infused into patients undergoing bone marrow transplantation. Despite its intravenous application, the impact of DMSO on vascular cells has not been assessed.
– In human endothelial cells, monocytes, and vascular smooth muscle cells (VSMC), DMSO inhibited tissue factor (TF) expression and activity in response to tumor necrosis factor-alpha or thrombin in a concentration-dependent manner. DMSO did not exert any toxic effects as assessed by phase-contrast microscopy, trypan blue exclusion, and lactate dehydrogenase release. Real-time polymerase chain reaction revealed that inhibition of TF expression occurred at the mRNA level. This effect was mediated by reduced activation of the mitogen-activated protein kinases c-Jun terminal NH2 kinase (51+/-6%; P=0.0005) and p38 (50+/-3%; P<0.0001) but not p44/42 (P=NS). In contrast to TF, DMSO did not affect expression of TF pathway inhibitor or plasminogen activator inhibitor-1. In vivo, DMSO treatment suppressed TF activity (41%; P<0.002) and prevented thrombotic occlusion in a mouse carotid artery photochemical injury model. DMSO also inhibited VSMC proliferation (70%; P=0.005) and migration (77%; P=0.0001) in a concentration-dependent manner; moreover, it prevented rapamycin and paclitaxel-induced upregulation of TF expression.
– DMSO suppresses TF expression and activity, as well as thrombus formation; in addition, it inhibits VSMC proliferation and migration. Given its routine use in modern clinical practice, we propose DMSO as a novel strategy for coating drug-eluting stents and treating acute coronary syndromes.
Mesh:Animals,Carotid Artery Thrombosis,Cell Movement,Cell Proliferation,Cells, Cultured,Dimethyl Sulfoxide,Disease Models, Animal,Gene Expression Regulation,Humans,Mice,Muscle, Smooth, Vascular,Myocytes, Smooth Muscle,Thromboplastin,Thrombosis

Oral dimethyl sulfoxide for systemic amyloid A amyloidosis complication in chronic inflammatory disease: a retrospective patient chart review. [16799886]
Amyloid A amyloidosis is an obstinate disease complication in chronic inflammatory disease, and there are few effective therapies. The objective of this study was to investigate the effect of oral dimethyl sulfoxide (DMSO) on amyloid A amyloidosis.
– Fifteen secondary amyloid A amyloidosis patients (4 men, 11 women; age, 23-70 years) were treated with DMSO between 1995 and 2003. DMSO was administered orally in all patients at a dose of 3-20 g/day. The clinical symptoms together with the renal and gastrointestinal functions were evaluated before and after treatment.
– Among the 15 patients, amyloid A amyloidosis was a complication of rheumatoid arthritis (RA) in 10, of Crohn’s disease in 4, and of Adult Still’s disease in 1. Nine cases mainly involved the kidney, with renal dysfunction and proteinuria, five mainly involved the gastrointestinal tract, with protein-losing gastroenteropathy and intractable diarrhea, and one involved both gastrointestinal and renal amyloidosis. DMSO treatment was successful in 10 (66.7%) of the 15 patients (RA, 6/10; Crohn’s disease, 4/4; Adult Still’s disease, 0/1). Eight weeks of DMSO administration improved the renal function and proteinuria in five out of ten renal amyloidosis patients, but had no effect on those patients with severe and/or advanced renal dysfunction. With regard to gastrointestinal amyloidosis, gastrointestinal symptoms, including diarrhea and protein-losing gastroenteropathy, were improved in six patients. No serious side effects were encountered with the DMSO treatment.
– Oral administration of DMSO is an effective treatment for amyloid A amyloidosis, especially for gastrointestinal involvement and the early stage of renal dysfunction.
Mesh:Administration, Oral,Adult,Aged,Amyloidosis,Diarrhea,Dimethyl Sulfoxide,Female,Humans,Male,Medical Records,Middle Aged,Retrospective Studies,Serum Amyloid A Protein,Stomach Diseases

