Effect Of Dimethyl Sulphoxide Research Articles

Antimycobacterial activity of isoniazid + prothionamide + dapsone against a number of randomly selected 'wild' strains of Mycobacterium tuberculosis.

46 strains of Mycobacterium tuberculosis were studied as to their susceptibility to isoniazid (INH) or to INH + prothionamide (PTH) in the presence or absence of dapsone (DDS) by microdilution transfer plate technique. Synergy with DDS as defined by Berenbaum in 1978 was seen in 78% with INH and in 91% with INH + PTH. It concerned the minimal inhibitory concentration, whereas the minimal bactericidal concentration (MBC) was unaffected in the case of INH and it was increased in only 52% with INH + PTH. The latter MBC proportion mentioned would be decreased to roughly 16% accepting an only twofold decrease in the MBC as possibly due to dilution errors. The possible effect of dimethyl sulphoxide on the reported results is discussed.

The effect of solvents upon the yield of revertants in the Salmonella/activation mutagenicity assay.

The effects of dimethylsulphoxide and acetone have been investigated in the Salmonella/activation mutagenicity assay using 2-aminoanthracene and benzo(a)pyrene as test compounds. Varying mutagenic responses were found with the solvents mutagenic responses were found with the solvents after treatment of the bacteria with 2-aminoanthracene. This was observed in two laboratories. Differences were not as evident after treatment with benzo(a)pyrene. In addition, different amounts of dimethylsulphoxide were used to dissolve amounts of dimethylsulphoxide were used to dissolve 2-aminoanthracene and varying mutagenic responses were obtained. These observations suggest that the choice and amount of solvent for individual test compounds may be critical in terms of determining a mutagenic response.

Raman and infrared study on the effects of dimethylsulphoxide (DMSO) on water structure

AbstractRaman and infrared spectra of liquid dimethylsulphoxide (DMSO) and DMSO‐water mixtures in a wide range of concentrations are reported and discussed. It is found that changes in the vibrational spectra can be related to a gradual insertion of water molecules in the cluster structure of liquid DMSO. In the more dilute aqueous solutions a gradual lowering of the νs=0 stretching frequency is observed and this can be related to the cooperative character of DMSO–water interactions. The interpretation of the spectra is in agreement with the capacity of DMSO for ‘breaking’ the structure of water in the more concentrated aqueous solutions and ‘enhancing’ it in very dilute solutions.

Effect of dimethylsulphoxide on the functional characteristics of isolated perfused rat liver

Exposure of rat liver, perfused with 7% BSA in Krebs-Ringer bicarbonate buffer, to 1.4 m Me 2SO at 35 °C had no effect on the release of potassium from the livers, but the rate of urea synthesis fell from 0.6 to 0.1 μmol/min. Bile production also decreased and the total amount collected during perfusion was only half that produced by controls. After perfusion for 4 hr at 35 °C control livers and those exposed to Me 2SO started to release GOT into the perfusate but livers exposed to the cryoprotective compound released the enzyme at a faster rate. Exposure of livers to Me 2SO at 5 °C resulted in potassium being released at a slower rate (0.98 μmol/min) than from cooled controls (1.19 μmol/min) and urea synthesis was decreased from 0.8 to 0.2 μmol/min. Bile production also declined but, because bile flow normally ceases during hypothermia, the effect on this aspect of liver function was probably less than was found at 35 °C. Release of GOT from livers exposed to Me 2SO at 5 °C was quite different from that observed at 35 °C; the enzyme appeared in the perfusate after about 8 hr and it was present in much lower concentration than was found with appropriately cooled controls which started to release the enzyme after 6 hr. Thus, exposure of rat liver to Me 2SO at 5 °C appears to be slightly less damaging than exposure at 35 °C and it may even have a beneficial effect on some aspects of liver function in vitro.

The effect of dimethyl sulphoxide on electron transport in chloroplasts

The effect of DMSO (dimethyl sulphoxide) on electron transport in chloroplast membranes has been studied. It has been found that concentrations of DMSO up to 20% ( v v ) do not inhibit electron transport in freshly isolated chloroplasts, but that higher concentrations start to cause inhibition. However, in chloroplasts that have been aged for 8 to 24 hours by storage at 4° C, the addition of DMSO at concentrations up to 20% causes stimulation of electron transport. Possible mechanisms for this effect are discussed.

Effect of Dimethyl Sulphoxide on the Expression of Nitrogen Fixation in Bacteria

Storage in dimethyl sulphoxide (DMSO) of Escherichia coli K12 hybrids carrying nif+ genes from Klebsiella pneumoniae can result in selection of a defective nitrogen-fixing phenotype. Similar results are obtained with E. coli K12 hybrids containing the nitrogen-fixing capacity from Rhizobium trifolii. DMSO appears to affect particular inner membrane proteins associated with energy metabolism in E. coli K12 and four chromosomal regions (chlD, chlG, his and unc) are associated with resistance to DMSO.

Some effects of dimethyl sulphoxide (DMSO) on the frog neuromuscular junction.

