Showing papers on "Sister chromatid exchange published in 1980"
TL;DR: The frequency of unequal crossing over, as measured by the deletion or duplication of an inserted genetic marker (LEU2), is sufficient to maintain the sequence homogeneity of the rDNA repeat units.
Abstract: Unequal sister chromatid exchanges occur at the ribosomal DNA locus of yeast during mitotic growth. The frequency of unequal crossing over, as measured by the deletion or duplication of an inserted genetic marker (LEU2), is sufficient to maintain the sequence homogeneity of the rDNA repeat units.
395 citations
TL;DR: It is shown that the chronic treatment of a Chinese hamster ovary and a SV40-transformed human skin fibroblast cell line with non-toxic levels of MNNG renders the cells resistant to the induction of sister chromatid exchange (SCE) by further alkylation damage.
Abstract: When Escherichia coli is chronically exposed to very low, nontoxic doses of a monofunctional alkylating agent (notably N-methyl-N′-nitro-nitrosoguanidine, MNNG), the adaptive DNA repair pathway is induced which enables the bacteria to resist the killing and mutagenic effects of further alkylation damage1–3. Mutation resistance in adapted bacteria is achieved, at least partly, by a greatly increased capacity of the cells to eliminate the minor DNA alkylation product O6-methyl-guanine4–6, which has been strongly implicated as premu-tagenic7,8 and precarcinogenic9. We now show that the chronic treatment of a Chinese hamster ovary (CHO) and a SV40-transformed human skin fibroblast (GM637) cell line with non-toxic levels of MNNG renders the cells resistant to the induction of sister chromatid exchange (SCE) by further alkylation damage. CHO cells also become resistant to killing (GM637 cells have not yet been tested). Having ruled out explanations such as changes in cell cycle distribution, mutagen permeability and mutagen detoxification, we conclude that resistance is probably achieved by the cells becoming more efficient at repairing alleviation damage, analogous to the adaptive response of E. coli1.
210 citations
TL;DR: Analysis of sister chromatid exchange formation in cytological systems has already provided information about chromosome structure and has been used to detect the effects of clastogens and to differentiate between chromosome fragility diseases.
Abstract: Sister chromatid exchanges (SCEs) represent the interchange of DNA replication products at apparently homologous loci. These exchanges presumably involve DNA breakage and reunion, although little is known about the molecular basis of sister chromatid exchange formation, and information about the biological significance of exchanges is largely circumstantial. In spite of these uncertainties, analysis of sister chromatid exchange formation in cytological systems has already provided information about chromosome structure and has been used to detect the effects of clastogens and to differentiate between chromosome fragility diseases.
187 citations
TL;DR: The SCEs of patients under chemotherapy were about five times higher than those of healthy subjects, and the oncology nurses had a higher SCE frequency than other hospital nurses, but this difference was not statistically significant.
Abstract: In oncology units, personnel handling chemotherapeutic drugs may occasionally be exposed to small amounts of genotoxic agents. This exposure was obviously the cause of the increased frequencies of sister chromatid exchange (SCE) observed in nurses in daily contact with cytostatics (N = 20, mean SCEs/cell +/- SE 9.4 +/- 0.3) as compared to a group of office workers (N = 10, mean SCEs/cell 8.1 +/- 0.3). The oncology nurses also had a higher SCE frequency than other hospital nurses (N = 10, mean SCEs/cell 8.7 +/- 0.2), but this difference was not statistically significant. The SCEs of patients under chemotherapy were about five times higher (mean SCEs/cell 36.8 +/- 0.6) than those of healthy subjects.
131 citations
TL;DR: Data provide direct evidence that genetically responsive mouse embryos (early postimplantation stage) possess the subcellular processes necessary for induction of enzymes that metabolize benzo[a]pyrene to its chemically active forms(s).