Dimethyl sulfoxide potentiates death receptor-mediated apoptosis in the human myeloid leukemia U937 cell line through enhancement of mitochondrial membrane depolarization. [15998540]
Dimethyl sulfoxide (DMSO) is a widely used prototypical chemical inducer of cell differentiation. In the present study, the effects of DMSO on susceptibility of human myeloid leukemia U937 cells towards ligation of distinct death receptors (DRs) were investigated. DMSO sensitized cells towards induction of apoptosis by anti-Fas antibody, tumour necrosis factor-alpha or Apo2 ligand/TNF-related apoptosis-inducing ligand (TRAIL). Apart from increasing Fas levels, DMSO did not affect expression of proteins in death signal transduction, such as Bcl-2 family proteins, FADD, caspase-3 and -8, the inhibitor of apoptosis proteins (IAPs) or cFLIP(L). However, DMSO significantly potentiated mitochondrial membrane depolarization, suggesting that this mechanism might be involved in sensitisation of myeloid cells to DR-mediated apoptosis.
Mesh:Adaptor Proteins, Signal Transducing,Apoptosis,Apoptosis Regulatory Proteins,CASP8 and FADD-Like Apoptosis Regulating Protein,Caspase 3,Caspase 8,Caspases,Cryoprotective Agents,Dimethyl Sulfoxide,Fas-Associated Death Domain Protein,Humans,Intracellular Signaling Peptides and Proteins,Leukemia, Myeloid,Membrane Glycoproteins,Mitochondria,Mitochondrial Membranes,Proto-Oncogene Proteins c-bcl-2,TNF-Related Apoptosis-Inducing Ligand,Tumor Necrosis Factor-alpha,U937 Cells,fas Receptor

Toxicity to topical dimethyl sulfoxide in a pediatric patient with anthracycline extravasation. [15770831]
Accidental extravasation of vesicant chemotherapy may cause important tissue injuries. Nowadays, the majority of authors propose topical dimethyl sulfoxide (DMSO), with or without local cooling, as the treatment of choise efor anthracyclines extravasation. No significant toxicity has been reported when DMSO is used as topical treatment. This report describes a case of local toxicity consisting of severe pain after its use in a pediatric patient. An illustration shows the extravasation area.
Mesh:Antibiotics, Antineoplastic,Antineoplastic Combined Chemotherapy Protocols,Child, Preschool,Dimethyl Sulfoxide,Extravasation of Diagnostic and Therapeutic Materials,Female,Humans,Leukemia, Myelomonocytic, Acute

[Treatment of pulmonary amyloidosis with dimethyl sulfoxide–a case report]. [15500151]
Metastatic lung tumor was suspected in a 52-year-old woman who showed multiple nodules on her chest radiographs. Conventional examinations did not define the diagnosis, and so a biopsy was performed using video-assisted thoracoscopic surgery. Pathological examination demonstrated deposits of amorphous materials which were stained red by Congo red staining, even after potassium permanganate treatment. Green birefringence was also observed in the deposits under a polarized light microscope. A diagnosis of localized pulmonary amyloidosis with AL type amyloid protein was made, and therapy with dimethyl sulfoxide (10 ml/day) was started. During the two-year therapy, little exacerbation on pulmonary nodules was observed. It was suggested that dimethyl sulfoxide inhibited the progression of the disease.
Mesh:Amyloidosis,Biopsy,Dimethyl Sulfoxide,Female,Humans,Lung,Lung Diseases,Middle Aged,Tomography, X-Ray Computed

Massive intracranial hemorrhage associated with the ingestion of dimethyl sulfoxide. [15171490]
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.
Mesh:Diagnosis, Differential,Dimethyl Sulfoxide,Fatal Outcome,Humans,Intracranial Hemorrhages,Male,Middle Aged,Poisoning,Seizures,Solvents,Tomography, X-Ray Computed