1. Dimethyl sulphoxide (DMSO) partially reversed neuromuscular blockade brought about by the action of (+)-tubocurarine or Mg(2+) on the frog sartorius nerve-muscle preparation.2. The amplitude and duration of the endplate potential (e.p.p.) were increased by DMSO at concentrations of 70 mM or greater.3. Miniature endplate potentials were raised in frequency, prolonged in duration and increased in amplitude by DMSO at concentrations of 141 mM or greater, but the increase in amplitude was generally less than in the case of the e.p.p.4. The resting muscle membrane potential was significantly depolarized by DMSO at 70 mM or greater concentrations, both at the endplate and remote from an endplate.5. The reversal of neurmuscular blockade by DMSO can be explained in terms of its previously reported ability to inhibit cholinesterase activity, together with the depolarizing action on muscle.

Asymmetric induction in the cyclisation of o-allylphenol with chiral mercury(II) carboxylates. The effect of dimethyl sulphoxide

The reactions of o-allylphenol with mercury(II) salts of a range of chiral carboxylic acids, followed by reductive demercuration, give optically active 2,3-di-hydro-2-methylbenzofuran; optical yields are influenced by the addition of dimethyl sulphoxide (DMSO), the maximum effect occurring with 4 mol of DMSO per mol of carboxylate.

Effect of dimethyl sulphoxide on growth, sporulation and spore germination of Rhizopus arrhizus fischer.

Influences of various levels of dimethyl sulphoxide (DMSO) ranging from 0.04–1.28 M on growth, sporulation and spore germination ofRhizopus arrhizus in liquid and semi-solid media were investigated. Light enhanced the inhibitory effect of DMSO on growth and sporulation in both media. Inhibition of spore germination was observed with direct treatment with DMSO. The inhibition was higher in spores obtained from cultures grown on the DMSO semi-solid media.

The effect of dimethylsulphoxide on the permeability of the lysosomal membrane

The latency of acid phosphatase in sucrose homogenates of rat liver and Tetrahymena pyriformis was found to decrease progressively on exposure to concentrations of dimethylsulphoxide between 5 and 25% (v/v). A progressive decrease in latency was also found in homogenates of rat liver prepared with potassium gluconate although, in this instance, the extent of the decrease was much less than with homogenates prepared in sucrose. With homogenates of rat liver prepared in ß-glycerophosphate, dimethylsulphoxide in concentrations up to 10% had little effect on the latency of acid phosphatase, although it decreased on exposure to higher concentrations.

The effect of dimethylsulphoxide on the permeability of the lysosomal membrane

The latency of acid phosphatase in sucrose homogenates of rat liver and Tetrahymena pyriformis was found to decrease progressively on exposure to concentrations of dimethylsulphoxide between 5 and 25% (v/v). A progressive decrease in latency was also found in homogenates of rat liver prepared with potassium gluconate although, in this instance, the extent of the decrease was much less than with homogenates prepared in sucrose. With homogenates of rat liver prepared in β-glycerophosphate, dimethylsulphoxide in concentrations up to 10% had little effect on the latency of acid phosphatase, although it decreased on exposure to higher concentrations.

Effect of dimethyl sulphoxide on charge transfer complexes between serotonin-, tryptophan and flavin mononucleotide under low temperatures.

The colors of serotonin-FMN and tryptophan-FMN complexes are not changed upon addition of dimethyl sulphoxide at the concentration of 10%, which is routinely used for cell preservation, at 20°. However, the addition to the extent of 50% and above does affect the colors of these complexes. The detailed measurement of the differences in the absorption spectra suggested that dimethyl sulphoxide weakens both the serotonin-FMN and tryptophan-FMN interactions at 20°. In contrast with the observation at 20°, the addition of DMSO under freezing conditions results in the disappearance of colors of the charge transfer complexes while raising the temperature to 20° promptly restores the original color. This disappearance and reappearance of colors, accompanied by freezing and thawing, could be repeated several times.

The effect of dimethyl sulphoxide on the structure of water

The constancy of v(OH) and v(OD) profiles shows that the addition of a few mole % DMSO to water does not change the average value or the width of distribution of hydrogen-bond energies.

Interaction of solvents with membranal and soluble potassium ion-dependent enzymes.

The effects of dimethyl sulphoxide and glycerol on ox brain microsomal Na(+)+K(+)-stimulated adenosine triphosphatase (EC 3.6.1.3), K(+)-stimulated p-nitrophenyl phosphatase and K(+)-dependent muscle pyruvate kinase (EC 2.7.1.40) were studied. Dimethyl sulphoxide at concentrations below 20% (v/v) was found to stimulate the p-nitrophenyl phosphatase and pyruvate kinase by increasing their affinity for K(+) but to inhibit the Na(+)+K(+)-stimulated adenosine triphosphatase. The latter enzyme activity was also inhibited by glycerol, which like dimethyl sulphoxide, stimulated the K(+)-activated p-nitrophenyl phosphatase at a wide range of concentrations. The solvent effects were promptly reversed by dilution. Similarity was found between glycerol and dimethyl sulphoxide, on one hand, and ATP, on the other, in their stimulatory effect and their ability to increase the ouabain- and oligomycin-sensitivity of the K(+)-stimulated p-nitrophenyl phosphatase. However, only the solvents, not the ATP, increased the binding of K(+) by the microsomes. From the above findings it is suggested that solvents may act on K(+)-dependent enzymes by altering the state of solvation of the activating cation as well as by changing the enzyme structure.

