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Showing papers on "Sister chromatid exchange published in 1983"


Journal ArticleDOI
TL;DR: These techniques, which are considerably less cumbersome and time-consuming than the use of radioactive isotopes of thymidine, can be used for further human studies of cell kinetics and chromosomal replication in both normal and malignant cells.
Abstract: Using a monoclonal antibody to bromodeoxyuridine (BUdR) and immunohistochemistry, we measured the incorporation of this thymidine analogue into the DNA of human normal and malignant cells exposed in vivo. BUdR given as a constant intravenous infusion for 12 or 24 h daily for up to 13 d resulted in a steady-state plasma level of 10(-6) M during the infusion. We demonstrated extensive incorporation of BUdR into both normal skin, normal bone marrow, and malignant melanoma cells. In addition, this infusion of BUdR was adequate to identify sister chromatid exchanges from human marrow chromosomes exposed in vivo. Using this constant infusion, significant but reversible (acute) toxicity was observed with myelosuppression and skin photosensitivity. These techniques, which are considerably less cumbersome and time-consuming than the use of radioactive isotopes of thymidine, can be used for further human studies of cell kinetics and chromosomal replication in both normal and malignant cells.

324 citations


Journal ArticleDOI
TL;DR: Phagocytes in inflammatory lesions enzymatically reduce oxygen to reactive metabolites, which include Superoxide anions, hydrogen peroxide, and ...
Abstract: CHRONIC inflammation can be associated with cancer.1 Phagocytes in inflammatory lesions enzymatically reduce oxygen to reactive metabolites, which include Superoxide anions, hydrogen peroxide, and ...

252 citations


Journal ArticleDOI
TL;DR: The results show a large variability in the individual SCE base-line frequency, and the importance of the proliferating rate of the culture in determining the SCE frequency is stressed.

235 citations


Journal Article
TL;DR: Treatment with either X-rays or UV was effective in producing mutants resistant to 6-thioguanine, but treatment with hematoporphyrin derivative photoradiation did not induce any mutagenic activity above background levels.
Abstract: Cell culture studies have been performed to compare the mutagenic potential and the induction of sister chromatid exchanges for hematoporphyrin derivative photoradiation, ionizing radiation, and UV radiation. The mutation frequency in Chinese hamster ovary cells at the hypoxanthine-guanine phosphoribosyltransferase locus was measured using resistance to 6-thioguanine. Phenotypic expression time prior to mutation selection was also examined. Treatment with either X-rays or UV was effective in producing mutants resistant to 6-thioguanine, but treatment with hematoporphyrin derivative photoradiation (at comparable toxicity levels) did not induce any mutagenic activity above background levels. The hematoporphyrin derivative incubation and photosensitization conditions used in this study did induce sister chromatid exchanges at frequencies comparable to those induced by X-rays but at lower frequencies than for UV treatments.

108 citations


Journal ArticleDOI
TL;DR: A quick and easy method for partially coating 5-bromo-2′-deoxyuridine tablets with paraffin before they were subcutaneously implanted in mice increased availability of the chemical from 8 to more than 24 h and significantly reduced the baseline level of sister-chromatid exchanges.

92 citations


Journal ArticleDOI
TL;DR: The data indicate that catechol and hydroquinone can be optimally metabolized to produce reactive species, presumably benzo(semi)quinones, under conditions of lower metabolic activity than those necessary for phenol and benzene.

