[Mechanisms of hemopoiesis inhibition and recovery after the administration of carminomycin and rubomycin in an experiment]. / Mekhanizmy podavleniia i reparatsii gemopoéza pri vvedenii karminomitsina i rubomitsina v éksperimente.

The experiments on 766 albino non-inbred rats and 270 mice BALB/c showed that when there were no basic differences in the mechanism of the anthracycline myeloinhibitory effect associated with a decrease in the number of the exogenic trunk hemopoietic cells, inhibition of the bone marrow proliferative activity and a decreased rate of the hemopoietic elements differentiation, carminomycin induced a more pronounced and persisting impairment of the hematopoietic tissue proliferation, as compared to rubomycin on their administration in doses equivalent by the total toxicity.

[Effect of carminomycin on bone marrow cell proliferative activity and differentiation rate]. / Vliianie karminomitsina na proliferativnuiu aktivnost' i skorost' differentsirovki kletok kostnogo mozga.

Autoradiographic investigations with the use of 3H-thymidine were performed on 140 noninbred albino rats. The fate of the label in the cells of the myeloid series was followed in the experimental and control groups. The animals of the experimental group were treated with carminomycin in the LD50 30 minutes after injecion of 3H-thymidine. The mitotic cycle of the nondifferentiated cells and promyelocytes + myelocytes in the control animals was equal to 24 hours, the period and rate of the metamyelocyte maturation being 10 hours and 0.81 per cent/hour respectively. The mitotic cycle of the nondifferentiated cells and promyelocytes + myelocytes during the first division after carminomycin administration increased up to 48 hours due to the block of G2-period, the period and rate of the metamyelocyte maturation being 18 hours and 0.43 per cent/hour respectively. The myelotoxic effect of carminomycin was due to the damage of the dividing cells in G2-period of the mitotic cycle, decreased rate of differentiation and death of the cells after or during the first and second divisions.

[Mechanism of the myeloinhibitory effect of carminomycin]. / K mekhanizum mieloingibiruiushchego éffekta karminomitsina.

The proliferative activity and level of aberrant mitoses in the cells of the bone marrow were studied experimentally on 223 noninbred mice treated with carminomycin administered intraperitoneally in single (LD50) and repeated doses. When the antibiotic was used in a single dose the values of the mitotic activity of the bone marrow elements did not correspond to the severity of depression and thir quantitative composition, which was explained by an impairement of the mitosis quality and possible interkinetic destruction of a significant part of both erythroid and immature myeloid cells capable of division at early stages after the exposure. At the same time the level of the bone marrow devastation under conditions of the treatment with repeated doses was mainly determined by inhibition of the erythronormoblast proliferative activity.