Stimulatory effect of dimethylsulfoxide on [3H]thymidine incorporation into DNA in Novikoff hepatoma cells

Barra, Rosemary; Hicks, Herbert; Koch, Michael; Lea, Michael A.

doi:10.1016/0020-711x(78)90051-4

Cited by 13 publications

(6 citation statements)

References 15 publications

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“…Other effects of EGF, such as stimulation of DNA synthesis, requires a longer exposure to EGF [39,40]. DMSO does stimulate DNA synthesis in Novikoff hepatoma cells [41] and in the skin of hairless mice [42]. Whether DMSO stimulates DNA synthesis through an EGF receptor-dependent mechanism is not known.…”

Section: Discussionmentioning

confidence: 99%

Dimethyl sulfoxide decreases specific EGF binding

Earp

Blaisdell

Lin

1984

J of Cellular Biochemistry

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Dimethyl sulfoxide (DMSO) stimulates tyrosine phosphorylation of the hepatic EGF receptor in isolated membrane preparations. To determine whether DMSO affects EGF binding, primary cultures of rat hepatocytes were incubated with 1-10% DMSO for 30 min prior to the addition of 125I-EGF. DMSO (1-2%) reduced specific 125I-EGF binding; the effect was maximal (a 40-60% reduction) at 5-7.5% DMSO and was reversed by removing the DMSO. Scatchard analysis showed that the reduction in binding was due to a change in receptor affinity. The decrease in binding was not seen when other, slightly less polar, solvents (eg, acetone and ethanol) were tested. DMSO also reduced 125I-EGF binding to purified rat liver plasma membranes. This reduction was seen in the absence of added ATP and in membranes that had been pretreated with TLCK, a tyrosine kinase inhibitor. Thus, completion of the receptor autophosphorylation reaction was not necessary to effect the change. The data are consistent with a DMSO-induced alteration of receptor conformation that reversibly reduces receptor affinity.

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Section: Discussionmentioning

confidence: 99%

Dimethyl sulfoxide decreases specific EGF binding

Earp

Blaisdell

Lin

1984

J of Cellular Biochemistry

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“…DMSO treatment enchanced albumin production in transformed hepatocytes [9], and decreased the binding of EGF to its receptor [12]. Addition of DMSO selectively enhanced the incorporation of [3H]thymidine into cultured Novikoff hepatoma cells [13] but retarded the growth of murine erythroleukemia cells and led to the differentiation process [14]. Addition of DMSO selectively enhanced the incorporation of [3H]thymidine into cultured Novikoff hepatoma cells [13] but retarded the growth of murine erythroleukemia cells and led to the differentiation process [14].…”

Section: Introductionmentioning

confidence: 99%

Effect of dimethyl sulfoxide on mouse embryo fibroblasts: inhibition of plasminogen activator inhibitor deposition and interference with early events of serum‐stimulated growth

Nagashunmugam

Srinivas

Shanmugam

1989

Biology of the Cell

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Quiescent and serum-stimulated cultures of Swiss mouse embryo fibroblasts (MEF) showed alterations in cell morphology including an enlargement in size upon treatment with 2% dimethyl sulfoxide (DMSO). Treatment of MEF and monkey kidney epithelial cells (MK2) with 2% DMSO at the early periods of serum-stimulated growth inhibited RNA, protein and DNA synthesis. DMSO treatment of cells at late stages of serum-stimulated growth (MEF after 1 hr and MK2 cells after 3 hr of stimulation) had little effect on DNA and protein synthesis although cell enlargement occurred in these cells. When the [35S]methionine labelled proteins of the control and the DMSO treated cells were analysed by high resolution polyacrylamide gel electrophoresis, no apparent difference was observed in the pattern of intracellular proteins of these cells. In contrast, the extracellular levels of two serum-induced secreted proteins of MEF (Mr 48,000 and 26,000) were dramatically reduced by DMSO treatment. The DMSO sensitive 48 kDa protein was found to be the major component of the extracellular matrix, while the 26 kDa protein was not. The 48 kDa protein was identified as plasminogen activator inhibitor (PAI-1). Densitometric quantitation showed a gradual accumulation of this protein in the matrix of serum-stimulated cells. The deposition of this protein in the matrix was inhibited by DMSO. Flow-cytometric quantitation of indirect immunofluorescence indicated higher intracellular levels of the 48 kDa protein in fetal calf serum (FCS) + DMSO treated cells, suggesting that the low level of this protein in the medium of DMSO treated cells is probably due to lack of transport of this protein from the cells into the medium.

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“…Short-term pre-exposure of Novikoff hep atoma cells to DMSO stimulated [3H]-thymidine and [3H]-uridine incorporation into DNA and RNA, respectively, but did not alter incorporation of [3H]-amino acids into cellular protein [Barra et al" 1978]. Incuba tion of mouse and rat hepatoma cells in DMSO-containing growth medium for lon ger periods of time, however, resulted in a dose-dependent stimulation in albumin ac cumulation and secretion in both cell types and diminished the expression of gamma glu tamyl transpeptidase in rat hepatic tumor cells [Higgins and BorenJ'reund, 1980].…”

Section: Introductionmentioning

confidence: 99%

Response of Mouse Liver Tumor Cells to the Differentiation-Inducing Agent Dimethylsulfoxide

Higgins

1982

Pharmacology

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The effects of the differentiation-inducing agent dimethylsulfoxide (DMSO) on the growth and protein composition of murine hepatic tumor cell (BW77-1) cultures were investigated using various concentrations of the polar solvent in the growth medium. A 4-day exposure to DMSO in concentrations of 0.5, 1 and 3% reduced final hepatocyte population density to 63, 43 and 15% of control values, respectively, while the amount of transferrin in the cellular and extracellular compartments increased in a dose-dependent fashion. The biochemical basis for elevated transferrin extractable per 10⁶ BW77-1 cells in DMSO-stimulated cultures was due to increases in both the transferrin contribution to total cellular protein and the mean protein content per cell. This stimulation in cellular protein levels was reflected in the incorporation of [³H]-amino acids into cell-associated 10% trichloroacetic acid-insoluble material. Cultures of transformed liver epithelial cells thus appear to respond to in vitro DMSO exposure by increasing their accumulation of a late-stage hepatocyte gene product.

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Stimulatory effect of dimethylsulfoxide on [3H]thymidine incorporation into DNA in Novikoff hepatoma cells

Cited by 13 publications

References 15 publications

Dimethyl sulfoxide decreases specific EGF binding

Dimethyl sulfoxide decreases specific EGF binding

Effect of dimethyl sulfoxide on mouse embryo fibroblasts: inhibition of plasminogen activator inhibitor deposition and interference with early events of serum‐stimulated growth

Response of Mouse Liver Tumor Cells to the Differentiation-Inducing Agent Dimethylsulfoxide

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