Abstract: Mouse embryos explanted at 7 1/2 or 8 1/2 days of gestation were cultured in medium containing benzo[a]pyrene and supplemented with 5-bromodeoxyuridine to allow detection of sister chromatid exchanges. The murine Ah locus regulates the inducible metabolism of polycyclic hydrocarbons such as benzo[a]pyrene. A high frequency of sister chromatid exchange was induced by benzo[a]pyrene in embryos from three Ah-"responsive" inbred strains (BALB/cDub, C3H/AnfCum, and C57BL/6N); there was little or no increase in two Ah-"nonresponsive" inbred strains (AKR/J and DBA/2J). Benzo[a]pyrene also induced sister chromatid exchanges in the Ah-responsive recombinant inbred line B6NXAKN-12 but not in the Ah-nonresponsive recombinant inbred line B6NXAKN-3. Sister chromatid exchange in cultured Ah-responsive mouse embryos was thus shown to be a sensitive assay. These data provide direct evidence that genetically responsive mouse embryos (early postimplantation stage) possess the subcellular processes necessary for induction of enzymes that metabolize benzo[a]pyrene to its chemically active forms(s). Both the Ah regulatory gene product (a cytoslic receptor) and the structural gene product (inducible cytochrome P1-450) therefore appear to be functional at an early embryonic age. Furthermore, this metabolic capacity may play an important role in the damage to embryonic cells by polycyclic hydracarbons.
114 citations
TL;DR: The differences in both the type and magnitude of the response of bone marrow cellular populations, as determined by different cytogenetic end points in male and female DBA/2 mice exposed to benzene or to phenobarbital and benzene, suggest not only that a metabolite of benzene is responsible for the observed effects, but that different metabolites may be involved in different end points.
Abstract: Exposure of adult male and female DBA/2 mice to 3100 ppm benzene for 4 hr significantly increased the frequency of sister chromatid exchanges in bone marrow cells of both sexes, inhibited marrow cellular proliferation (but only in male mice), and did not significantly increase the frequency of chromosomal aberrations in either sex. Phenobarbital pretreatment synergistically interacted with benzene exposure to further increase sister chromatid exchanges in female mice, induce greater inhibition of cellular proliferation in male mice, and induce a significant level of chromatid-type chromosomal aberrations in both sexes. During the second day after exposure to benzene there was increased inhibition of cellular proliferation in male mice and both new DNA damage and persistance of old DNA damage in female mice. The differences in both the type and magnitude of the response of bone marrow cellular populations, as determined by different cytogenetic end points in male and female DBA/2 mice exposed to benzene or to phenobarbital and benzene, suggest not only that a metabolite of benzene is responsible for the observed effects, but that different metabolites may be involved in different end points.
112 citations
Journal Article•
109 citations
TL;DR: The sister chromatid exchange frequencies of newly established and old cell lines derived from patients with lymphatic tumors or leukemia were compared to the SCE rates of lymphoblastoid cell lines of normal controls and all cell lines from malignant tumors displayed significantly higher SCE values than the control lines.
Abstract: The sister chromatid exchange (SCE) frequencies of six freshly established and two old cell lines derived from patients with lymphatic tumors or leukemia were compared to the SCE rates of lymphoblastoid cell lines of normal controls. All cell lines from malignant tumors displayed significantly higher SCE values than the control lines. In general, the SCE rates seem to be correlated to the number of chromosomal markers and the degree of karyotypic instability of each line.
103 citations
01 Jan 1980
TL;DR: Some of the problems and perspectives of the SCE test are explored and some of the results obtained so far are reviewed.
Abstract: The recent introduction of the sister-chromatid exchange (SCE) test has revolutionized the cytogenetic approach to the identification of biologically hazardous chemicals. Increasingly, laboratories are turning to this technique in preference to scoring chromosome aberrations. This chapter explores some of the problems and perspectives of the SCE test and reviews some of the results obtained so far.
101 citations
94 citations
TL;DR: A close correlation was observed between the ability to induce SCEs or chromosomal aberrations and the mutagenic potency in bacteria and the results from microbial reversion assays.