  • can cause hemorrhage in patients with metastaic brain lesions

Anti-angiogenic effects of dimethyl sulfoxide on endothelial cells. [12951474]
Dimethyl sulfoxide (DMSO) has anti-inflammatory and analgesic properties and is the only intravesical agent approved by the FDA for the treatment of interstitial cystitis. While it is known that DMSO has numerous biological effects on cell differentiation and alteration of cell-surface carbohydrate structures, the anti-inflammatory mechanism of DMSO has been not clear yet. Therefore, further investigation of DMSO in terms of inflammation therapy is needed. This study assessed the in vitro anti-angiogenic effects of DMSO on human aorta endothelial cells to clarify one of the mechanisms of its anti-inflammatory activity. DMSO did not affect expression of E-selectin on endothelial cells in the presence of TNF-alpha. Furthermore, DMSO effectively inhibited capillary tube formation; this mechanism would be due to suppression of matrix metalloproteinase-2 (MMP-2) production. These results provide useful knowledge about the anti-inflammatory effects of DMSO and the regulatory mechanism of MMP-2.
Mesh:Angiogenesis Inhibitors,Cells, Cultured,Dimethyl Sulfoxide,E-Selectin,Endothelial Cells,Enzyme-Linked Immunosorbent Assay,Gelatin,Humans,Matrix Metalloproteinase 2,Microtubules

! !
Intermittent use of topical dimethyl sulfoxide in macular and papular amyloidosis. [9888342]
Severe and therapy-resistant pruritus is the most prominent feature of macular (MA) and lichen (LA) amyloidosis that leads to further amyloid deposition by recurrent frictional trauma to the epidermis. Of the various therapeutic modalities with variable success, the most encouraging and beneficial effect has been observed with topical dimethyl sulfoxide (DMSO) therapy. In a previous study, we achieved marked clinical improvement in nine of 10 patients in a daily treatment regimen over 6-20 weeks, but relapses occurred in the post-treatment follow-up period. The aims of this study are to investigate whether the patients would benefit from intermittent therapy and to determine the optimal application interval of DMSO to maintain the relief of symptoms.
– Thirteen patients with histopathologically verified cutaneous amyloidosis (five MA, two LA and six biphasic) were enrolled in the study. They were treated once daily with a 50 or 100% DMSO solution until pruritus disappeared. Then, DMSO was applied at increasing intervals until the widest effective application interval for maintenance of relief was reached. Patients were regularly followed-up by a scoring system for pruritus, papules, and pigmentation, control biopsies, photographs, blood biochemistry, and side-effects.
– The mean time required for the disappearance of pruritus was 4.1 weeks. Remarkable flattening of the papules was achieved after an average therapy period of 9 weeks. After a total therapy period of 6.5 months, a nearly 50% remission in pigmentation and >70% flattening of papules were achieved. The widest effective DMSO application interval was 8.6 days. The side-effects of therapy were contact urticaria, desquamation, burning sensation, and garlic-like breath odor, which were more prominent with the higher concentration of DMSO. In interval therapy, side-effects were tolerated more easily than in daily therapy. No reduction of amyloid deposits was revealed in control biopsies.
– Locally applied DMSO can break the vicious “pruritus-amyloid deposition-pruritus” cycle in patients with MA and LA. In addition to its daily use, interval therapy seems to maintain this effect and enables patients to tolerate side-effects more easily.
Mesh:Administration, Topical,Adult,Amyloidosis,Dimethyl Sulfoxide,Drug Administration Schedule,Female,Humans,Male,Middle Aged,Pruritus,Skin Diseases

