• BMB Reports
• /
• v.43 no.9
• /
• pp.622-628
• /
• 2010

Dimethyl sulfoxide (DMSO) can be reduced to dimethyl sulfide by MsrA, which stereospecifically catalyzes the reduction of methionine-S-sulfoxide to methionine. Our previous study showed that DMSO can competitively inhibit methionine sulfoxide reduction ability of yeast and mammalian MsrA in both in vitro and in vivo, and also act as a non-competitive inhibitor for mammalian MsrB2, specific for the reduction of methionine-R-sulfoxide, with lower inhibition effects. The present study investigated the effects of DMSO on the physiological antioxidant functions of methionine sulfoxide reductases. DMSO elevated hydrogen peroxide-mediated Saccharomyces cerevisiae cell death, whereas it protected human SK-Hep1 cells against oxidative stress. DMSO reduced the protein-carbonyl content in yeast cells in normal conditions, but markedly increased protein-carbonyl accumulation under oxidative stress. Using Msr deletion mutant yeast cells, we demonstrated the DMSO's selective inhibition of the antioxidant function of MsrA in S. cerevisiae, resulting in an increase in oxidative stress-induced cytotoxicity.

• BMB Reports
• /
• v.42 no.9
• /
• pp.580-585
• /
• 2009

Dimethyl sulfoxide (DMSO) is widely used in chemistry and biology as a solvent and as a cryoprotectant. It is also used as a pharmaceutical agent for the treatment of interstitial cystitis and rheumatoid arthritis. Previous reports described DMSO as being reduced by methionine-S-sulfoxide reductase (MsrA). However, little is known about the DMSO reduction capability of methionine-R-sulfoxide reductase (MsrB) or its effect on the catalysis of methionine sulfoxide reduction. We show that mammalian MsrB2 and MsrB3 were unable to reduce DMSO. This compound inhibited MsrB2 activity but did not inhibit MsrB3 activity. We further determined that DMSO functions as an inhibitor of MsrA and MsrB2 in the reduction of methionine sulfoxides via different inhibition mechanisms. DMSO competitively inhibited MsrA activity but acted as a non-competitive inhibitor of MsrB2 activity. Our study also demonstrated that DMSO inhibits in vivo methionine sulfoxide reduction in yeast and mammalian cells.

• Journal of Yeungnam Medical Science
• /
• v.5 no.2
• /
• pp.111-119
• /
• 1988

To elucidate the effects of dimethyl sulfoxide on myocardial and endothelial cells in culture, the cells were exposed to 10% dimethyl sulfoxide in culture medium for 1 hour at 48 hours after cell isolation. The general morphology and the cytochemical reaction of marker enzymes for mitochondria and Golgi complexes were investigated. The results were summarized as follows. : 1. DMSO induced elongation and narrowing of the cells and increase of mitochondrial reaction in myocardial cells. 2. DMSO induced destruction and disruption of myofibrils in myocardial cells resulting in increase of contractile activities. 3. In the endothelial cells, DMSO suppressed proliferative activities but thiamine pyrophosphatase reactions were enhanced indicating increase of Goigi complex activity. 4. DMSO seemed to hamper with the adhesiveness and motility of the endothelial cells causing the decrease of the number of cells in vitro.

• The Korean Journal of Physiology and Pharmacology
• /
• v.5 no.2
• /
• pp.157-163
• /
• 2001

The effects of dimethyl sulfoxide (DMSO) were studied in two groups of Xenopus oocytes, one expressing ATP sensitive $K^+\;(K_{ATP})$ channel comprised of sulfonylurea receptor SUR1 and inwardly rectifying $K^+$ channel subunit Kir6.2, and the other expressing renal $K_{ATP}$ channel ROMK2. At concentrations of $0.3{\sim}10%$ (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 $K_{ATP}$ channel expressed in Xenopus oocyte through a protein-specific mechanism(s) that remains to be further elucidated.

