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  • 1
    Electronic Resource
    Electronic Resource
    Mechanism for the changes in levels of glutathione upon exposure of cultured mammalian cells to tertiary-butylhydroperoxide and diamide (1993)
    Springer
    Archives of toxicology 67 (1993), S. 401-410 
    Details
    ISSN: 1432-0738
    Keywords: Glutathione ; Oxidized glutathione ; tertButylhydroperoxide ; Reactive oxygen radicals ; Glutathione synthesis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Qualitative and quantitative changes associated with cellular glutatione (GSH) in response to oxidants were investigated in cultured Chinese hamster V79 cells. Incubation of cells with benzoylperoxide (BZP), tert-butylhydroperoxide (t-BuOOH), hydrogen peroxide or diamide for 1 h reduced the level of total GSH (GSH + GSSG). Among the oxidants, t-BuOOH and diamide caused an increase in levels of glutathione disulfide (GSSG) and a resultant increase in the ratio of the level of GSSG to the level of total GSH, suggestive of the induction within the cells of a pro-oxidant state by the oxidants. o-Phenanthroline, a chelator of divalent ion, almost completely suppressed the decrease in levels of total GSH caused by t-BuOOH while it did not suppressed either increases in levels of GSSG or increases in the ratio of the levels of GSSG to that of total GSH caused by the hydroperoxide. These results suggest that reactive oxygen radicals are involved in the decrease in levels of GSH by treatment with t-BuOOH but not in the increase in the level of GSSG. After treatment with either t-BuOOH or diamide for 1 h, the level of GSH rapidly increased to more than twice the control level during 15–45 min of post-treatment incubation. o-Phenanthroline almost completely suppressed the increase in levels of GSH caused by t-BuOOH, while it did not affect the changes caused by diamide, suggesting a difference between the mechanisms by which t-BuOOH and diamide cause increases in levels of GSH. It seems likely that reactive oxygen radicals participate not only in the decrease in levels of GSH caused by t-BuOOH but also in the rapid increase that occurs after such treatment. Hence, the first decrease in levels of GSH by the hydroperoxide may be causally related to the latter increase. The amount of [35S]-cysteine taken up by cells after treatment with t-BuOOH was about one half of that taken up by control cells. By contrast, the rate of incorporation of radioactive cysteine into acid-soluble material increased to more than twice that of the controls after treatment with t-BuOOH. The increase in the rate of incorporation of [35S]cysteine into acid-soluble material caused by t-BuOOH was not a consequence of inhibition by the hydroperoxide of utilization of cysteine for protein synthesis. Inhibition of protein synthesis by cycloheximide caused neither an increase in the incorporation of cysteine into acid-soluble material nor an increase in rate of biosynthesis of GSH. Incorporation of radioactive cysteine into the cysteine moiety of GSH and the disappearance of the radioactivity from the cysteine fraction were enhanced after treatment with t-BuOOH. These data indicate that biosynthesis of GSH de novo is enhanced by t-BuOOH.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01977401
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  • 2
    Electronic Resource
    Electronic Resource
    Arsenic compound-induced increases in glutathione levels in cultured Chinese hamster V79 cells and mechanisms associated with changes in γ-glutamylcysteine synthetase activity, cystine uptake and utilization of cysteine (1997)
    Springer
    Archives of toxicology 71 (1997), S. 730-740 
    Details
    ISSN: 1432-0738
    Keywords: Key words Arsenic compounds ; Glutathione ; γ-glutamylcysteine synthetase ; Cystine uptake
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Increases in the glutathione (GSH) level in cultured Chinese hamster V79 cells incubated with arsenic compounds were investigated in terms of changes in the activity of γ-glutamylcysteine synthetase (γ-GCS), rate of cystine uptake, and utilization of cysteine. Arsenite at subtoxic concentrations caused a marked increase of the GSH level at 8 h after addition and then declined. Increase in the GSH level caused by arsenite was associated with an increase in the rate of cystine uptake, but not in γ-GCS activity. Increase in the rate of uptake of cystine was attributed mainly to an increase in the utilization of cysteine in the synthesis of GSH. Dimethylarsinic acid (DMAA) also caused an increase in the GSH level in a time- and concentration-dependent manner. Increase in the GSH level was accompanied by increases in γ-GCS activity and in the uptake of cystine. DMAA caused a reduction in the rate of utilization of cysteine for protein synthesis while enhancing the rate of cysteine utilization for GSH synthesis. Cycloheximide inhibited increases in γ-GCS activity caused by DMAA and in the rate of cystine uptake caused by arsenite and DMAA. The cystine transport system is suggested to be induced by arsenite and DMAA with γ-GCS induced in cells incubated with DMAA. Among the arsenic compounds, methylarsonic acid (MAA) was not effective in causing an increase in the GSH level. Accordingly, increases in the GSH level caused by arsenite and DMAA may be specific phenomena in which the cells responded to the arsenicals by increasing the GSH level.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002040050454