Dimethyl sulfoxide (DMSO) causes a reversible inhibition of telomerase activity in a Burkitt lymphoma cell line. [9680092]
Telomerase is an enzyme that is required for maintenance of telomeres. This enzyme has been shown to be present in germline tissues and majority of tumors and tumor cell lines. The regulation of telomerase is an area of active investigation in different models because, potentially, inhibition of this enzyme could be important in cancer therapy. To study the regulation of this enzyme in lymphoma cell lines, we used DMSO to produce a reversible G0/G1 arrest in Raji cell line, as shown earlier [Sawai M, Takase K, Teraoka H, Tsukada K. Reversible G1 arrest in the cell cycle of human lymphoid cell lines by dimethyl sulphoxide. Exp Cell Res 1990;187:4-10].
– In this study, we use a highly quantifiable conventional (non-amplified) assay to study the effect of DMSO on telomerase. In addition, we studied cellular proliferation and cell cycle profiles of the cells treated and, subsequently, released from DMSO induced blockage.
– In this model, DMSO reversibly inhibited telomerase activity that could be restored after release from the blockage. The inhibition of telomerase seems to parallel cellular proliferation and it appears that telomerase is regulated upon entry into the cell cycle. This view is consistent with other previously published views on relationship of telomerase with exit from cell cycle.
– Our observations demonstrate a novel effect of DMSO on cellular mechanisms in Raji cell line. It may provide an attractive model to further study regulation of telomerase in this cell line.
Mesh:Burkitt Lymphoma,Cell Cycle,Cell Division,Dimethyl Sulfoxide,Enzyme Inhibitors,Humans,Telomerase,Tumor Cells, Cultured

Dimethyl sulfoxide-induced apoptosis in human leukemic U937 cells. [8721951]
Dimethyl sulfoxide (DMSO), which induces differentiation of myeloid cells, was found to cause apoptosis in human leukemic U937 cells. Apoptosis was assessed by DNA electrophoresis and flow cytometry. The time needed to induce apoptosis varied from a few hours to 2-3 days, depending on the concentration of DMSO used. The plasma membrane remained intact long after DNA fragmentation had occurred. DMSO-induced apoptosis was inhibited by zinc ions and, to a lesser extent, by the protein kinase C activator: phorbol 12-myristate 13-acetate (PMA). Cycloheximide and actinomycin D did not prevent DMSO-induced apoptosis, showing that U937 cells do not require protein or RNA synthesis to undergo apoptosis. DMSO induced apoptosis despite the expression of the anti-apoptotic Bcl-2 protein in U937 cells. The amount of Bcl-2 remained unchanged during DMSO-induced apoptosis.
Mesh:Apoptosis,Cell Line,Cell Membrane,Cell Survival,Cycloheximide,DNA, Neoplasm,Dactinomycin,Dimethyl Sulfoxide,Electrophoresis, Agar Gel,Flow Cytometry,Humans,Kinetics,Leukemia,Protein Kinase C,Tetradecanoylphorbol Acetate,Time Factors,Tumor Cells, Cultured,Zinc

