Biomedical subjects
Publications and source records attributed to G Obe.
The trifunctional alkylating chemical mutagen trenimon increases the frequency of sister chromatid exchanges in human leukocyte chromosomes in vitro, as revealed by a BUdR-Giemsa method. Treatment with lead acetate exhibited negative results in this respect. The use of sister chromatid exchanges as possible indicators for mutagenic activities is discussed.
In human leukocyte cultures st up with TC medium 199,DNA synthesis and mitotic indices were analysed by means of 3H-thymidine autoradiography and cell counting. DNA synthesis starts at around 28 hrs. The frequencies of labelled cells rise slowly and reach a maximum of around 24%. The first mitoses appear at around 38 hrs but up to 49 hrs only very few mitoses can be seen. After that time the mitotic indices rise and reach values of up to 11% cultivation in the presence of BudR for 72 hrs and staining with Hoechst 33258 stain revealed that first, second and third mitoses occur together in the cultures at this time. Irradiation of whole blood and cultivation for 72 hrs leads to mitoses containing dicentric and ring chromosomes with and without fragments, to interphases with micronuclei, to premature chromosome condensations (PCC) and to polyploid mitoses indicating that at this time first and further mitoses are present.
In the Chinese hamster bone marrow chromosomal aberrations were induced after whole body irradiation with Co-60 gamma rays in vivo. Aberrant mitoses give rise to lagging chromatin that forms micronuclei. Eventually the micronuclei are slowed down in their cell cycles in comparison to the main nuclei. The mitotic chromatin of the main nuclei induces premature chromosome condensation (PCC) in the micronuclei that are still in the interphase state of their cell cycles.
Evidence is presented for the occurrence of premature chromosome condensation (PCC) from micronuclei even in the first in vitro mitoses in a case of Fanconi's anemia.
In lymphocytes of a 7-year-old boy with Fanconi's anemia the frequencies and sites of sister-chromatid exchanges (SCE) were studied with the BrdU-Giemsa method. The average frequency of SCE (8.8 per metaphase) and the inter- and intrachromosomal distribution of SCE was not significantly different from the controls.
The Chinese hamster bone marrow was used as a test system in vivo to analyse the chromosome-danaging effect of bleomycin. Both chromosome and chromatid aberrations were found. Mitoses with aberrations (Ma) show a linear dose-effect relationship after a recovery time of 24 h, the same hold true for cells with micronuclei (Cm) and for mitoses with premature chromosome condensation (PCC). The dose-effect relationships for Ma, Cm and PCC run parallel to each other with Ma at the highest and PCC at the lowest level (Ma greater than Cm greater than PCC). The time-effect relationships for Ma, Cm and PCC show that after 12 h recovery time there are no PCCs but the highest frequencies of Ma and Cm indicating that most cells are in their first post-treatment mitoses or Gi-phases at this fixation time. In addition to the frequency determinations autoradiographic analysis were performed to clarigy the nature of the PCCs. The results are interpreted as follows: bleomycin induces chromosomal aberrations that in turn give rise to micronuclei by means of lagging chromatin, main and micronuclei eventually become asynchronous in their cell cycles and mitosing main nuclei induce PCC in the micronuclei.
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Premature chromosome condensation (PCC) was induced in human leukocytes in vitro by a bifunctional alkylating agent 2,5-bis-(methoxyethoxy)-3,6-bis-ethylene-imino-p-benzoquinone (A 139), bleomycin and X-rays. Analysis shows that PCC originates from micronuclei that have been slowed down in their cell cycles in respect to the main nuclei. The mitosing chromatin of the main nuclei induced PCC in the associated micronuclei. Morphologically the PCC was mostly of the S-phase type with the chromatin exhibiting a more or less pulverized appearance; in some experiments this was verified by incorporation of (3H) thymidine (TdR). In a few cases the PCC looked like G2-phase PCC with ladder-like chromosomes. GI-phase PCC was not found. PCC of the type described in this work may be used as an indicator of induced lagging of chromatin that can be the result of chromosomal aberrations or of nondisjunction.
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