[Cytogenetic analysis of lymphocytes from epileptic dogs].
Explore the source record for details and available documents.
Animals↗
Biomedical subjects
G Obe
Publications and source records attributed to G Obe.
The restriction endonuclease Alu I induces chromosomal aberrations in human peripheral lymphocytes in vitro.
The restriction endonuclease Alu I (recognition site AG/CT) produces chromosomal aberrations in isolated human peripheral lymphocytes in vitro. The aberrations are of the chromosome-type when the cells are treated in G1 and of the chromatid-type when the cells are treated in late S, early G2. Additional treatment with ammonium sulphate leads to higher aberration frequencies than treatment with Alu I alone.
Ammonium Sulfate↗
How do in vivo mammalian assays compare to in vitro assays in their ability to detect mutagens?
Explore the source record for details and available documents.
Animals↗
Chromosomal damage induced in human lymphocytes by low doses of D-T neutrons.
Unstable chromosome aberrations induced by in vitro irradiation with zero plus seven low doses of 14.8 MeV D-T neutrons in the range 3.55-244 mGy have been analysed in human peripheral blood lymphocytes. In order to obtain the required large numbers of scored cells for such low doses, fourteen laboratories participated in the experiment. The dose responses for dicentrics, excess acentrics and total aberrations, fitted well to the Y = alpha D model. The alpha coefficient of yield for dicentrics, 1.60 +/- 0.07 X 10(-2) Gy-1, compares well with the values obtained in previous studies with D-T neutrons at somewhat higher doses. Results from a previous collaborative study using 250 kVp X-rays over a comparable dose range indicated the possible existence of a threshold below 50 mGy. In the present study there is no clear evidence for neutrons for such a threshold. However, the data were insufficient to permit the rejection of a possible threshold below approximately 10 mGy.
Chromosome Aberrations↗
Elevation of Alu I-induced frequencies of chromosomal aberrations in Chinese hamster ovary cells by Neurospora crassa endonuclease and by ammonium sulfate.
The frequencies of chromosomal aberrations induced by the restriction endonuclease Alu I (recognition site AG/CT) can be elevated to a similar extent by additional treatments with a single-strand-specific endonuclease from Neurospora crassa (EC 3.1.30.1), or with ammonium sulfate in which the Neurospora endonuclease is suspended. These data indicate that Alu I does not produce DNA single-strand breaks in the chromatin of living cells, which can be recognized by the Neurospora endonuclease. The salt may induce conformational changes in the chromatin which make more recognition sites available for Alu I. Experiments with recovery times between the treatments with Alu I and the salt indicate that Alu I can act in the nucleus for at least 40 min.
Ammonium Sulfate↗
Metabolism of ethanol in vitro produces a compound which induces sister-chromatid exchanges in human peripheral lymphocytes in vitro: acetaldehyde not ethanol is mutagenic.
Ethanol (EtOH) in the presence of the EtOH-metabolizing enzyme, alcohol dehydrogenase (ADH) leads to the induction of sister-chromatid exchanges (SCEs) in human peripheral lymphocytes in vitro. Acetaldehyde (AA) induces SCEs, whose frequencies are lowered in the presence of the AA-metabolizing enzyme, aldehyde dehydrogenase (ALDH). EtOH in the presence of ADH produces more SCEs than EtOH in the presence of ADH and ALDH. These data are interpreted to show that not ethanol itself, but its first metabolite acetaldehyde is mutagenic.
Acetaldehyde↗
The restriction endonuclease Alu I induces chromosomal aberrations and mutations in the hypoxanthine phosphoribosyltransferase locus, but not in the Na+/K+ ATPase locus in V79 hamster cells.
The restriction endonuclease Alu I induces chromosomal aberrations and mutations in the hypoxanthine phosphoribosyltransferase (HPRT) locus as measured by 6-thioguanine resistance (TGr) in V79 hamster cells. Alu I does not induce mutations in the Na+/K+ ATPase locus as measured by ouabain resistance (OUAr). The data are interpreted to mean that most if not all Alu I-induced TGr mutations represent chromosomal aberrations.