Dimethyl sulfoxide suppresses apoptosis in Burkitt’s lymphoma cells. [7843285]
Previous reports have suggested that dimethyl sulfoxide (DMSO) may be a useful reversible G1 arresting agent for synchronizing Raji Burkitt’s lymphoma cells (K. Takase et al. (1992) Cell Growth Differ. 3, 515-521; M. Sawai et al. (1990) Exp. Cell Res. 187, 4-10). We have therefore critically evaluated several aspects of DMSO’s effects using Daudi and Ramos Burkitt’s lymphoma (BL) cells. In BL cells starved in the presence or absence of DMSO for 4 to 6 days (approximately four to six doubling times), the following observations were noted: (A) Both Daudi and Ramos cells show increased cell synchrony accompanied by apoptosis when starved in RPMI 1640 supplemented with 10% fetal calf serum (FCS). Inclusion of 1.5% DMSO causes a diminution in apoptosis with minimal effects on synchrony. (B) Lowering the FCS concentration to 5% induces apoptosis. DMSO-mediated protection from apoptosis is observed in Daudi but not in Ramos. (C) When human serum (10%) is used instead of FCS, Daudi cells show no apoptosis and DMSO is without effect on cell cycle distribution. By contrast, Ramos cells show significant apoptosis, which is prevented by the inclusion of DMSO. (D) When starved in a chemically defined medium (AIM-V), both Daudi and Ramos cells show significant apoptosis. DMSO protects Ramos from apoptosis under these conditions. (E) Upon removal of DMSO, both Daudi and Ramos cells reenter the cell cycle but with significant apoptosis. (F) The protective effect of DMSO from apoptosis is observed in a narrow range of concentration between 1 and 2%. At higher concentration, DMSO itself induces apoptosis. These results suggest that DMSO itself prevents apoptosis, an effect which may present as an apparent effect on cell synchrony.
Mesh:Apoptosis,B-Lymphocytes,Blood,Burkitt Lymphoma,Cell Cycle,Cell Differentiation,Culture Media,DNA, Neoplasm,Dimethyl Sulfoxide,Humans,Tumor Cells, Cultured
– in lymphoma The protective effect of DMSO from apoptosis is observed in a narrow range of concentration between 1 and 2%. At higher concentration, DMSO itself induces apoptosi

[DMSO induced differentiation of human gastric adenocarcinoma cell line MGC 80-3]. [7801721]
The in vitro effects of dimethyl sulfoxide (DMSO) on MGC 80-3 cells were studied by light microscopy, transmission electron microscopy and biochemical methods. The results indicated that the inhibitory effects of DMSO on the growth of MGC 80-3 cells was concentration dependent and 1.5% DMSO was suitable in the present study. The growth rate, mitotic index, colony forming efficiency and Con A-aggregation of the cells treated with 1.5% DMSO in vitro for 7 days was reduced respectively by 35.15%, 18/1000, 90% and 55.8%. It was remarkable that the activity of membrane-associated alkaline phosphatase, which is not presented in normal human gastric mucosa, was decreased by 90% in the treated cells. There was a 75% decrease of the rate of tumorigenesis in the treated cells as compared with the tumorigenic rate of the untreated MGC 80-3 cells inoculated into nude mice. Gross morphological changes of MGC 80-3 cells treated with 1.5% DMSO were evident including enlargement and flatness of the cells, stumpy microvillies instead of long and rigid ones, and extremely well-developed Golgi apparatus and rough endoplasmic reticulum. This data indicated that DMSO was able to induce differentiation of MGC 80-3 cells and change their malignant phenotypes.
Mesh:Adenocarcinoma,Animals,Cell Transformation, Neoplastic,Dimethyl Sulfoxide,Female,Humans,Male,Mice,Mice, Inbred BALB C,Mice, Nude,Stomach Neoplasms,Tumor Cells, Cultured

Dimethyl sulfoxide inhibits the binding of granulocyte/macrophage colony-stimulating factor and insulin to their receptors on human leukemia cells. [8439959]
Numerous agents can induce the terminal differentiation of leukemia cells in vitro, and this action has been found to be of therapeutic value in the treatment of acute promyelocytic leukemia. The proximal site of action of the prototypical chemical inducer of differentiation, dimethyl sulfoxide (DMSO), is not known. In this study, DMSO was found to rapidly cause a 45% to 85% reduction in the specific binding of the growth factors granulocyte/macrophage colony-stimulating factor and insulin to their respective cell surface receptors on HL-60 human acute promyelocytic leukemia cells. Significant inhibition of binding was first observed after 30 min of DMSO treatment, occurred at both 4 degrees C and 37 degrees C, and was due to a DMSO-induced decrease in apparent receptor affinity, with little change in receptor number. A similar inhibition of insulin binding was seen with a second inducer of differentiation, hexamethylene bisacetamide. Kinetic studies demonstrated that DMSO enhanced the rate of insulin dissociation from its receptor. The inhibition of insulin binding by DMSO was also observed in a cell-free extract, suggesting that the effect was not a cell-mediated response to DMSO treatment. DMSO blocked the insulin-induced stimulation of protein tyrosine phosphorylation. These studies suggest that one action of DMSO may be the disruption of the structure and/or organization of cell surface receptors that regulate growth and differentiation.
Mesh:Cell Differentiation,Dimethyl Sulfoxide,Granulocyte-Macrophage Colony-Stimulating Factor,Humans,Insulin,Leukemia, Promyelocytic, Acute,Receptor, Insulin,Receptors, Granulocyte-Macrophage Colony-Stimulating Factor,Tumor Cells, Cultured

