1,721,001 research outputs found
Chromosomal aberrations and sister-chromatid exchanges in Chinese hamster cells treated in vitro with hexavalent chromium compounds.
No full textChinese hamster cells (CHO line) were treated in vitro for 30--39 h with hexavalent chromium compounds (K2Cr2O7 and Na2CrO7), at concentrations ranging from 0.1 to 1.0 microgram of Cr6+ per ml, in medium containing BUdr. Chromosomal aberrations and sister-chromatid exchanges were scored on BUdr-labelled 2nd division metaphases, collected at the end of treatment and stained with Giemsa. Treatment with mitomycin C 0.009--0.030 microgram/ml) was carried out as a control for the responsiveness of the cell system to chromosomal damage. Both chromium compounds induced marked mitotic delays. Chromosomal aberrations were increased about 10-fold by exposure to Cr6+ (1.0 microgram/ml). The principal aberrations observed were single chromatid gaps, breaks and interchanges, whose frequencies increased proportionally to the concentration of chromium. Dicentric chromosomes, isochromatid breaks, chromosome and chromatid rings were also induced. The frequenyc of sister-chromatid exchanges was hardly doubled 30 h after exposure to Cr6+ at 0.3 microgram/ml, whereas it was trebled 39 h after treatment, in the cells whose division cycle had been slowed down by chromium
DNA adducts in Mytilus galloprovincialis and Zosterisessor ophiocephalus collected from PAC-polluted and reference sites of the Venice lagoon.
No full textMediterranean mussels (Mytilus galloprovincialis) and bottom-dwelling grass gobies (Zosterisessor ophiocephalus) were collected from the Venice lagoon both in front of the open sea and from the industrial area of Porto Marghera. DNA adducts were measured by means of the nuclease P1-enhanced 32P-DNA postlabelling assay. Autoradiograms of gill DNA from animals of the industrial area showed a tract of unresolved adducts along the diagonal radioactive zone. Such adducts were detected at low but significant levels in different sampling periods only in mussels and fish collected at Porto Marghera. The presence of bulky aromatic DNA adducts in native mussels is consistent with previous results on the appearance of a weak adduct in gill DNA of Mytilus galloprovincialis treated with benzo(a)pyrene. However, the mechanisms leading to DNA damage and the fate ofthe initial lesions in marine invertebrates exposed to genotoxic agents are still poorly understood
Biomonitoring of human populations exposed to PAH: DNA adduct formation in blood lymphocytes of human populations exposed to PAH
No full textCytotoxic and clastogenic effects of soluble chromium compounds on mammalian cell cultures.
Full text linkThe inhibition of cell growth, the reduction of cell survival and the induction of chromosome aberrations and of sister chromatid exchange (SCE) have been determined in cultured hamster cell lines (BHK and CHO) treated with 11 water-soluble compounds of hexavalent and trivalent chromium. All Cr6+ compounds inhibit growth of BHK cells and reduce survival of CHO cells to levels comparable to those obtained only after exposure to 100--1000 times higher Cr3+ concentrations. The cytotoxicity curves obtained with the different Cr6+ compounds are almost overlapping, whereas marked differences of activity are noticeable among Cr3+ compounds. Giant cells are obtained after exposure to Cr6+ and Cr3+ compounds, as shown by the rise of DNA and RNA per cell, and are due to the blockage of the cell cycle without sudden inhibition of macromolecular syntheses. Both Cr6+ and Cr3+ compounds are able to induce chromosome aberrations, whereas Cr3+ is absolutely incapable of inducing SCE, only Cr6+ being active. The frequency of chromosome aberrations is increased about 10-fold after exposure to 1.0 micrograms/ml Cr6+, whereas it is only doubled after treatment with up to 150 micrograms/ml Cr3+. On the other hand, in spite of the sensitivity of CHO cells to the induction of SCE by mitomycin C, the frequency of SCE hardly doubles after exposure to Cr6+ compounds. The present data confirm that Cr6+ compounds are characterized by a marked cytotoxicity and clastogenic action on mammalian cell cultures and show that Cr3+ compounds, though cytotoxic only at extremely high concentrations and not increasing the frequency of SCE, are not completely without cytogenetic effect, as they are able to induce chromosome aberrations
Cytotoxic and clastogenic effects of soluble and insoluble compounds containing hexavalent and trivalent chromium.
