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Chinese Hamster V79 Cells (chinese + hamster_v79_cell)
Selected AbstractsExamination of cytotoxicity and mutagenicity of AH26 and AH Plus sealersINTERNATIONAL ENDODONTIC JOURNAL, Issue 5 2003I. Mileti Abstract Aim ,To study in vitro the cytotoxic and mutagenic effects of AH26 and AH Plus. Methodology ,Cytotoxic effects on Chinese hamster V79 cells were determined by counting viable cells following incubation with eluations of AH26 and AH Plus. In one set of experiments, the materials were mixed, set for 1 h and then eluted with dimethyl sulphoxide (DMSO) for 1 h, 24 h and 7 days. In the other set, AH26 and AH Plus were mixed and set for 1 h, 24 h and 7 days in physiological saline then crushed and eluted in DMSO for 24 h. The cytotoxic effects of these eluates were evaluated. Three concentrations were chosen to examine the mutagenic effects of AH26 and AH Plus: 5.57, 16.7 and 55.7 ,g mL,1. The structural chromosomal aberration analysis and micronucleus test were performed on human lymphocytes according to standard procedures. Results ,Dose,response curves of cell survival were obtained. Both materials were shown to be cytotoxic in doses larger than 55.7 ,g mL,1, except for AH26, after 7 days setting time. AH Plus was also shown to be toxic in concentrations of 16.7 ,g mL,1, except after 7 days setting time. Neither AH26 nor AH Plus induced a significant increase of chromosomal aberrations or micronuclei induction at any setting time or concentration. Conclusion ,There was no mutagenicity found for AH26 and AH Plus on human lymphocytes in highly controlled conditions in vitro. [source] Inhibition of human cytochrome p450 1b1 further clarifies its role in the activation of dibenzo[a,l]pyrene in cells in cultureJOURNAL OF BIOCHEMICAL AND MOLECULAR TOXICOLOGY, Issue 3 2007Brinda Mahadevan Abstract Metabolic activation and DNA adduct formation of the carcinogenic aromatic hydrocarbon dibenzo{a,l}pyrene (DBP) was investigated in human mammary carcinoma MCF-7 cells and human cytochrome P450 (CYP) 1B1-expressing Chinese hamster V79 cells in culture. It has been shown that DBP is metabolically activated to DNA-binding diol epoxides both in vitro and in vivo. To further establish the role of human CYP1B1 in the activation of DBP, both cell lines were cotreated with DBP and a selective chemical inhibitor of CYP1B1, 2,4,3, ,5,-tetramethoxy-stilbene (TMS). Results from DBP,DNA adduct analyses revealed the complete inhibition of DNA binding when cells were cotreated with DBP and TMS in comparison to DBP alone. Inactivation of CYP1B1 by TMS was also demonstrated through a decrease in the 7-ethoxyresorufin O -deethylase (EROD) activity in microsomes isolated from these cells. Emodin, 3-methyl-1,6,8-trihydroxyanthraquinone, an active ingredient of an herb, has been recently shown of being able to induce CYP1 gene expression. Examination of human CYP1B1 induction and EROD activity confirmed an increase in protein levels upon cotreatment with emodin and DBP. Despite increases in protein levels and enzyme activity, there was no significant change in DBP,DNA binding levels at very low substrate concentrations (17 nM). The data obtained in this study emphasize the central role of CYP1B1 in the activation of DBP in human cells in culture. © 2007 Wiley Periodicals, Inc. J Biochem Mol Toxicol 21:101,109, 2007; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/jbt.20168 [source] Real-time cellular uptake of serotonin using fluorescence lifetime imaging with two-photon excitationMICROSCOPY RESEARCH AND TECHNIQUE, Issue 4 2008Stanley Walter Botchway Abstract The real-time uptake of serotonin, a neurotransmitter, by rat leukemia mast cell line RBL-2H3 and 5-hydroxytryptophan by Chinese hamster V79 cells has been studied by fluorescence lifetime imaging microscopy (FLIM), monitoring ultraviolet (340 nm) fluorescence induced by two-photon subpicosecond 630 nm excitation. Comparison with two-photon excitation with 590 nm photons or by three-photon excitation at 740 nm shows that the use of 630 nm excitation provides optimal signal intensity and lowered background from auto-fluorescence of other cellular components. In intact cells, we observe using FLIM three distinct fluorescence lifetimes of serotonin and 5-hydroxytryptophan according to location. The normal fluorescence lifetimes of both serotonin (3.8 ns) and 5-hydroxytryptophan (3.5 ns) in solution are reduced to ,2.5 ns immediately on uptake into the cell cytosol. The lifetime of internalized serotonin in RBL-2H3 cells is further reduced to ,2.0 ns when stored within secretory vesicles. Microsc. Res. Tech., 2008. © 2007 Wiley-Liss, Inc. [source] Cysteine enhances clastogenic activity of dimethylarsinic acidAPPLIED ORGANOMETALLIC CHEMISTRY, Issue 7 2002Mari Kitamura Abstract The effects of cysteine on dimethylarsinic acid (DMA)-induced cytotoxicity and chromosomal aberration were studied using Chinese hamster V79 cells. The IC 50 of DMA, i.e. the concentration resulting in a 50% decrease in cell population of viable cells, was 130,µg,ml,1 (0.94 mM), whereas that in the presence of 50,µg,ml,1 (0.28 mM) cysteine was 20,µg,ml,1 (0.14 mM). The mitotic index with co-administration of 50,µg,ml,1 (0.36 mM) DMA and 50,µg,ml,1 cysteine was 1.4 times that with 50,µg,ml,1 DMA alone. Whereas 82% of cells divided twice with 25,µg,ml,1 (0.18 mM) DMA alone, most cells divided only once with co-administration of 25,µg,ml,1 DMA and 50,µg,ml,1 cysteine. These results indicated that the increase in mitotic index by cysteine was due to enhancement of mitotic arrest by DMA. With co-administration of 25,µg,ml,1 DMA and 50,µg,ml,1 cysteine, tetraploidy was 14.3% higher and fivefold by that with 25,µg,ml,1 DMA only. Cysteine at 50,µg,ml,1 enhanced induction of chromosomal aberrant cells by DMA. 100,µg,ml,1 (0.72 mM) DMA induced 91% chromosomal aberrant cells in the presence of cysteine, and 12% in the absence of cysteine. Chromatid breaks and chromatid gaps were the most frequent types of aberration induced by co-administration of DMA and cysteine or DMA alone. Co-administration of DMA and cysteine produced many attenuated chromosomal figures. The attenuated chromosomal figures always had several chromatid gaps and chromatid breaks. Our findings may provide clues to arsenic carcinogenesis in humans. Copyright © 2002 John Wiley & Sons, Ltd. [source] | |||||||||||||