• Korean Journal of Ichthyology
• /
• v.19 no.2
• /
• pp.173-177
• /
• 2007

A series of experiments were conducted to compare the effects of various diluents and cryoprotectants on the motility and survival rate in cryopreservation of the red seabream, Pagrus major sperm. Sperm was efficiently cryopreserved using 300 mM glucose as a diluent. Two cryoprotectant, dimethyl sulfoxide (DMSO) and glycerol, were added to 300 mM glucose to formulate the extenders at concentrations between 5% and 30% by volume for freezing. The highest post-thawed sperm motility and survival rate were obtained with 10% DMSO.

• Journal of the Korean Chemical Society
• /
• v.19 no.1
• /
• pp.3-10
• /
• 1975

The partial molal volumes and relative viscosities of tetraethylammonium chloride in a series of dimethyl sulfoxide (DMSO)-water mixtures were measured at $30^{\circ}C$. A maximum structuredness of solvent, that leads to a minimum viscosity A-coefficient and a maximum viscosity B-coefficient of the Jones-Dole equation(${\eta}_r=1+AC^{1/2}$ + BC), was found at 0.2${\sim}$0.3 mole fraction of DMSO. The solvent structure, that leads to a minimum partial molal volume due to the maximum electrostrictive effect of chloride ion and to a minimum viscosity B-coefficient, was found at 0.4${\sim}$0.5 mole fraction of DMSO. An approximate relationship between the limiting effective flowing volume, $V_e^{\circ}$, and the B-coefficient was found to be B = 2.5 $V_e^{\circ}$ in the Einstein equation.

• The Korean Journal of Physiology and Pharmacology
• /
• v.11 no.5
• /
• pp.227-231
• /
• 2007

The classic type of transient receptor potential channel(TRPC) is a molecular candidate for $Ca^{2+}$-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 $50{\mu}M$ 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 $6{\pm}1%$ of the initial peak amplitude 60 sec after CCh application and to $1{\pm}0.5%$ after 120 sec. But, in the presence of 0.01%, 0.1% and 1% DMSO, TRPC5 current spontaneously declined to $55{\pm}2%,\;68{\pm}1%\;and\;100{\pm}0.2%$ of the initial peak amplitude 60 sec after CCh application and to $38{\pm}2%,\;61{\pm}1%\;and\;100{\pm}1%$ after 120 see, respectively. The results suggest that DMSO can internally attenuate the desensitization of TRPC5 current through unknown mechanisms that remain to be elucidated.

• Korean Journal of Food Science and Technology
• /
• v.32 no.1
• /
• pp.42-49
• /
• 2000

A new method for the quantitative determination of capsaicinoids in microcapsule has been developed. Among seventeen solvents tested for solubilizing wall material (gum arabic and modified starch) of microcapsule, dimethyl sulfoxide (DMSO) was selected as an optimal solvent. The most appropriate mixing ratio of microcapsule to DMSO for solubilizing wall material was 1 to 10(w/v). Appropriate carriersolubilizing temperature and time were $55^{\circ}C$ and 30 min, respectively. Also conditions for extracting oleoresin from the solubilized microcapsule were studied. The mixing ratio of ethanol to DMSO was optimal at 8 to 1(v/v). Optimized vortexing time was 5 min at 40㎐. Pecipitant was obtained by centrifugation at 21000 rpm for 15 min. The precipitant was reextracted with ethanol. The extracted supernatants were combined and adjusted to final volume of 25 ml. Extracted solutions were analyzed for quantitation of total capsaicinoids by employing HPLC and for quantitation of total carotenoids by spectrophotometric method. This method can be used to monitor changes of capsacinoid during manufacturing or storage of red pepper oleoresin microcapsule powder.

• Journal of the korean veterinary medical association
• /
• v.22 no.5
• /
• pp.266-283
• /
• 1986

• KSBB Journal
• /
• v.27 no.5
• /
• pp.313-318
• /
• 2012

Dimethyl sulfoxide (DMSO) increased the intracellular calcium ion concentration in stably transfected Drosophila melanogaster S2 cells expressing recombinant cyclooxygenase 1 (COX-1). DMSO did not increase the Drosophila NOS (dNOS) transcript level in calcium chelator-treated cells. Expression of recombinant COX-1 due to DMSO was diminished in cells treated with calcium chelators or channel blockers. Our results indicate that an increased intracellular calcium ion concentration due to DMSO is associated with up-regulation of the dNOS gene, leading to enhanced expression of COX-1.