Abstract: The induction of sister-chromatid exchanges (SCEs), chromosomal aberrations and polyploids was investigated in cultured Chinese hamster cells treated with pesticides or a related compound positive in microbial reversion assays. The chemicals tested were captan, captafol, 1,2-dibromoethane (EDB), 1,2-dibromo-3-chloropropane (DBCP), 5-nitro-1-naphrhonitrile (NNN), p-dimethylaminobenzenediazo sodium sulfonate (DAPA), 2-hydrazinoethanol (HEH), vamidothion, dichlorovos (DDVP), N-nitroso-ethylenethiourea (N-nitroso-ETU), and 2,4-dinitrophenyl thiocyanate (NBT). A significant and dose-dependent increase in the frequency of SCEs and chromosomal aberrations was observed in the cell cultures treated with captan, captafol, EDB, DBCP, HEH, DDVP, vamidothion, DAPA or N-nitroso-ETU or NBT produced a significant increase in the frequency of polyploid cells, whereas the other agents did not. When compared with results from microbial reversion assays, a close correlation was observed between the ability to induce SCEs or chromosomal aberrations and the mutagenic potency in bacteria (r:0.71-0.84).
TL;DR: It is confirmed that cyclophosphamide induced chromosome breakage and SCE only in the presence of a metabolic activating system (liver S9) and after metabolism, cycloph phosphamde was more active than the other agents in inducing SCE.
Abstract: The effects of cyclophosphamide and three of its known metabolites (nitrogen mustard, acrolein, and nor-nitrogen mustard on chromosome breakage and sister chromatid exchange (SCE) were analyzed in vitro with and without the presence of a metabolic activating system (liver S9). We confirmed that cyclophosphamide induced chromosome breakage and SCE only in the presence of S9. After metabolism, cyclophosphamde was more active than the other agents in inducing SCE. Thus, the agent(s) directly responsible for this induction of a high SCE rate was not analyzed in this study. On the other hand, acrolein was most toxic to cell proliferation and most active in inducing chromosome breakage. The cytogenetic toxicity of these agents in comparison with their mutagenic and therapeutic activities is discussed.
TL;DR: Peripheral blood lymphocytes from 32 male rotogravure workers with daily exposure to toluene were studied for chromosome aberrations and sister chromatid exchange and a significant increase was observed among smokers, both exposed and occupationally unexposed, compared to nonsmoking referents.
Abstract: Peripheral blood lymphocytes from 32 male rotogravure workers with daily exposure to toluene were studied for chromosome aberrations and sister chromatid exchange. Neither of these two cytogenetic parameters differed significantly from the corresponding frequencies in 15 unexposed control subjects. However, a significant increase in sister chromatid exchange was observed among smokers, both exposed and occupationally unexposed, compared to nonsmoking referents.
TL;DR: The mutagenicity of lead chromate in human lymphocytes appears to be entirely due to the chromate ion since chromosome aberrations were induced by potassium chromate but not lead chloride.
Abstract: Possible mutagenic activity of lead chromate in mammalian cells was studied using assays for chromosome aberrations and sister-chromatid exchanges in cultured human lymphocytes, and DNA fragmentation as detected by alkaline-sucrose gradient sedimentation in cultured Chinese hamster ovary (CHO) cells. Lead chromate caused dose-related increases in chromosome aberration and sister-chromatid exchange in human lymphocytes. No increase in DNA damage was observed in CHO cells, possibly due to the relative insensitivity of the CHO cells and the limited solubility of lead chromate in tissue culture medium. The mutagenicity of lead chromate in human lymphocytes appears to be entirely due to the chromate ion since chromosome aberrations were induced by potassium chromate but not lead chloride.
TL;DR: There was no difference in the SCE rate between smokers and nonsmokers, nor was there any difference between heavy and light smokers.
Abstract: The incidence of sister chromatid exchanges in smokers and nonsmokers was investigated. There was no difference in the SCE rate between smokers and nonsmokers, nor was there any difference between heavy (>10 per day) and light (<10 per day) smokers.