78 citations


Journal Article
TL;DR: The results show that erythrocytes are essential for the activation of Styrene in the lymphocyte test system, which probably results from the conversion of styrene into styrene 7,8-oxide by oxyhemoglobin.
Abstract: Styrene induces sister chromatid exchanges (SCEs) in human whole-blood lymphocyte cultures without exogenous metabolizing systems, which indicates that styrene is metabolically activated in this in vitro system. Whole-blood lymphocyte cultures from 11 male donors showed a clear increase in SCEs after a 48-hr treatment with styrene (2 mM) or with the reactive metabolite styrene 7,8-oxide (0.15 mM). Styrene (0.5 to 4 mM) induced a distinct dose-dependent increase of SCEs in whole-blood cultures (with 200 to 400 million red blood cells/ml) but only a slight effect in purified lymphocyte cultures (with 20,000 red blood cells/ml). SCE induction by styrene (2 mM) depended on the amount of red blood cells (0.02 to 2000 million/ml) added to the purified lymphocyte cultures. Cyclophosphamide, studied for comparison, clearly increased SCEs irrespective of the presence of erythrocytes. The results show that erythrocytes are essential for the activation of styrene in the lymphocyte test system. This activation probably results from the conversion of styrene into styrene 7,8-oxide by oxyhemoglobin.

76 citations


Journal ArticleDOI
11 Mar 1983-Science
TL;DR: Results based on breathing zone exposure and task frequency estimates over a 6-month period for 14 workers suggest that sister chromatid exchanges are a sensitive indicator of exposure and that cumulative dose and dose rate are important predictors of sister Chromatid exchange response.
Abstract: Sister chromatid exchange rates increased significantly in the peripheral lymphocytes of a small group of hospital workers exposed to ethylene oxide for as little as 3.6 minutes per day regularly over a period of months. Results based on breathing zone exposure and task frequency estimates over a 6-month period for 14 workers suggest that sister chromatid exchanges are a sensitive indicator of exposure and that cumulative dose and dose rate are important predictors of sister chromatid exchange response.

71 citations


Journal ArticleDOI
TL;DR: The majority of the high (12-fold elevated) baseline sister-chromatid exchanges (SCEs) that occur in the CHO mutant line EM9 appear to be a consequence of incorporated Brd Urd, and they arise during replication of DNA containing BrdUrd in a template strand.
Abstract: The majority of the high (12-fold elevated) baseline sister-chromatid exchanges (SCEs) that occur in the CHO mutant line EM9 appear to be a consequence of incorporated BrdUrd, and they arise during replication of DNA containing BrdUrd in a template strand. In normal CHO cells the alkaline elution patterns of DNA newly replicated on a BrdUrd-containing template are significantly altered compared with those seen during the replication on an unsubstituted template. The nascent DNA synthesized on such an altered template is delayed in reaching mature size, possibly because replication forks are temporarily blocked at sites occurring randomly along the template. Transient blockage of replication forks may be a prerequisite for SCE. The delay in replication on BrdUrd-substituted templates was greater in EM9 cells than in parental AA8 cells and was also greater in AA8 cells treated with benzamide, an inhibitor of poly(ADPR) polymerase, than in untreated AA8 cells. Under these conditions, treatment with benzamide also produced a 7-fold increase in SCEs in AA8. An EM9-derived revertant line that has a low baseline SCE frequency showed less delay in replication on BrdUrd-substituted templates than did EM9. However, under conditions where the template strand contained CldUrd, which was shown to produce 4-fold more SCEs than BrdUrd in AA8 cells, the replication delay in AA8 was not any greater in the CldUrd-substituted cells. Thus, other factors besides the delay appear to be involved in the production of SCEs by the template lesions resulting from incorporation of the halogen-substituted pyrimidine molecules.

58 citations


Journal ArticleDOI
TL;DR: The four major trihalomethanes (THMs) found in chlorinated drinking water have been investigated for their ability to induce sister chromatid exchanges (SCEs) and cell-cycle delays in human lymphocytes in vitro and to induce SCEs in mouse bone marrow cells in vivo.

