Expression of disodium cromoglygate ‘protective’ effects observed during V79 cell proliferation

Horáková, K; Vlčková, Angelika; Lukácová, D

doi:10.1016/0009-2797(93)90002-g

Cited by 5 publications

(3 citation statements)

References 13 publications

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“…In agreement with our study, benfluron caused cell cycle arrest in S and G2/M phases in V79 cells (Horáková et al, 1988). The treatment of V79 cells with BF in combination with disodium cromoglycate resulted in cell cycle arrest in late S and G2/M phases as well (Horáková et al, 1993). Our finding is also in agreement with the results of Seifrtová et al (2011), who detected mainly G2/M or S phase cell cycle arrest in MOLT-4 and Jurkat cells after the treatment with mitoxantrone.…”

Section: Discussionsupporting

confidence: 93%

Benfluron Induces Cell Cycle Arrest, Apoptosis and Activation of p53 Pathway in MOLT-4 Leukemic Cells

Seifrtová,

Cochlarová,

Havelek

et al. 2015

Fol. Biol.

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The aim of our study was to determine the effect of potential anti-tumour agent benfluron on human leukemic cells MOLT-4 and elucidate the molecular mechanisms of response of tumour cells to this chemotherapeutic agent. It has been shown that the mechanisms of action of benfluron are complex, but the molecular pathways of the cytostatic effect have remained unknown and the present study contributes to their elucidation. In this work, benfluron reduced viability of the treated cells and induced caspase-mediated apoptosis. The programmed cell death was associated with activation of caspases 8, 9 and 3/7. Moreover, exposure of cells to benfluron resulted in accumulation of the cells primarily in late S and G2/M phases. The changes in the levels of key proteins show that benfluron provoked activation of p53 and induced phosphorylation of p53 on serine 15 and serine 392. The application of benfluron led to phosphorylation of Chk1 on serine 345 and phosphorylation of Chk2 on threonine 68 in the treated cells. Higher doses of benfluron caused phosphorylation of ERK1/2 on threonine 202 and tyrosine 204, whereas JNK and p38 kinases were not activated. In conclusion, benfluron induces apoptosis, cell cycle arrest in late S and G2/M phases, and activates various signalling pathways of the DNA damage response.

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Section: Discussionsupporting

confidence: 93%

Benfluron Induces Cell Cycle Arrest, Apoptosis and Activation of p53 Pathway in MOLT-4 Leukemic Cells

Seifrtová,

Cochlarová,

Havelek

et al. 2015

Fol. Biol.

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“…Then the cell sheets were harvested in triplicate with trypsin. 9 Aliquots of this suspension were used for cell count and protein content determinations. 10 Bovine serum albumin was used as the standard.…”

Section: In Vitro Studymentioning

confidence: 99%

Effect of cyclosporin A in Lewis rats in vivo and HeLa cells in vitro

Sovcikova

Tulinská

Kubová

et al. 2002

J of Applied Toxicology

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The aim of this study was to compare the effect of cyclosporin A (CsA) in inbred Lewis rats with published assessment of immunotoxicity in 'classical' outbred Wistar rats. A second purpose was to consider the contribution of a panel of in vitro assays in cell cultures when added to an immunotoxicity study in vivo. The in vivo effect of CsA was investigated in a 28-day subacute immunotoxicity study in male Lewis rats at three different concentrations: 1.25, 5 and 20 mg kg(-1). The highest dose of CsA exceeded the maximum tolerated dose. A drop in body, spleen and popliteal lymph node weight of exposed animals displayed symptoms of toxicity. At a high toxic dose, haematological changes showed a decrease in the leucocyte count and in the percentage of lymphocytes, and an increase in the percentage of polymorphonuclear leucocytes. The haematocrit was significantly dose-dependently suppressed in all rats exposed to CsA. A similar dose-dependent depression of the mean cell volume of erythrocytes was found in rats given high and middle doses of CsA. The phagocytic activity of polymorphonuclear leucocytes and monocytes also was significantly dose-dependently suppressed. No significant changes in primary antibody response to sheep erythrocytes or in vitro proliferative response of spleen lymphocytes to mitogens were found in those rats.A battery of in vitro cytotoxicity methods was selected for the evaluation of metabolic and functional activity of subcellular organelles (mitochondria, lysosomes) and for the detection of drug-induced superoxide-mediated damage in HeLa cells. This cell line was chosen because it has a lower activity of superoxide dismutase (SOD) than normal cells and is sufficiently sensitive for the detection of the induction of oxygen radicals. The in vitro results indicated a direct relationship between CsA cytotoxicity and a change in the mitochondrial enzyme activity, as well as an induction of superoxide production. The results of the study indicated that a combination of selected in vivo and in vitro methods is an inexpensive way to obtain more complex information on cell status affected by xenobiotics.

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“…[1][2][3][4][5][6] DSCG inhibits mediator releases from a wide range of cells 2,5 and affects cell differentiation. [7][8][9] The human leukemia (HL)-60 is a cell line that can be used in an experimental model providing the possibility to examine the regulation of arachidonic acid (AA) metabolism in myeloid cells. HL-60 cells can be differentiated into morphologically mature granulocyte like cells, 10,11 which produce a various kind of arachidonate metabolites including leukotrienes.…”

Section: Introductionmentioning

confidence: 99%

Disodium cromoglycate suppresses the induction of cysteinyl leukotriene synthesis during granulocytic differentiation in HL-60 cells

Zaitsu¹,

Honjo²,

Ishii³

et al. 2004

Respiratory Medicine

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Expression of disodium cromoglygate ‘protective’ effects observed during V79 cell proliferation

Cited by 5 publications

References 13 publications

Benfluron Induces Cell Cycle Arrest, Apoptosis and Activation of p53 Pathway in MOLT-4 Leukemic Cells

Benfluron Induces Cell Cycle Arrest, Apoptosis and Activation of p53 Pathway in MOLT-4 Leukemic Cells

Effect of cyclosporin A in Lewis rats in vivo and HeLa cells in vitro

Disodium cromoglycate suppresses the induction of cysteinyl leukotriene synthesis during granulocytic differentiation in HL-60 cells

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