TL;DR: Both styrene and its presumed active metabolite styrene oxide show dose response as potent inducers of sister chromatid exchanges (SCEs) in human lymphocyte cultures.
Abstract: Both styrene and its presumed active metabolite styrene oxide show dose response as potent inducers of sister chromatid exchanges (SCEs) in human lymphocyte cultures. The SCE inducing and clastogenic capacity of styrene in lymphocytes in vitro can be explained by gas chromatographically measurable increase of styrene oxide in styrene treated cultures.
01 Jan 1980
TL;DR: Of the synthetic bases which may be incorporated in DNA, two of the most interesting are the thymine analogs, 5-bromouracil and 5-iodouracicil.
Abstract: Of the synthetic bases which may be incorporated in DNA, two of the most interesting are the thymine analogs, 5-bromouracil and 5-iodouracil. DNAs containing these bases have a number of altered properties which have been used to advantage by molecular biologists.
TL;DR: Workers in the Swedish paint industry exposed to a mixture of organic solvents, mainly containing xylene or toluene, were investigated for genotoxic effects and there was no correlation between SCE and chromosome breaks.
Abstract: Workers in the Swedish paint industry exposed to a mixture of organic solvents, mainly containing xylene or toluene, were investigated for genotoxic effects. No difference in the frequency of sister chromatid exchanges (SCE), 0.192 and 0.193 per chromosome, respectively, was noted in the peripheral lymphocytes of the exposed group of 17 workers and their matched reference group. No correlation was found between xylene or toluene exposure and SCE frequency nor between total solvent exposure and SCE frequency. The frequency of chromosome aberrations was also investigated for the five most exposed workers and their matched referents, and no difference was found. There was no correlation between SCE and chromosome breaks.
TL;DR: All 4 CS cell strains proved to be hypersensitive to UV for both of these end-points, but no close correlation between levels of SCE and lethality was observed.
Abstract: Ultraviolet light-induced sister-chromatid exchanges (SCE) and cell killing were investigated in 4 fibroblast cell strains from patients with the sun-sensitive disease Cockayne's syndrome (CS) All 4 CS cell strains proved to be hypersensitive to UV for both of these end-points, but no close correlation between levels of SCE and lethality was observed Cell strains from two individuals heterozygous for CS were indistinguishable from wild-type
Journal Article•
TL;DR: The results argue that promotion by TPA does not proceed by a mechanism involving genetic recombination or the altered expression of newly mutated alleles.
Abstract: The potent tumor promoter 12- O -tetradecanoylphorbol-13-acetate (TPA) was tested for its ability ( a ) to induce sister chromatid exchange, ( b ) to increase the rate of transition at the adenine phosphoribosyltransferase ( aprt ) locus from the presumptive heterozygous state (+/-) to the homozygous state (-/- or -), and ( c ) to enhance the frequency of mutations expressed after ultraviolet radiation mutagenesis. We have found no significant effect of TPA in any of these experiments. Sister chromatid exchange frequencies in both V79 and Chinese hamster ovary cells remained unchanged by TPA treatment under various conditions, a result inconsistent with the hypothesis that an important effect of TPA might be to increase the rate of chromosomal mitotic recombination (and hence segregation of recessive mutations) in a manner akin to increased chromatid recombination. We have also been unable to obtain evidence for mitotic recombination affecting the aprt locus in Chinese hamster ovary cells for which the rate of change to a high level of resistance to azaadenine was measured. The rate of 8.6 × 10-7 mutation (and/or segregations) per cell generation assessed by fluctuation analysis was not increased by the continuous presence of TPA, 4 µg/ml, in the medium. In the third set of experiments, mutant frequencies in Chinese hamster ovary cells after ultraviolet mutagenesis were measured for the markers ouabain resistance, thioguanine resistance, and azaadenine resistance, under conditions with and without pretreatment with TPA before mutant selection. No convincing enhancement in mutation expression was observed. In summary, these results argue that promotion by TPA does not proceed by a mechanism involving genetic recombination or the altered expression of newly mutated alleles.