53 citations


Journal ArticleDOI
TL;DR: The results show that the in vivo SCE method may be useful for the identification of genotoxins and that the outcome of the test is, for certain chemicals, dependent upon the route of exposure.
Abstract: Chemically-induced sister-chromatid exchange (SCE) was measured in vivo in bone marrow of Chinese hamsters Chemicals were administered either intraperitoneally or orally and increased SCE frequencies were noted with 6 of 6 direct-acting genotoxins and with 9 of 14 activation-dependent genotoxins Metronidazole, O -toluidine, 4-nitro- O -phenylenediamine and 2-nitro- p -phenylenediamine, compounds which have shown either mutagenic or carcinogenic activity, did not induce SCE in vivo 4 non-genotoxins and 4 different control treatments did not induce SCE The results show that the in vivo SCE method may be useful for the identification of genotoxins and that the outcome of the test is, for certain chemicals, dependent upon the route of exposure

Journal ArticleDOI
C C Huang, C S Han, X F Yue, C M Shen, S W Wang, F G Wu, B Xu 
TL;DR: HRT and HHRT were highly toxic, but they induced no increases in SCE frequency, indicating that cytotoxicity of a compound does not necessarily correlate with SCE induction.
Abstract: Growth inhibition in the Chinese hamster cell line V79 and in the human lymphoid cell line Raji and induction of sister chromatid exchange(s) (SCE) in V79 cells after treatment with six anticancer drugs [harringtonine (HRT), homoharringtonine (HHRT), camptothecin (CPT), hydroxycamptothecin (HCPT), lycobetaine (LBT), and oxalysine (OXL)] developed in the People's Republic of China were studied. OXL is a new antibiotic; all other drugs are plant extracts. All drugs caused a dose-dependent growth inhibition in both cell types, as evidenced by decreases in plating efficiencies of V79 cells and in viable cell counts of Raji. However, the degree of inhibition differed widely among the drugs. HRT, HHRT, CPT, and HCPT were the most potent growth inhibitors, LBT was next, and OXL was the least effective inhibitor. SCE analyses were made in V79 cells treated with a drug in the presence or absence of the metabolic activation system S9 mixture (S9 mix), except for the HRT assay in which the S9 mix was not used. CPT, HCPT, and LBT induced a dose-dependent increase in SCE frequencies, while HRT, HHRT, and OXL caused no SCE induction at any dose level used. CPT was the most powerful SCE inducer. HCPT induced SCE but at a much reduced rate when compared to that of CPT. LBT was a weak SCE inducer; SCE induction was seen only in cultures treated with 40 micrograms or more LBT/ml. Addition of the S9 mix did not alter SCE frequencies, indicating that the drugs were direct-acting agents. HRT and HHRT were highly toxic, but they induced no increases in SCE frequency, indicating that cytotoxicity of a compound does not necessarily correlate with SCE induction.

Journal ArticleDOI
TL;DR: These studies strongly suggest that most of the Bloom syndrome SCEs occur during the second cell cycle when BrdUrd-containing DNA is used as template for replication and that the normal level of BS SCE observed at the first mitosis of the hybrid cells is the result of SCE inhibition resulting from the fusion with normal cells.
Abstract: When Bloom syndrome (BS) cells labeled with bromodeoxyuridine (BrdUrd) for one round of DNA replication were fused with nonlabeled normal cells, the hybrid cells had a normal level of sister chromatid exchange (SCE) at the first mitosis after fusion. However, when normal cells treated with mitomycin C (MC) were fused with nontreated normal cells, the MC-induced SCE was not affected by fusion with normal cells. Single and twin SCEs were analyzed in the Colcemid-induced endoreduplicated normal and BS lymphoid B cells from diplochromosomes. In normal cells, the same number of SCEs occurs in each of the two cell cycles; the SCE ratio of single (6.30 SCEs per cell) to twin (2.92 SCEs per cell) was 2:1 on the endoreduplicated-cell basis, showing 1:1 on the diploid-cell basis. In BS cells, the SCE ratio of single (144.8 SCEs per cell) to twin (5.9 SCEs per cell) was 25:1 on the endoreduplicated-cell basis and was 12:1 on the diploid-cell basis. These studies strongly suggest that most of the BS SCEs occur during the second cell cycle when BrdUrd-containing DNA is used as template for replication and that the normal level of BS SCE observed at the first mitosis of the hybrid cells is the result of SCE inhibition resulting from the fusion with normal cells.