Cytotoxicity of dimethyl sulfoxide and antineoplastic combinations against human tumors. [3369622]
Five human tumor reference cell lines were tested in vitro against 0 percent, 5 percent, and 10 percent DMSO; four antineoplastic agents; and combinations of 5 percent or 10 percent DMSO plus each antineoplastic agent. Synergistic cytotoxicity between DMSO and antineoplastic agents against each cell line were demonstrated. We have concluded that delivery of standard doses of antineoplastic agents in 5 percent or 10 percent DMSO may be useful in the treatment of some tumors because of the marked increase in tumoricidal effect seen with some DMSO and drug combinations. Alternatively, lower doses of antineoplastic agents might be delivered in DMSO, producing the same cytotoxic effect as a full dose of drug without DMSO but with less systemic toxicity.
Mesh:Antineoplastic Agents,Antineoplastic Combined Chemotherapy Protocols,Cisplatin,Dimethyl Sulfoxide,Doxorubicin,Drug Screening Assays, Antitumor,Drug Synergism,Fluorouracil,Humans,Tumor Cells, Cultured,Vinblastine

Effect of dimethyl sulfoxide on human carcinoma cells, inhibition of plasminogen activator synthesis, change in cell morphology, and alteration of response to cholera toxin. [3837848]
Human carcinoma HEp-3 lost its tumorigenic and metastatic potential upon prolonged culture in vitro. This change was accompanied by a reduced production of plasminogen activator (PA) of the urokinase type (uPA), which is secreted by HEp-3 cells, a change in response to effectors that modulate uPA production, and an alteration of cell morphology. Similar but more rapid changes occurred when malignant HEp-3 cells were exposed to dimethyl sulfoxide (DMSO). uPA activity in the culture medium dropped below 50% of the control level within 6 h after the addition of DMSO and became undetectable after 24 h of treatment. This drop in uPA activity was not caused by an increased production of PA inhibitors. The cell-associated uPA decreased to 25 to 30% of the control level within 6 h of DMSO treatment and remained at this level for at least 96 h; the reduced uPA production was partially accounted for by a rapid decrease in the functional and chemical concentration of uPA mRNA. In contrast, the concentrations of most of the abundant mRNA species did not appear to be significantly affected, and cell growth was only slightly inhibited in the presence of DMSO. Malignant HEp-3 cells treated with DMSO responded to cholera toxin with an enhanced production of uPA, and their morphology became indistinguishable from that of nonmalignant HEp-3 cells grown in vitro for prolonged periods of time. All of the above changes were fully and rapidly reversible. The inhibitory effect of DMSO on PA production appears to be specific for uPA of human cell lines.
Mesh:Cell Line,Cholera Toxin,Dimethyl Sulfoxide,Humans,Neoplasms,Plasminogen Activators