TL;DR: The data indicate that chromatid and isochromatid deletions have different molecular steps in their formation, and that different molecular mechanisms are also involved in the symmetrical and unsymmetrical rejoining in Chromatid interchanges.
Abstract: Repair- and recombination-defective mutations at two loci (mei-9 and mei-41) of Drosophila melanogaster have been examined for their effects on the induction of chromosome aberrations by x-rays and the formation of sister chromatid exchanges (SCEs). Irradiation of larval neuroblast cells during the S phase with x-rays showed that mutants at both of these loci are about 10 times more sensitive than wild type to the induction of chromosome aberrations. The pattern of induced aberrations was characteristic for each mutant locus: in cells bearing mei-9 mutations most breaks were chromatid deletions, whereas in the presence of mei-41 mutations similar frequencies of chromatid and isochromatid deletions were observed. Furthermore, chromatid interchanges could not be induced in cells carrying mei-9 alleles; therefore these mutations define a step necessary for chromatid rejoining. mei-41 alleles also define a function involved in the formation of chromatid interchanges; total exchanges were less frequent than expected from nonmutant controls; and the proportion of exchanges arising by symmetrical rejoining was markedly reduced. These data indicate that chromatid and isochromatid deletions have different molecular steps in their formation, and that different molecular mechanisms are also involved in the symmetrical and unsymmetrical rejoining in chromatid interchanges. Neuroblast cells of larvae bearing mei-9 and mei-41 alleles were also treated for 13 hr with 5-bromodeoxyuridine at 9 μg/ml in order to differentiate sister chromatids for the scoring of SCEs. Whereas mei-41 had a normal level of SCEs, mei-9 exhibited a frequency of SCEs that was about 70% that of the control. Because both mei-9 and mei-41 mutations result in defective meiotic recombination, these data suggest that they define steps shared by symmetrical interchange formation and meiotic recombination that do not participate in the formation of most SCEs.
TL;DR: For a series of mutagens, induction of SCE does not necessarily result from a single specific DNA lesion, therefore, SCE can be considered a qualitative indicator of potential mutagenic events.
Abstract: The mechanism of induction of sister chromatid exchange (SCE) was investigated by treating Chinese hamster V-79 cells with two ethylating and two methylating mutagens at doses, taken from linear response curves, that produced 30 SCE/cell. Concentrations of the DNA alkylation products were measured or calculated at 11 DNA base sites and at the phosphodiester bond. Ethyl methanesulfonate, N-methyl- and N-ethyl-N-nitrosourea produced comparable concentrations (3.3 to 3.5 micromol product/mol DNA phosphate) of O6-alkylguanine. Hence, alkylation at O6 of guanine appears relevant to SCE induction for these mutagens. Since alkylation at O6 of guanine has been positively correlated with mutagenesis in V-79 cells, these findings support the suggestion that SCE and mutagenesis can result from a common DNA lesion. Methyl methanesulfonate (MMS) produced very little O6-methylguanine, but did produce 3-methylthymine and 3-methyladenine, either of which might account for the MMS-induced SCE. Thus, for a series of mutagens, induction of SCE does not necessarily result from a single specific DNA lesion. Therefore, SCE can be considered a qualitative indicator of potential mutagenic events.
TL;DR: Sister chromatid exchange (SCE) frequency was not increased in G0 lymphocytes following irradiation up to 400 rads and increased BrdUrd concentration only slightly increased the sensitivity of the SCE technique to irradiation doses of 50 rads.
Abstract: Sister chromatid exchange (SCE) frequency was not increased in G0 lymphocytes following irradiation up to 400 rads. Lymphocytes irradiated after 42 or 60 hours of culture showed a dose-dependent increase in exchange frequency at 100 and 200 rads. SCE was not increased in cells irradiated in G2 (68.5 hours).
Lymphocytes maintained in a 5-Bromodeoxyuridine (BrdUrd) free medium and irradiated 42 hours after culture initiation showed an increase in SCE if BrdUrd was added immediately after irradiation, but no increase was found if there was a 5 hour holding period prior to the addition of BrdUrd.