Journal ArticleDOI
TL;DR: Results suggest that poly(ADP-ribose) is important in the repair of DNA damage after exposure to alkylating agents and exercises a regulatory role in stabilizing chromatin structure whenever strand breaks occur in DNA.
Abstract: Benzamide and 3-aminobenzamide, inhibitors of poly(ADP-ribose) polymerase, synergistically enhanced the frequencies of unscheduled DNA synthesis and sister chromatid exchanges in Chinese hamster ovary (CHO) cells treated with N-methyl-N'-nitro-N-nitrosoguanidine (MNNG). These inhibitors also increased methyl methanesulfonate (MMS)- or MNNG-induced DNA strand breaks and significantly retarded the rejoining of strand breaks in CHO and HeLa S3 cells. These results suggest that poly(ADP-ribose) is important in the repair of DNA damage after exposure to alkylating agents and exercises a regulatory role in stabilizing chromatin structure whenever strand breaks occur in DNA.

Journal ArticleDOI
TL;DR: Results demonstrate that mitotic inhibition and aberrations are more sensitive indicators of BaP-induced damage than are developmental effects and suggest that cytogenetic analysis be included in the standard 48-hr sea urchin bioassay procedure when testing contaminants suspected of being mutagens.
Abstract: The teratogenic effects of environmental levels of the mutagen, benzo(a)pyrene (BaP), were investigated using the purple sea urchin (Strongylocentrotus purpuratus) and were related to embryonic cytotoxicity and genotoxicity as evidenced by the presence of aberrant chromosome arrangements during mitosis. Developmental abnormalities were observed in gastrulae treated with initial BaP concentrations of 1 to 50 ng/ml relative to solvent (ethanol)-treated control embryos. However, genotoxic effects were significant at the lowest BaP dose tested, 0.5 ng/ml. When compared to seawater and ethanol control embryos, fewer mitotic figures and increased frequencies of abnormal mitoses were present in BaP-treated gastrulae. Micronucleus formation, a widely used test of genotoxicity in mammals, was observed in embryos exposed to 1 to 50 ng/ml BaP. Grossly abnormal test embryos had high incidences of mitotic aberrations and were composed of large numbers of pycnotic, karyolytic, and multinucleated cells. The results from this cytogenetic analysis demonstrate that mitotic inhibition and aberrations are more sensitive indicators of BaP-induced damage than are developmental effects and suggest that cytogenetic analysis be included in the standard 48-hr sea urchin bioassay procedure when testing contaminants suspected of being mutagens. Cytologic-cytogenetic analysis is particularly suited for use with invertebrates and appears to be as sensitive as more laborious and expensive routine cytogenetic methods which involve karyotyping such as the sister chromatid exchange test.

Journal ArticleDOI
TL;DR: A progressive dose- and time-related enhancement in SCE frequencies induced by Cr3+ compounds in delayed cells was observed, and by prolongation of treatment time up to 48 h, a progressive doses-and-time- related enhancement inSCE frequencies was observed.
Abstract: The induction of sister chromatid exchanges (SCEs) in Chinese hamster V79 cells exposed to soluble CrCl3 and insoluble Cr2O3, compounds of trivalent chromium (Cr3+), was determined. Their ability to induce SCEs was compared with those of three hexavalent chromium (Cr6+) compounds: K2CrO4, Na2CrO4 and Na2Cr2O7. Both the delay in progression through the cell cycle induced by Cr3+ compounds and the SCE frequencies in the delayed cells were also evaluated. The exposure for 28 h to CrCl3 and Cr2O3 at concentrations of 9.7-39 micrograms and of 34-136 micrograms of Cr3+ per ml, respectively, induced a statistically significant (p less than 0.001) dose-dependent increase in SCEs up to 1.9-fold (CrCl3) and 4-fold (Cr2O3) over control levels. Compared with the effective concentrations of Cr6+ compounds, which produced up to 4-fold increase of SCEs, inducing concentrations of CrCl3 and Cr2O3 were 300- and 1000-fold higher in terms of chromium. By prolongation of treatment time up to 48 h, a progressive dose- and time-related enhancement in SCE frequencies induced by Cr3+ compounds in delayed cells was observed. Lower concentrations of Cr2O3, without effect after 28 h of treatment, induced an increase of SCEs by prolongation of exposure time.

