In vitro culture of Toxoplasma gondii in HL-60 cells cnd cell-mediated immunity against Toxoplasma in dimethylsulfoxide(DMSO)-induced HL-60 cells, i.e., differentiation into granulocytes, were pursued. HL-60 cells were treated with various concentrations of DMSO, and 1.3%(v/v) for 3 day incubation was chosen as the optimal condition for differentiation into granulocytes. The degree of differentiation was assayed in physiological and functional aspects in addition to morphological point. When treated with 1.3% DMSO for 3 days, HL-60 cells did not synthesize DNA materials beyond background level, and showed active chemotactic response to chemotactic peptide, formyl-methionyl-leucyl-phenylalanine(FMLP). Morphologically promyelocytes of high nuclear/cytoplasmic(N/C) ratio changed to granulocytes of relatively low N/C ratio. The relationships between HL-60 cells or DMSO-induced HL-60 cells and Toxoplasma were examined after stain with Giemsa and fluorescent dye (acridine orange). HS-60 cells did not show any sign of toxoplasmacidal activity but showed intracellular proliferation of Toxoplasma to form rosette for 72 hr co-culture. In contrast, DMSO-induced HL-60 cells phagocytosed Toxoplasma within 1 hr, and performed a process of intracellular digestion of Toxoplasma thereafter. With the above results, it is suggested that phagosome-lysosome fusion is one of the critical events for the parasitism by Toxoplasma or for susceptibility of host cells. The in vitro culture system of this study has offered a defined condition to study the protozoan parasite-host cell interactions.
parasitology-protozoa ; Toxoplasma gondii ; HL-60 cells ; dimethylsulfoxide ; in vitro culture ; dimethylsulfoxide

No abstract available.
Cystitis, Interstitial* ; Dimethyl Sulfoxide*

The classic type of transient receptor potential channel (TRPC) is a molecular candidate for Ca2+-permeable cation channel in mammalian cells. TRPC5 is rapidly desensitized after activation by G protein-coupled receptor. Herein we report the effect of dimethyl sulfoxide (DMSO) on the desensitization of TRPC5. TRPC5 was initially activated by muscarinic stimulation with 50microM carbachol (CCh) and then decayed rapidly even in the presence of CCh (desensitization). DMSO in the pipette solution slowed the rate of this desensitization. Under the control conditions, TRPC5 current spontaneously declined to 6+/-1% of the initial peak amplitude 60 sec after CCh application and to 1+/-0.5% after 120 sec. But, in the presence of 0.01%, 0.1% and 1% DMSO, TRPC5 current spontaneously declined to 55+/-2%, 68+/-1% and 100+/-0.2% of the initial peak amplitude 60 sec after CCh application and to 38+/-2%, 61+/-1% and 100+/-1% after 120 sec, respectively. The results suggest that DMSO can internally attenuate the desensitization of TRPC5 current through unknown mechanisms that remain to be elucidated.
Carbachol ; Dimethyl Sulfoxide*

PURPOSE: To investigate the effect of intravitreal melatonin on retina in rabbit. METHODS: In four pigmented rabbit, melatonin was intravitreally injected 100 mu g/0.1 ml, 300 mu g/0.1 ml concentration in left eye, DMSO was injected in right eye as control. we examined gross fundus finding and electroretinogram and then light and electronic microscopic findings at 24 hours and 1 week with both eye. RESULTS: intravitreally melatonin injected eye at 100 mu g/0.1 ml, 300 mu g/0.1 ml concentration and control eye at 1 day and 1 week, significant difference was not shown in gross fundus finding, electroretinogram, light and electronic microscopic finding. Additionally edema, toxic effect change was not found in retina. CONCLUSIONS: Intravitreally injected melatonin has not influenced on retina grossly, histologically, physiologically at 100 mu g/0.1 ml and 300 mu g/0.1 ml concentration. Further study is required about toxic effect of melatonin over 300 mu g/0.1 ml concentration and clinical usefulness of melatonin in retina.
Dimethyl Sulfoxide ; Edema ; Intravitreal Injections ; Melatonin* ; Retina*

The present study was to assess the effect of ultrarapid freezing on the development of 1-cell mouse zygote using cryoprotectants, DMSO (dimethyl sulfoxide) or PROH (1,2-propanediol). We investigated the effect of the type and concentration of cryoprotectant, and of the temperature and time of prefreezing equilibration on their capacity to develop to the blastocyst stage in vitro. The concenration, the equilibration temperature, and the exposure time seemed to serve as an important factor in ultrarapid freezing of 1-cell mouse zygotes. In addition to the exposure time and the concentration of cryoprotectant appeared to play a key role in the development of the embryo. In general, the development of the embryo was more effective at 3degrees C than 23degrees C and 4.5 M than 3 M for 3 to 5 minutes. At 23degrees C the development of the embryo was stimulated by DMSO while at 3degrees C it was stimulated by PROH. Thus it has been suggested that there exists a correlation between the concentration of cryoprotectants and exposure time in the development of the embryo. In conclusion, we found that for ultrarapid freezing of mouse 1-cell embryos in DMSO, or PROH-based solution, viability shown optimum depending on the cryoprotectant, the concentration of the cryoprotectant and on the temperature and the duration of equilibration.
Animals ; Blastocyst ; Dimethyl Sulfoxide ; Embryonic Structures ; Freezing* ; Mice* ; Zygote*