The effect on induced SCE frequency of heightened radiosensitivity due to increased amounts of BrdUrd was also investigated. When the BrdUrd concentration was increased from 10 μg/ml to 50 μg/ml, the percent increase in X-ray-induced SCE was lower at 50 μg/ml. In addition, increased BrdUrd concentration only slightly increased the sensitivity of the SCE technique to irradiation doses of 50 rads.
Journal Article•
TL;DR: Peripheral lymphocytes from cancer patients receiving mitomycin C treatment were examined for cytogenetic effects and the significance of the specific kinetics of change in the sister chromatid exchnage frequency after in vivo treatments is discussed in relation to cancer chemotherapy.
Abstract: Peripheral lymphocytes from cancer patients receiving mitomycin C treatment were examined for cytogenetic effects The treatment consisted of iv injections of mitomycin C at a dose of 4 mg given twice a week for 2 weeks The lymphocytes were cultured in vitro for 72 hr with phytohemagglutinin and 5-bromodeoxyuridine, and then sister chromatid exchanges were scored Before treatment with mitomycin C, the frequencies of sister chromatid exchanges in lymphocytes of cancer patients were similar to those of healthy controls After the first and second treatments in vivo with mitomycin C, the frequencies of sister chromatid exchanges increased with time, reached a peak in about 24 hr, and then returned to the pretreatment level in about 48 hr, in contrast to the case of in vitro exposure to mitomycin C After the third and fourth injections, however, the frequency increased further and did not return to the original level The significance of the specific kinetics of change in the sister chromatid exchange frequency after in vivo treatments is discussed in relation to cancer chemotherapy
TL;DR: 12-O-Tetradecanoylphorbol 13-acetate (TPA), a known tumor promoter, enhances the morphologic transformation of Syrian hamster embryo cells induced by low transforming concentrations of N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) without potentiation of cell lethality or of changes in sister chromatid exchanges (SCEs) or chromosomal aberration frequencies.
Abstract: 12-O-Tetradecanoylphorbol 13-acetate (TPA), a known tumor promoter, enhances the morphologic transformation of Syrian hamster embryo cells induced by low transforming concentrations of N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) (0.025-0.1 microgram/ml) without potentiation of cell lethality or of changes in sister chromatid exchanges (SCEs) or chromosomal aberration frequencies. When MNNG was added to logarithmically growing cultures and TPA was added 2, 24, or 48 hr later, no changes in SCE frequency relative to MNNG alone occurred. Similar results were obtained with TPA in cells that had been exposed to MNNG in stationary growth phase. Whereas no transformation occurred with TPA alone and pretreatment with TPA did not affect MNNG transformation, its addition 2 hr after MNNG reduced transformation frequency but addition 24-72 hr after MNNG increased the transformation frequency up to 6-fold. TPA had a minimal effect on increasing the transformation frequency (2-fold) induced by MNNG at 0.25 micrograms/ml, a high concentration. Of three polycyclic hydrocarbons, perylene, benzo[g,h,i]perylene, and benz[a]anthracene, known as weak or noncarcinogens, only benz[a]anthracene induced a very low transformation frequency; however, after TPA, transformation occurred with all three. Because the number of cells whose transformation was initiated by low doses of carcinogen is much larger than the number of cells giving rise to transformed colonies in the absence of TPA, the frequency of the initial event is greater than can be expected from point mutations. Furthermore, the promotional aspect of transformation is not accompanied by a parallel increase in SCE.
TL;DR: An apparently reverse finding of decreased sister-chromatid exchanges may be a manifestation of the subtler effect of the environmental chemical on the DNA replication mechanism.