brain hypertension treatment
Dimethyl sulfoxide for the treatment of intracranial hypertension: a preliminary trial. [6462399]
Dimethyl sulfoxide (DMSO) has shown promise as a drug for the treatment of intracranial hypertension. In this report, we describe our experience in six patients, two who received a bolus administration of 10% DMSO and four who received a 20% solution titrated against the intracranial pressure (ICP). Five of the patients in this series suffered from severe head injury, and one had a cortical venous thrombosis associated with pregnancy. The first two patients were treated with a rapid infusion of a 10% solution of DMSO. Initially, the ICP was satisfactorily controlled using this method. Over time, however, fluid overload, severe electrolyte disturbances, and an ultimate loss of ICP control occurred. In subsequent patients, a 20% solution titrated against the ICP was used. Although ICP control was better achieved using this method of administration, problems with fluid management and electrolytes occurred again despite a high level of vigilance. In addition, because of the solvent properties of DMSO and its propensity over time to dissolve most standard intravenous infusion systems, mechanical difficulties in its administration were encountered in all six patients. The mechanism of action of DMSO is not well understood. It differs from the barbiturates, but acts too rapidly to function solely as a diuretic. The drug is extremely complex to use, and difficulties with its administration may make its risks ultimately greater than its potential benefits. Until more laboratory data are available concerning its use and better delivery systems are developed, neurosurgeons are cautioned against treating intracranial hypertension with DMSO.
Mesh:Adult,Brain Injuries,Dimethyl Sulfoxide,Dose-Response Relationship, Drug,Female,Hematoma, Epidural, Cranial,Hematoma, Subdural,Hemodynamics,Humans,Intracranial Embolism and Thrombosis,Intracranial Pressure,Male,Middle Aged,Pregnancy,Pseudotumor Cerebri,Water-Electrolyte Balance

Dimethyl sulfoxide in the management of patient with brain swelling and increased intracranial pressure after severe closed head injury. [2290457]
The results of a prospective study on the effects of dimethyl sulfoxide (DMSO) in patients with severe closed head injuries causing brain edema and increase in intracranial pressure (ICP) are presented. 10 patients were selected and carefully analyzed according to Glasgow coma scale (GCS) scores and severity of brain edema. The results demonstrate that DMSO rapidly reduces the raised ICP, increases the cerebral perfusion pressure (CPP) and improves the neurological course and outcome without affecting the systemic blood pressure and patient responsiveness except only in one patient. We also point out that the rebound effect does not occur.
Mesh:Adolescent,Adult,Brain Concussion,Brain Edema,Child,Dimethyl Sulfoxide,Female,Glasgow Coma Scale,Humans,Intracranial Pressure,Male,Middle Aged,Pseudotumor Cerebri,Survival Rate

Inability of dimethyl sulfoxide to increase brain uptake of water-soluble compounds: implications to chemotherapy for brain tumors. [3978658]
There is conflicting evidence as to whether dimethyl sulfoxide (DMSO) can reversibly open the blood-brain barrier and augment brain uptake of water-soluble compounds, including anticancer agents. To investigate this, 125I-human serum albumin, horseradish peroxidase, or the anticancer drug melphalan was administered iv to rats or mice, either alone or in combination with DMSO. Some animals received an additional ip priming dose of DMSO. The regional brain concentrations of each substance were measured after the animals were killed. DMSO administration did not significantly increase the brain uptake of any of the compounds as compared to control uptakes. These results do not support prior reports that DMSO increases the permeability of water-soluble agents across the blood-brain barrier.
Mesh:Animals,Blood-Brain Barrier,Brain,Brain Neoplasms,Cerebrovascular Circulation,Dimethyl Sulfoxide,Horseradish Peroxidase,Humans,Male,Melphalan,Osmolar Concentration,Rats,Rats, Inbred F344,Rats, Inbred Strains,Serum Albumin,Solubility
– doesn’t mention molecular weights. Perhaps more BS