Effect of dimethyl sulphoxide on charge transfer complexes of D-amino acid oxidase under low temperatures.

Effect of dimethyl sulphoxide on charge transfer complexes of D-amino acid oxidase under low temperatures.

The effect of dimethyl sulphoxide on the radiation response of the rough-skinned newt (Taricha granulosa).

SummaryNewts were collected, acclimatized, and maintained unfed at 10°c both before and after irradiation. Exposures ranging up to 30 kR were given with 300 kVp x-rays and 60Co gamma-rays. Half the newts were pre-treated with the maximum sublethal dose of dimethyl sulphoxide DMSO (i.p.), the remainder were untreated.The mean survival-time—exposure curves for both groups of animals were typically sigmoid. However, the mean survival times of the DMSO-treated newts were significantly longer for all exposures between 200 R and 15 kR. Absolute protection was afforded by DMSO up to 500–600 R, while the lethal threshold dose for untreated irradiated newts was 100–200 R.The degree of radioprotection afforded by DMSO varied according to the time of administration, concentration of DMSO, and radiation exposure. DMSO prevented skin ulceration and caused splenomegaly and hepatomegaly after 650 R, which in turn was associated with a degree of plethora and haemoconcentration, or possibly real polycythaemia.

Effects of dimethyl sulphoxide, dimethyl formamide and dimethyl acetamide on myocardial contractility and enzyme activity

DMSO, DMF and DMA were all shown to increase the force of contraction of the electrically-driven guinea-pig left atrium. These responses were not altered by α- or β-adrebergic receptor antagonists nor by reserpine-pretreatment of guinea-pigs. The effect of DMSO on intact muscle was completely reversible, in contrast to DMF and DMA, which were toxic at high concentrations. All three solvents stimulated Ca 2+ transport and inhibited Na +, K + -dependent ATPase activity, DMSO stimulated adenyl cyclase but did not affect the degree of stimulation induced by isoproterenol, whereas DMF inhibited both the basic activity and the isoproterenol-induced stimulation. The relative potencies of these solvents (DMF > DMSO = DMA) in increasing myocardial contractility correlates with their ability to stimulate microsomal Ca 2+ transport. The greater inhibition of Na +, K + -ATPase by high concentrations of DMF and DMA, and the inhibition of adenyl cyclase by DMF, may account for the greater toxicity of these compounds in atria, compared with DMSO.

Effect of Dimethylsulphoxide on the Germination of Spores of Lycogala epidendrum

RECENT researches on dimethylsulphoxide (DMSO) have emphasized the capacity of this solvent to penetrate cellular membranes easily and rapidly. Jacob, Bischel and Herschler1 reported an effect of increased membrane permeability in tissue of dogs and in plants. Sciuchetti and Born2 found that DMSO apparently enhances the response of Datura tatula to a growth retardant when the DMSO is combined with the retardant. Activation of spores of Bacillus pantothenticus spores after exposure to DMSO has been reported by Widdowson3. DMSO is a reaction solvent4 and has been shown to increase the rates of many chemical reactions. Considering the possibility that DMSO activates or accelerates the initiation of metabolic processes in spores slow to germinate, the effect of this solvent on spore germination was investigated.

Anion-exchange separation of metal ions in dimethyl sulphoxide-methanol-hydrochloric acid

The effect of dimethyl sulphoxide on the anion-exchange behaviour of many metals m a methanolic system with hydrochloric acid was explored. Distribution coefficients for 26 elements were determined in a mixed solvent system of dimethyl sulphoxide-methanol-0.6 M hydrochloric acid, in which the proportions of dimethyl sulphoxide and methanoi were varied. Lead(II) and silver(I) complexes are soluble in this system. Interesting effects were noted for gold(III), iron(III), molybdenum(VI) and uranium(VI). As a measure of the usefulness of the systems studied, 27 anion-exchange separations of two- to four-component mixtures of metal ions were carried out, each with quantitative results.

Effects of Dimethyl Sulphoxide and of Vitamin A on Human Platelets

SummaryDimethyl sulphoxide (DMSO) causes some release of amino acids, adenine nucleotides, and acid phosphatase and β-glucuronidase activities from washed human platelets. Addition of vitamin A with DMSO greatly enhances the effect; but vitamin A in ethanol added to platelets fails to release amino acids and nucleotides. Release appears to be due to a change in permeability of the platelet membrane, not to the discharge of contents of intracellular structures. Lipid peroxidation of membrane phospholipids, or a similar reaction, may be involved. Thrombin causes a different type of alteration in platelet permeability.The results suggest that DMSO should not be used as a preservative for platelets. They may have some bearing on the mechanisms of toxicity of DMSO and vitamin A.