Abstract: Cytogenetic and cytokinetic changes were examined using the differential staining method for sister chromatids in cultured lymphocytes from 16 female workers who had been occupationally exposed to up to 40 ppm of benzene for 1–20 years. While no increases in the number of structural and numerical chromosome aberrations nor any changes in cell-cycle kinetics were observed, a slight decrease in the frequency of sister-chromatid exchanges was detected. This apparently reverse finding of decreased sister-chromatid exchanges may be a manifestation of the subtler effect of the environmental chemical on the DNA replication mechanism. Possible dose-effect relationship in benzene-induced chromosome aberrations was discussed.
TL;DR: Observations in some human genetic mutant cells defective in their ability to repair DNA damage indicate that sister chromatid exchanges and chromosome aberrations are cytological manifestations of replication-mediated dual-step repair pathways that are in operation to tolerate DNA damage when damage-bearing DNA enters and passes through semiconservative replication.
Abstract: Apparent association between the ability to induce chromosome aberrations and sister chromatid exchanges and mutagenic-carcinogenic potential found in a variety of physical and chemical agents has led us to speculate that these cytogenetic changes might be reflection of DNA damage and repair and might provide indices of mutagenic changes. However, the mechanisms of their formation and their relation to DNA repair as well as the mechanism of their linking to mutation are by no means well understood. Studies in some human genetic mutant cells defective in their ability to repair DNA damage indicate, as a testable proposition, that sister chromatid exchanges and chromsome aberrations are cytological manifestations of replication-mediated dual-step repair pathways that are in operation to tolerate DNA damage when damage-bearing DNA enters and passes through semiconservative replication. The observations are also in line with idea that the majority of sister chromatid exchanges can arise when damage DNA attempts replication possibly by a process relating with the replicative bypass repair mechanisms such as those proposed by Fujiwara and Tatsumi [34] and Higgins et al. [54], while chromosome aberration formation and some fraction of sister chromatid exchanges are related with the postreplication repair processes which attempt to rescue damaged template post-replicationally by de novo synthesis or recombination type repair systems. The former sister chromatid exchange-relating process seems to link mutation to less extent, if any, than the latter process, which is caffeine sensitive and likely to be error-prone.
TL;DR: It is shown here that a storage effect can be demonstrated for sister chromatid exchange (SCE) and, to a much greater extent, for chromosome structural changes in human lymphocytes exposed to mitomycin C and stored for various periods before stimulation with phytohaemagglutinin (PHA).
Abstract: Two of the distinctive differences between the mutagenic repsonse of Drosophila sperm exposed to X rays and to alkylating agents, are: (1) an increase in the incidence of chromosomal structural changes with increasing storage time (days, or weeks) prior to fertilisation following treatments with chemical mutagens, but not X rays, and (2) the frequent occurrence of F1 individuals mosaic for either mutation or chromosome structural change after chemical treatment, but not after X-ray radiation1. Similar time-dependent increases in mutations and chromosome aberrations have also been reported for fungal spores2 and plant seed root meristem cells3 exposed to alkylating agents, but no enhancing effect of storage could be demonstrated in confluent human fibroblasts exposed to an alkylating agent in vitro4. We show here that a storage effect can be demonstrated for sister chromatid exchange (SCE) and, to a much greater extent, for chromosome structural changes in human lymphocytes exposed to mitomycin C and stored for various periods before stimulation with phytohaemagglutinin (PHA). Moreover, mitomycin C-treated G0 cells, which normally develop only chromatid-type aberrations, also yield chromosome-type changes after storage. This result implies a time-dependent alteration in the induced lesions following storage, and predicts a decreasing incidence of mosaicism with increasing storage time—a result that has indeed previously been reported for stored Drosophila sperm5.
TL;DR: The genotoxic risk caused by environmental chemicals may be detected by analyzing the frequency of sister chromatid exchanges in peripheral blood lymphocytes, and it is also observed to be significantly higher in lymphocytes of laboratory personnel.
Abstract: The genotoxic risk caused by environmental chemicals may be detected by analyzing the frequency of sister chromatid exchanges in peripheral blood lymphocytes Up to now the frequency of sister chromatid exchange has been correlated with smoking habits, and it is also observed to be significantly higher in lymphocytes of laboratory personnel