Journal ArticleDOI
TL;DR: It was observed that mitotic index and cell cycle duration were affected by low temperature, and an increase as well as decrease in incubation temperature of cells leads to a higher frequency of sister chromatid exchanges in human lymphocytes.
Abstract: The effect of temperature variation on sister chromatid exchange (SCE) frequencies in human lymphocytes was studied. An increase as well as decrease in incubation temperature of cells leads to a higher frequency of sister chromatid exchanges than in cultures grown at 37°C. In addition, it was observed that mitotic index and cell cycle duration were affected by low temperature.

Journal ArticleDOI
TL;DR: Acetaldehyde caused a dose-dependent linear increase in the induction of sister chromatid exchanges in lymphocytes from both Germans and Japanese, causing significantly higher rates of SCE at acetaldehyde doses above 360 μM.
Abstract: Acetaldehyde, the first metabolite of ethanol oxidation, caused a dose-dependent linear increase in the induction of sister chromatid exchanges in lymphocytes from both Germans and Japanese Japanese, possessing only aldehyde dehydrogenase II isozyme (ALDH I deficient phenotype) and showing adverse effects after alcohol ingestion, did not differ in SCE rates from Germans and Japanese possessing isozymes I and II At acetaldehyde concentrations above 360 μM, a significant chromosome breaking effect and a definite delay in cell cycle events, as evaluated by the BdUrd labeling technique, was registered in all individuals Pyridoxal 5′-phosphate showed no protective effect against acetaldehyde-induced SCE formation in our system A 24-h extension of the normal culture period revealed significantly higher rates of SCE at acetaldehyde doses above 360 μM

Journal ArticleDOI
TL;DR: Results demonstrate for the first time that SCE can be detected in cultured lymphocytes of rodents following inhalation exposures and are consistent with the occurrence of elevated SCE frequencies in occupationally-exposed workers.

Journal Article
TL;DR: Aphidicolin, a specific inhibitor of DNA polymerase alpha, was found to induce high frequencies of endoreduplication in Chinese hamster V79 cells in a dose-dependent manner, consistent with the hypothesis thatDNA polymerase beta might be responsible for endore DUplication as was reported in mouse trophoblast cells.
Abstract: Aphidicolin, a specific inhibitor of DNA polymerase α, was found to induce high frequencies of endoreduplication in Chinese hamster V79 cells in a dose-dependent manner. The aphidicolin-induced endoreduplication was observed when cells were incubated at 37° but not at 41°. Since it is known that DNA polymerase β is more thermally labile than is DNA polymerase α, the data are consistent with the hypothesis that DNA polymerase α might be responsible for endoreduplication as was reported in mouse trophoblast cells. From the induced diplochromosomes, it was observed that the two unifilarly 5-bromodeoxyuridine-substituted chromatids are generally paired and located inside, whereas the two bifilarly 5-bromodeoxyuridine-substituted chromatids are flanking outside regardless of the presence of sister chromatid exchange or intradiplochromatid interchange.

Journal ArticleDOI
TL;DR: Of five tobacco alkaloids tested, only anatabine led to a dose-dependent enhancement of the number of sister-chromatid exchanges (SCE) in Chinese hamster ovary cells (CHO).
Abstract: Of five tobacco alkaloids tested, only anatabine led to a dose-dependent enhancement of the number of sister-chromatid exchanges (SCE) in Chinese hamster ovary cells (CHO). Nicotine and nornicotine at high concentrations increased the baseline frequency of SCEs moderately. Anabasine and myosmine had no influence on the spontaneous frequency of SCEs.

