| Research Abstract |
Acute chromosome-damaging and chromatid-rearranging capacities of various mutagens and carcinogenes such as 7,12-dimethy 1 benz (a) anthracene (DMBA), and N-nitroso-N-methylurea (NMU) were studied using rat bone marrow cells, liver cells and fibroblasts in vivo and in vitro. The frequency of chromosome aberrations (CA) and sister chromatid exchange (SCE) after administration of above-mentioned carcinogens was tested under various stimuli. Athough the incidence of DMBA- and NMU-induced CA in the normal rats was 28% and 33%, it was 17% and 24% in the polycythemic rats. However, the incidence of CA in anemic rats was 45% and 56% and in polycythmic rats administrated with 6 Units of erythropietin at the time of DMBA injection was 41% and 47%. In the other words, the induction of CA by DMBA was enhanced by anemia and suppressed by polycythemia. The low incidence of CA in polycythmic rats was reversed by stimulation of erythropoietin injected at the time of DMBA and NMU treatment. CA were distributed nonrandomly in chromo somes 1 and 2. One region, the 40% region from the centromere (1q31), of the long arm of chromosome 1, and three regions, 30,55 and 80% from the centromere (2q21,2q25,2q41), of chromosome 2 were extremely susceptible to DMBA and NMU in the hematopoietic state. The frequency of SCE was increased under the condition of anemia and that of SCE was decresed under the condition of polycythemia. In liver cell obtained hepatectomized rats, the frequency of SCE induced by DMBA was enhanced with addition of the LGF in vivo (from 13.5% to 28.3%). In fibroblasts, the frequency of SCE induced by NMU was enhanced inthe ratio of 1.5 times with addition of the FGF in cultured medium in vitro.
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