Transformation in the presence of dimethyl sulfoxide facilitates recovery of Epstein-Barr virus. [6298146]
Human umbilical cord blood lymphocytes were immortalized by infection with Epstein-Barr virus (EBV) in the presence of various concentrations of dimethyl sulfoxide (DMSO). 13 continuous lymphoblastoid cell lines were established. DMSO did not affect the efficiency of transformation and establishment of these lines. After a period of 2 months in culture, the lines were tested for EBV production by lethal irradiation (6,000 rad) from a 60Co source and subsequent cocultivation with primary umbilical cord lymphocytes. Cell lines transformed in the presence of 2% DMSO yielded transforming activity in 46.6% of test cultures, compared with 9.5% for lines established without DMSO in the medium. These findings imply that a permanent change in the host/virus relationship resulted from a brief exposure (48 h) to DMSO at the time of transformation.
Mesh:Cell Line,Cell Transformation, Viral,Dimethyl Sulfoxide,Fetal Blood,Herpesvirus 4, Human,Humans,Lymphocytes

Dimethyl sulfoxide as a cholesterol-lowering agent in cultured fibroblasts exposed to low density lipoproteins. [7074119]
Confluent cultures of human skin fibroblasts were exposed to medium containing high levels of low density lipoproteins (LDL-cholesterol equivalent to 400 micrograms per ml) and 0 or 2% dimethyl sulfoxide (DMSO). The uptake and accumulation of cellular cholesterol from LDL were reduced significantly (30%) in the DMSO-treated cells as compared to the controls. The reduction in cellular sterol was due almost exclusively to a significant decrease (50%) in cholesterol ester accumulation. Incubation of cells with 125I-labelled LDL showed clearly that DMSO did not act by increasing the secretion of cholesterol from the cell, but rather by significantly decreasing the binding, internalization and degradation of exogenous LDL. De novo synthesis of cholesterol from [14C]acetate was measured and found to correlate inversely with cellular sterol levels in either control or DMSO-treated cells.
Mesh:Acetates,Anticholesteremic Agents,Cells, Cultured,Cholesterol,Cholesterol, LDL,Dimethyl Sulfoxide,Fibroblasts,Humans,Infant, Newborn,Kinetics,Lipoproteins, LDL,Male,Skin

  • significant decrease (50%) in cholesterol ester accumulation
  • significantly decreasing the binding, internalization and degradation of exogenous LDL
Reversible cellular damage by dimethyl sulfoxide reflected by release of marker enzymes for intracellular fractions. [7458406]
Irritative human skin reactions were induced by dimethyl sulfoxide (DMSO). Suction blisters were raised on these areas within 1.5 h after their induction and simultaneously on normal skin. The activities of marker enzymes for subcellular fractions in the suction blisters were determined. In suction blisters raised on the DMSO induced wheals significantly higher values of the cytosol enzyme lactate dehydrogenase and also some higher values of the lysosomal marker alpha-mannosidase were found than in blisters produced on normal skin. Membrane-bound marker enzymes for subcellular fractions were not elevated. Since the skin is macroscopically completely normal 24 h after application of DMSO, our results indicate that the induction of a certain membrane damage with release of intracellular enzymes does not necessarily lead to cellular necrosis.
Mesh:Aged,Blister,Cell Membrane,Dimethyl Sulfoxide,Humans,Male,Middle Aged,Skin,Subcellular Fractions

  • the induction of a certain membrane damage with release of intracellular enzymes does not necessarily lead to cellular necrosis

Inhibition of insulin receptor binding by dimethyl sulfoxide. [420863]
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.
Mesh:Depression, Chemical,Dimethyl Sulfoxide,Dose-Response Relationship, Drug,Humans,Lymphocytes,Receptor, Insulin
– reduced affinity of the insulin receptor

Activation of viruses in human tumors by 5-iododeoxyuridine and dimethyl sulfoxide. [5008440]
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.
Mesh:Adenocarcinoma,Cells, Cultured,Deoxyuridine,Dimethyl Sulfoxide,Endoplasmic Reticulum,Humans,Inclusion Bodies, Viral,Iodine,Male,Microscopy, Electron,Middle Aged,Oncogenic Viruses,Rhabdomyosarcoma

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