Journal ArticleDOI
TL;DR: Sister chromatid exchanges in chromosomes of group A, i.e., the group with the longest chromosomes, were significantly associated with asbestos exposure and cigarette smoking, with an interaction between the two.
Abstract: In vitro cytogenetic studies of amosite, chrysotile, and crocidolite asbestos have shown that these fibers may induce chromosome abnormalities and an elevated sister chromatid exchange (SCE) rate in mammalian cells. Twenty-five asbestos insulators (6 with radiographic asbestosis) were compared to 14 controls frequency matched for age and were found to have a marginally increased SCE rate in circulating lymphocytes with increasing years of exposure (P= 0.057). There was a significant association between SCE rate and smoking (P=0.002) after controlling for years of asbestos exposure and age. Smoking asbestos insulators had the highest SCE rate. Sister chromatid exchanges in chromosomes of group A, i.e., the group with the longest chromosomes, were significantly associated with asbestos exposure and cigarette smoking, with an interaction between the two.

Journal ArticleDOI
TL;DR: Asbestos caused no dose-related increase in sister-chromatid exchange levels in any of the cell types, but mitotic delay was induced in CHO-K1 cells and human fibroblasts and human lymphoblastoid cells.
Abstract: Possible mutagenic activity of the asbestos dusts crocidolite and chrysotile, and fine and coarse glass, was assessed in CHO-K1 cells, human fibroblasts and human lymphoblastoid cells using the sister-chromatid exchange assay and by examining the effects on cell kinetics. Asbestos caused no dose-related increase in sister-chromatid exchange levels in any of the cell types. However, mitotic delay was induced in CHO-K1 cells and human fibroblasts. The order of magnitude of induced delay in CHO-K1 cells was chrysotile > fine glass > crocidolite > coarse glass. Mitotic inhibition was more pronounced in these cells if they were still in suspension when initially exposed to the dusts compared with 1 h after plating.

Journal ArticleDOI
TL;DR: A reliable mouse peripheral blood lymphocyte culture assay has been developed for sister-chromatid exchange analysis and consistently yields sufficient numbers of metaphases from both B- and T-lymphocytes for SCE and chromosome-breakage studies.
Abstract: A reliable mouse peripheral blood lymphocyte culture assay has been developed for sister-chromatid exchange analysis. Crucial aspects for optimal mitogenesis include: (1) the addition of 5 × 105 leucocytes/ml culture; (2) the use of animals with leucocyte counts from 5 to 7 × 106/ml; and (3) the addition of 6% mouse plasma for the first 24 h of a total 54-h incubation. When 7 μg phytohemagglutinin/ml were used to stimulate T-lymphocytes, the mitotic index was 3.4 ± 0.3%, 28 ± 2.3% of the metaphases were in first-division, and the SCE frequency/metaphase was 7.3 ± 0.2 (n = 14 mice). When B-lymphocytes were stimulated with 60 μg lipopolysaccharide/ml, the mitotic index was 4.5 ± 0.3%, 64 ± 3.3% of the metaphases were in first-division, and the SCE frequency/metaphase was 4.6 ± 0.1 (n = 7 mice). This culture method consistently yields sufficient numbers of the metaphases from both B- and T-lymphocytes for SCE and chromosome-breakage studies.

Journal ArticleDOI
TL;DR: It is suggested that a genotoxic effect due to inorganic lead may occur in long-term lead-exposed men and that this effect could be related to a serious disease for which he was undergoing treatment.

Journal Article
TL;DR: Second- and third-division cell SCE data produced by the various protocols indicate persistence of SCE-inducing lesions with no evidence of repair, and first-cycle ethyl carbamate treatment was less effective than was second-cycle treatment in inducing SCEs.
Abstract: Various treatment protocols were designed to investigate sister chromatid exchanges (SCEs) induced over successive posttreatment cell cycles in bone marrow and alveolar macrophage cells following treatment of C57BL/6J × DBA/2J F1 mice by i.p. injection of ethyl carbamate (3.3 mmol/kg). The same initial extent of alkylation in bone marrow and alveolar macrophages was suggested by identical SCE frequencies produced in both cell types by a one-cycle exposure protocol. The relatively lower responses in bone marrow cells by all other protocols may be a result of its faster mean population-cycling time. Second- and third-division cell SCE data produced by the various protocols indicate persistence of SCE-inducing lesions with no evidence of repair. In spite of the demonstrated lack of repair, first-cycle ethyl carbamate treatment was less effective than was second-cycle treatment in inducing SCEs. These results could not be attributed to selection of less-damaged cells over 2 cycles or to enhanced bromodeoxyuridine sensitivity in the second-cycle treatment protocol. It is speculated that the apparent cancellation of SCEs occurring over two successive cycles in the two-cycle exposure protocol may indicate the transient presence of ethyl carbamate-induced DNA interstrand cross-links. A possible mechanism of action of ethyl carbamate involving the formation of a transient cross-link and a persistent DNA monoadduct is postulated.