Animals↗
Restriction endonuclease Bam H I induces chromosomal aberrations in Chinese hamster ovary (CHO) cells.
Treatment of Chinese hamster ovary (CHO) cells with the restriction endonuclease Bam H I (recognition site: G/GATCC) leads to high frequencies of chromosomal aberrations. Experiments with bromodeoxyuridine-labelled chromosomes show that the aberrations occur nearly exclusively in first post-treatment metaphases. The results are interpreted to mean that only some of the cells take up the enzyme and that these cells are the ones showing the aberrations. Cells which do not take up the enzyme show up as differentially stained metaphases and have no aberrations. Why some cells take up the restriction enzyme and others not is not known, possibly this is dependent on the physiological condition of the cells.
Animals↗
Epidemiological studies concerning chromosomal aberrations in alcoholics and smokers.
Explore the source record for details and available documents.
Adolescent↗
Spontaneous level of somatic chromosome aberrations in man.
Explore the source record for details and available documents.
Age Factors↗
The chromosome-breaking activity of the restriction endonuclease Alu I in CHO cells is independent of the S-phase of the cell cycle.
The restriction endonuclease Alu I induces chromosomal aberrations in living Chinese hamster ovary (CHO) cells. Multiple fixation times reveal that the chromosome-breaking activity of Alu I is similar to that of ionizing radiation in that it is independent of the S-phase of the cell cycle. These results indicate that DNA double-strand breaks are the ultimate lesions for the production of chromosomal aberrations in all stages of the cell cycle.
Animals↗
Influence of Neurospora endonuclease on trenimon-induced structural chromosomal aberrations and sister-chromatid exchanges in human peripheral lymphocytes and Chinese hamster ovary cells.
Human peripheral lymphocytes and Chinese hamster ovary cells were treated in the G1 phase of the cell cycle with the trifunctional alkylating agent trenimon (TRN) and post-treated with a single-strand specific endonuclease from Neurospora crassa (NE). TRN induces chromosomal aberrations of the chromatid type (CA) and sister-chromatid exchanges (SCE). NE post-treatment leads to an elevation of the frequencies of CA but not of SCEs. This indicates that TRN induced CA are the result of DNA double-strand breaks and that the SCEs originate from other types of lesions, most probably base damage.
Alkylating Agents↗
Mutagenicity of methyl 2-benzimidazolecarbamate, diethylstilbestrol and estradiol: structural chromosomal aberrations, sister-chromatid exchanges, C-mitoses, polyploidies and micronuclei.
Methyl 2-benzimidazolecarbamate (MBC), diethylstilbestrol (DES) and estradiol were tested with regard to their ability to induce C-mitoses, polyploidies, micronuclei, structural chromosomal aberrations and sister-chromatid exchanges (SCE) in human peripheral lymphocytes in vitro. The compounds did not induce structural chromosomal aberrations either in the presence or absence of metabolic activation. MBC and estradiol were negative in the SCE test. DES induced SCE rates which were not even twice the control level and which were independent of dose and of metabolic activation. All compounds induced C-mitoses, polyploidies and micronuclei. The micronuclei are interpreted as resulting from errors in the anaphase distribution of chromosomes by spindle disturbances rather than from structural chromosomal aberrations.
Benzimidazoles↗
On the origin of chromosomal aberrations in human peripheral lymphocytes in vitro. I. Experiments with Neurospora endonuclease and polyethylene glycol.