New born rat heart cells were dissociated using trypsin and/or collagenase to elucidate the dissociation efficiency of these two enzymes. And the effect of dimethyl sulfoxide during and immediately after cell dissociation was also investigated to clarify the so-called protective activity of dimethyl sulfoxide on cell performance. The results can be summarized as follows. 1. Cold trypsin 18 hours pretreatment followed by warm collagenase treatment resulted best cell viability and cell yield. 2. Single warm trypsin treatment gave the poorest result. 3. Dimethyl sulfoxide did not seem to play any protective role during or immediately after rat heart cell dissociation. It had very damaging effect on rat heart cells.
Animals ; Cell Survival ; Collagenases* ; Dimethyl Sulfoxide* ; Heart* ; Rats* ; Trypsin*

Various concentrations, including 100%, 75%, 50%, and 25% of dimethyl sulfoxide (DMSO) were applied on the back of albino rats, followed by ultraviolet irradiation after 30 minutes. Biopsy specimens were taken 6, 12, 24, 36, and 48 hours afters ultraviolet irradiation without local anesthesia. The macroscopic and histologic findings were as follows. 1. Mild degree of erytheme appeared only on the site of the highest concentration (100%) of DMSO. 2. Vacuolization of the prickle cells appeared slightly later on the sites of higher concentrations (75% and 100%) than those of lower concentrations and control. 3. After 48 hours post-irradiation, there was no detectable vacuolization on the sites of higher concentrations, whereas marked vacuolization still remained on the other sites. 4. More pronounced epidermal thickening could be observed on the sites of higher concentrations than the sites of lower concentrations and control. 5. The dermal edema was more completely disappeared on the sites of higher concentrations than the sites of lower concentrations and control, 48 hours after ultraviolet irradiation.
Anesthesia, Local ; Animals ; Biopsy ; Dimethyl Sulfoxide* ; Edema ; Rats

To elucidate arsenic-induced oxidative DNA damage, the genotoxicity of arsenic in human cells was comparatively studied with single cell gel electrophoresis (SCGE) assay in combination with the observation of the protective effects of dimethyl sulfoxide (DMSO) and catalase. Arsenic, at the concentration of 2.4 μM by coincubation for 24 hours, significantly induced DNA damage in HL60, a human promyelocytic leukemia cell line. In contrast, significant DNA damage was found in human mononucleocytes at the concentration of 4.8 μM or above. The cells were incubated separately with DMSO (12 mM/l), a well-known hydroxyl radical (OH-) scavenger, and catalase (1,300 U/ml), a hydrogen peroxide (H2O2) scavenger, for 6 hours and then further coincubated with various concentrations of arsenic for 24 hours at 37°C and 5% CO2. The findings showed that both DMSO and catalase significantly reduced the arsenic-induced tail moment, a parameter of total damaged DNA, in HL60 and mononucleocytes. Hence our findings indicate that arsenic, with micromolar concentrations, induces typical and various extents of DNA damage in human cells via reactive oxygen species in a dose-dependent manner.
Human ; DNA Damage ; Arsenic ; Dimethyl Sulfoxide ; Arsenic measurement

The Onyx system has been well established in recent years as a very important material in the treatment of arteriovenous malformations (AVMs). When using the Onyx, it is essential to wait for the creation of a plug around the tip of the catheter, which enables the effective forward penetration of Onyx. Recent reports have shown that the introduction of a dimethyl sulfoxide compatible dual-lumen balloon microcatheter improves the efficiency of AVM embolization. We report our recent experience of two cases of intracranial AVM embolization using Onyx and the transarterial balloon-assisted technique. In both cases, the procedures were successfully performed and the nidus of the AVM was totally occluded in a relatively short time. This technique may enable immediate forward flow and penetration of Onyx without concern about reflux. It may also reduce the procedure time and increase the angiographic occlusion rate. Navigation of the dual-lumen balloon microcatheter nevertheless remains a challenge.
Arteriovenous Malformations ; Catheters ; Dimethyl Sulfoxide ; Intracranial Arteriovenous Malformations*

The effects of dimethyl sulfoxide (DMSO) were studied in two groups of Xenopus oocytes, one expressing ATP sensitive K+ (KATP) channel comprised of sulfonylurea receptor SUR1 and inwardly rectifying K+ channel subunit Kir6.2, and the other expressing renal KATP channel ROMK2. At concentrations of 0.3~10% (vol/vol) DMSO inhibited whole cell Kir6.2/SUR1 currents elicited by bath application of sodium azide (3 mM) in a concentration-dependent manner. The inhibition constant and Hill coefficient were 2.93% and 1.62, respectively. ROMK2 currents, however, was not affected significantly by DMSO. The results support the idea that DMSO inhibits KATP channel expressed in Xenopus oocyte through a protein-specific mechanism(s) that remains to be further elucidated.
Adenosine Triphosphate ; Baths ; Dimethyl Sulfoxide* ; Oocytes* ; Sodium Azide ; Xenopus*