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  • 3
    Electronic Resource
    Electronic Resource
    Different effects of inorganic and dimethylated arsenic compounds on cell morphology, cytoskeletal organization, and DNA synthesis in cultured Chinese hamster V79 cells (1998)
    Springer
    Archives of toxicology 72 (1998), S. 566-573 
    Details
    ISSN: 1432-0738
    Keywords: Key words Arsenic compounds ; Microtubule network ; Mitotic arrest ; Multinucleated cells ; DNA synthesis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Changes in cytoskeletal organization of cultured V79 cells exposed to arsenite and dimethylarsinic acid (DMAA), a methylated derivative of inorganic arsenics, and related changes, such as mitotic arrest and induction of multinucleated cells, were investigated in comparison with their effects on DNA synthesis. DMAA caused mitotic arrest and induction of multinucleated cells with a delay of 12 h relative to the mitotic arrest. By contrast, arsenite at equitoxic concentrations to DMAA was less effective than DMAA in causing mitotic arrest and in inducing multinucleated cells. Post-mitotic incubation of cells arrested in metaphase by 6 h incubation with 10 mM DMAA showed that the incidence of multinucleated cells increased conversely with a rapid decrease in metaphase cells. This suggests that metaphase-arrested cells can escape from metaphase, resulting in the appearance of multinucleated cells. The mitotic arrest caused by DMAA was accompanied by disruption of the microtubule network. By contrast, both arsenite and DMAA did not cause disorganization of actin stress fibers even when incubated at concentrations that caused a marked retardation of cell growth. Cells exposed to arsenite for 6 h showed marked inhibition of DNA synthesis, whereas inhibition by DMAA was not observed. When incubation was prolonged by 18 h, the arsenite-induced inhibition of DNA synthesis was mitigated. By contrast, inhibition of DNA synthesis by DMAA occurred in parallel with an increase in the population of mitotic cells. These results suggest that DMAA caused growth retardation and morphological changes via disruption of the microtubule network, and that arsenite-induced retardation of cell growth and inhibition of DNA synthesis were not attributable to the cytoskeletal changes.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002040050544
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  • 4
    Electronic Resource
    Electronic Resource
    Cytotoxicological aspects of organic arsenic compounds contained in marine products using the mammalian cell culture technique (1998)
    New York, NY [u.a.] : Wiley-Blackwell
    Applied Organometallic Chemistry 12 (1998), S. 137-143 
    Details
    ISSN: 0268-2605
    Keywords: arsenobetaine ; arsenocholine ; trimethylarsine oxide ; tetramethylarsonium iodide ; organic arsenic compound ; arsenite ; arsenate ; marine organisms ; cytotoxicity ; chromosomal aberration ; sister chromatid exchange (SCE) ; Chemistry ; Industrial Chemistry and Chemical Engineering
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Chemistry and Pharmacology
    Notes: Arsenobetaine, arsenocholine, trimethylarsine oxide and tetramethylarsonium iodide, which are contained in marine fishery products, were examined for their potencies on cell growth inhibition, chromosomal aberration and sister chromatid exchange (SCE). Arseno- betaine, the major water-soluble organic arsenic compound in marine animals, exhibited very low cytotoxicity towards mammalian cells. This compound showed no cell growth inhibition at a concentration of 10 mg cm-3 and the cytotoxicity was lower than 1/14 000th of that of sodium arsenite and 1/1600th of that of sodium arsenate towards BALB/c 3T3 cells. The chromosomal aberrations caused by arsenobetaine at a concentration of 10 mg cm-3 consisted mainly of chromatid gaps and chromatid breaks, but in this concentration chromosomal breakage owing to its osmotic pressure is likely to be considerable. No SCE was observed at a concentration of 1 mg cm-3. Arsenocholine and trimethylarsine oxide also showed no cell growth inhibited at a concentration of 10 mg cm-3. However, tetramethylarsonium iodide inhibition the growth of BALB/c 3T3 at a concentration of 8 mg cm-3. These compounds exhibited a low ability to induce chromosomal aberrations at a concentration range of 2-10 mg cm-3 and no SCE was observed at a concentration of 1.0 mg cm-3. These results suggested that the major and minor organic arsenic compounds contained in marine fishery products are much less cytotoxic inorganic arsenic, methylarsonic acid and dimethylarsinic acid. © 1998 John Wiley & Sons, Ltd.
    Additional Material: 2 Ill.
    Type of Medium: Electronic Resource
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