Post-treatment of mutagen-treated human peripheral lymphocytes with a single-strand specific endonuclease from Neurospora crassa leads to a significant elevation of the rate of structural chromosomal aberrations. Our results indicate that DNA double-strand breaks (DSB) are ultimate lesions for the formation of chromosomal aberrations in the G1 and G2 phase of the cell cycle and probably also in the S-phase. Post-treatment of X-irradiated G2 cells with polyethylene glycol (PEG) leads to an elevation of the frequencies of chromatid type aberrations. This result is taken as an indication that nucleases from PEG-damaged lysosomes transform lesions in X-ray damaged chromosomes to DSB. With respect to the origin of chromosomal aberrations, our results are in favour of the breakage and reunion hypothesis of K. Sax , and not of Revell 's exchange hypothesis.
Cell Cycle↗
Molecular mechanisms involved in the production of chromosomal aberrations. III. Restriction endonucleases.
Chinese hamster ovary cells (CHO cells) and mouse fibroblasts (PG 19) were permeabilized with inactivated Sendai virus, treated with different types of restriction endonucleases (Eco RV, Pvu II, Bam HI, Sma I, Asu III, Nun II), and studied for the occurrence of chromosomal aberrations at different times following treatment. The pattern of chromosomal aberrations observed was similar to that induced by ionizing radiations. Restriction endonucleases that induce blunt double-strand breaks (Eco RV, Pvu II) were more efficient in inducing chromosomal aberrations than those that induce breaks with cohesive ends (Bam HI, Nun II, Asu III). Ring types were very frequent among the aberrations induced by restriction enzymes. Cytosine arabinoside, an inhibitor of DNA repair, was found to increase the frequencies of aberrations induced by restriction enzymes, indicating its effect on ligation of double-strand breaks. The relevance of these results to the understanding of the mechanisms of chromosomal aberration formation following treatment with ionizing radiations is discussed.
Animals↗
Liquid-holding experiments with human peripheral lymphocytes. II. Experiments with trenimon and 1-beta-D-arabinosylcytosine.
Liquid holding of trenimon-treated human peripheral lymphocytes in the G0 stage of the cell cycle leads to an elevation in the frequencies of chromosome aberrations and a decrease in the frequencies of chromatid aberrations. The frequencies of aberrant metaphases are not influenced significantly under these experimental conditions. Storage of trenimon-treated cells in the presence of 1-beta-D-arabinosylcytosine (araC) leads to an additional increase in the frequencies of chromosome-type aberrations, with an increase in the frequencies of aberrant metaphases as well. These findings are interpreted as DNA double-strand breaks being formed during the repair of damaged DNA, and that araC exaggerates this effect by inhibiting repair. AraC does not influence the frequencies of SCEs significantly, which indicates that either the lesions or the repair pathways leading to chromosome aberrations are different from those leading to SCEs.
Cells, Cultured↗
Mutagenic activities of cyclophosphamide (NSC-26271) and its main metabolites in Salmonella typhimurium, human peripheral lymphocytes and Chinese hamster ovary cells.
Cyclophosphamide (CPA) and its main metabolites were analyzed with respect to their mutagenic activities in Salmonella, human peripheral lymphocytes (PL), and Chinese hamster ovary (CHO) cells. In Salmonella, the compounds were activated with S9 mix from rat livers, which were unstimulated or stimulated with Aroclor 1254 or phenobarbital. For the enzyme inducers the following order of efficiency was found for all test compounds except carboxyphosphamide: phenobarbital greater than Aroclor 1254 greater than non-induced. The most potent mutagens in all 3 test systems were 4-OH-CPA, PAM and nor-HN2. S9 mix transforms 4-OH-CPA to strong mutagenic compounds in the Salmonella assay. All metabolites tested in the Salmonella assay were activated by S9 mix to higher mutagenic potential.
Animals↗
Mutagenicity of antiepileptic drugs. II. Phenytoin, primidone and phenobarbital.
The antiepileptic drugs, phenytoin, primidone and phenobarbital, were tested in Chinese hamster ovary (CHO) cells for their ability to induce sister-chromatid exchanges (SCEs) and structural chromosomal aberrations (CAs), with and without metabolic activation. SCEs and CAs were analyzed in the same cell population. The results are negative.
Animals↗