Journal Article
TL;DR: The results show that, although Adriamycin and menogarol differ significantly in their bacterial mutagenicity (Ames assay), they have similar genotoxic activity in several mammalian systems.
Abstract: Adriamycin and menogarol are anthracyclines which cause more than 100% increase in life span of mice bearing P388 leukemia and B16 melanoma. Unlike Adriamycin, menogarol does not bind strongly to DNA, and it minimally inhibits DNA and RNA synthesis at lethal doses. Adriamycin is a clinically active drug, and menogarol is undergoing preclinical toxicology at National Cancer Institute. In view of the reported mutagenicity of Adriamycin, we have compared the genotoxicity of the two drugs. Our results show that, although Adriamycin and menogarol differ significantly in their bacterial mutagenicity (Ames assay), they have similar genotoxic activity in several mammalian systems. Adriamycin is strongly mutagenic in the Ames assay with TA98 and TA100. Menogarol is nonmutagenic to TA98 and TA100. For the mammalian cell culture systems, V79 (Chinese hamster) cells are exposed for 2 hr to drug, following which cell survival, induction of sister chromatid exchanges, chromosome damage, and production of mutants resistant to 6-thioguanine are measured. The percentage of survival obtained with the two drugs ranges between 25 and 50% at 0.15 microgram/ml and 5 to 15% at 0.3 microgram/ml. At 0.15 microgram/ml, Adriamycin and menogarol increase the percentage of cells with chromosome damage from a background level of 8.8 to 30 and 22.5%, respectively. The same drug concentration causes a small but significant increase in sister chromatid exchange rate. Both drugs are equally active (increase mutation frequency about 3- to 6-fold above background) in producing 6-thioguanine-resistant mutants. The induction of micronuclei in polychromatic erythrocytes of rats is the most sensitive assay system. Both drugs cause 10- to 15-fold increase in micronuclei at nontoxic doses.

Journal ArticleDOI
TL;DR: A comparison of Vicia-faba-root S10 with rat-liver S9 was made in their capacity to bring about, in vitro, the metabolic activation of ethanol, maleic hydrazide and cyclophosphamide that can lead to the induction of sister-chromatid exchanges (SCEs) in CHO cells.
Abstract: A comparison of Vicia-faba -root S10 with rat-liver S9 was made in their capacity to bring about, in vitro, the metabolic activation of ethanol, maleic hydrazide (MH) and cyclophosphamide (CP) that can lead to the induction of sister-chromatid exchanges (SCEs) in CHO cells. When NADP was a cofactor in the S9 mix, ethanol, MH and CP all induced an increase of SCEs with rat-liver S9. With Vicia-root S10, however, ethanol induction of SCEs was very weak and no effect at all was observed with MH and CP. When NAD was a cofactor in the S9 mix, Vicia-root S10 activated ethanol and produced an increase in SCEs.

Journal ArticleDOI
TL;DR: The frequency of sister-chromatid exchanges in human lymphocytes cultured in vitro was not changed after a 30-min exposure to a 2 MHz focused, diagnostic ultrasound beam with a pulse repetition rate of 1000 Hz.

Journal ArticleDOI
TL;DR: The ability of simple alkylating carcinogens to induce sister-chromatid exchange (SCE) has been well established, although theAlkyl lesion(s) leading to SCE formation have not been delineated.