Full text linkCr(III) and Cr(VI) compounds of varying solubilities have been tested in vitro for their ability to inhibit cell growth and nucleic acid and protein syntheses in BHK cells, to induce alterations in the mitotic cycle in HEp cells, and to increase the frequency of chromosomal aberrations and sister chromatid exchanges (SCE) in CHO cells. All Cr(VI) compounds, and particularly those containing soluble Cr(VI), such as potassium dichromate and zinc yellow, differentially inhibit macromolecular syntheses in BKH cells, that of DNA being always the most affected. Among Cr(III) compounds, which generally have very low cytotoxicity, chromite is particularly active, and inhibits cell growth and DNA synthesis even more than the poorly soluble Cr(VI) compounds. Preincubation in growth medium, with or without metabolizing cell cultures, solubilizes considerable amounts of Cr(VI) from zinc yellow and chromite, but significant amounts are also obtained from the most insoluble Cr(VI) pigments. When BHK cells are treated with such preincubated solutions, reduction of soluble Cr(VI) to Cr(III) by cell metabolites is seen with all Cr(VI) compounds, accompanied by decreased cytotoxicity. The same differences between Cr(VI) and Cr(III) compounds apply to the cytotoxic effects on mitosis of HEp cells and the clastogenic effects on CHO cells. The activity of chromite, the only Cr(III) pigment capable of significantly increasing the frequency of SCE, is due to contamination with soluble Cr(VI). In contrast to the very low cytotoxicity of Cr(III), much higher chromium levels are detected in the cells incubated with soluble Cr(III) than with the same concentrations of soluble Cr(VI). 50% and 75% of chromium accumulated in the cells during treatments with Cr(VI) and Cr(III) respectively remains firmly bound to the cells, even when they are incubated for up to 48 h in normal growth medium. Chromium accumulated in the cells after treatment with Cr(III) is most probably bound to the cell membrane, whereas some of the Cr(VI) is transported through the cell membrane and reduced in the cell nucleus. The results of the present investigation are in agreement with those obtained with the same Cr(VI) and Cr(III) compounds in mutagenicity assays in bacteria and carcinogenicity tests in rodents. A re-evaluation of the mechanisms of chromium carcinogenisis is proposed
Cytogenetic alterations in Mytilus galloprovincialis as indicators of the presence of genotoxic pollutants in the marine environment: methodological aspets.
No full textRelease of mutagens from finished leather.
No full textExtracts of a leather widely used in the furniture and dress-making industries were tested for their mutagenic activity in the Salmonella/microsome assay. Extracts obtained after vigorous treatment of leather samples in a Soxhlet apparatus with toluene or ethanol were mutagenic in strain TA98 of S. typhimurium in the absence of S9 mix. The analysis of extracts of leather at various intermediate stages of processing showed that the mutagenic activity appeared after the coloration process. The responsible compound was identified to be an azo dye (Color Index: Acid Brown 83) whose mutagenic potency was about 4 revertants/micrograms
I coloranti azoici per cuoio: rischio mutageno e cancerogeno.
No full textThe paper reviews the carcinogenicity and mutagenicity data on azo dyes used in the leather industry. Two water soluble benzidine-based dyes were classified as "probably carcinogenic to humans" by the International Agency for Research on Cancer (IARC). No other dyes have been evaluated by the IARC. Of the 48 azo dyes assayed in the Salmonella/microsome test, 20 gave positive results. Attention is drawn to the important role of the in vivo metabolism of azo compounds, which includes a preliminary reduction of the azo bonds and subsequent release of the aromatic amines of the dye. A useful assay (Prival test) for evaluating the mutagenic properties of azo dyes involves a reductive step that permits the release of any genotoxic agents present in the compounds. A list of leather azo dyes is furnished that are considered as potentially harmful due to the presence of a carcinogenic aromatic amine (benzidine, p-aminobenzene and derivatives) in their formulae
Mutagenic activity of carbon black dyes used in the leather industry
No full textSeven carbon black pastes used as commercial leather dyes were tested for their mutagenicity in the Salmonella/microsome test (TA98 and TA100 strains). All the samples assayed either directly or after extraction with a 30-min sonication in benzene were devoid of mutagenicity both in the presence and absence of a metabolic activation preparation. After a 48-h extraction with boiling toluene in a Soxhlet apparatus, four samples were mutagenic in TA98 strain in the presence of S9 mix. The activity ranged from 1.3 to 9.6 induced revertants/mg equivalent of extract. A weak direct mutagenic activity in strain TA98 was shown by one extract. Polycyclic aromatic hydrocarbons (PAH) were determined in the toluene extracts by high resolution gas chromatography/mass spectrometry. The presence of PAH could explain the mutagenicity of only one sample (8.79 micrograms of total PAH/100 mg equivalents of extract), while low or undetectable levels of PAH were found in the other mutagenic extracts. The mutagenic activity was evident only after a vigorous extraction process, thus a low bioavailability of the mutagens present in these compounds is suggested
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