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Biomedical subjects

N I Riabchenko

Publications and source records attributed to N I Riabchenko.

At least 19 recordsLinked to original sources

[The effect of an injection of N-methylformamide into mice on the cell cycle and cell morphology of ascitic hepatoma 22A].

A cell differentiating agent N-methylformamide (MF) was studied for its antitumor activity against a murine ascitic hepatoma 22A. After a 48 hour NMF administration (i/p) the tumor cell number was monitored; the distribution of these cells in the cell cycle was registered by flow cytometry, ultrastructural changes were studied by electron microscope. The polar solvent MF inhibited tumor growth, reduced mitotic activity, and nuclear/cytoplasmic ratio, led to structural complication of endoplasmic reticulum and mitochondria. The analysis of these events is suggestive that in consequence of MF effect on tumor cells, proportion of G0/G1 and M cells was decreased, while the proportion of S and G2 cells was increased.

Animals

[DNA degradation and changes in the permeability and form of Ehrlich ascites tumor cells when incubated in an anaerobic medium without glucose].

After a 3-hour incubation of the Ehrlich ascite tumor cells in buffered Hanks solution, without glucose and oxygen, the extensive cell injuries were observed. The time-course of appearance of these injuries was as follows: cell blebbing, staining of the cells with trypan blue, and then their staining with ethidium bromide. The DNA degradation registered with fluorometric method coincided in time with cell staining with trypan blue. All injuries (except DNA degradation) were delayed at pH 6.0 compared with those at pH 7.3. Glucose added to the cell suspension greatly protected the cells from these injuries, although DNA degradation at pH 6.0 in these conditions was a little higher than that at pH 7.3.

Anaerobiosis

[Inhibition of transplantable tumors in mice by monomethylformamide].

The paper discusses the effect of a cell differentiation-inducing agent--monomethylformamide--on the growth of ascites hepatoma 22A, Ehrlich ascites tumor, thymoma EL-4, leukemia L1210, Lewis lung carcinoma and hemocytoblastosis La. A single injection of the drug into tumor-bearing mice inhibited the growth of the said neoplasms as shown by cell levels in ascites tumors, node size of Lewis lung carcinoma and survival in animals with hemocytoblastosis La. The analysis of the kinetics of inhibition of growth to be transient. For both tumors, the effect of 0.25 g/kg body weight and more showed exponential growth.

Animals

[Interphase death of lymphoid cells: role in the genesis of radiation sickness and molecular mechanisms].

An analysis of the data on the effect of lymphoid cells on the proliferation and differentiation of hemopoietic stem cells has led to a conclusion that radiation injury of lymphocytes plays an important role in the pathogenesis of the cerebrospinal syndrome. The molecular mechanisms of lymphocyte interphase death were considered. It was shown that due to some peculiarities in the energy supply of these cells the appearance of breaks in DNA causes the development of biochemical processes resulting in a decrease in NAD, an increase in the activity of nucleases, a decrease in ATP, and the accumulation of active metabolites of glycolysis. These reactions result in an increase in the disintegration of DNA, chromatin and pyknosis of lymphocyte nuclei.

Animals

[Effect of metronidazole on the intensity of cell respiration].

The time-course of the metronidazole (MZ) radiosensitizing effect after the administration of the agent to mice 7 days following the inoculation of ascites tumor cells is better correlated with the time-course of the MZ content in the above cells than with the time-course of their potential respiration intensity evaluated by the polarographic method in a closed unit. Five minutes after MZ administration the depression of respiration intensity reached 50% and might contribute to the radiosensitizing effect. After MZ administration not only "metronidazole" but also "oxygen" waves were recorded in ascites tumors of mice using the polarographic method.

Animals

[Effect of cycloheximide on the alkaline and acid DNAse activity in rat cells].

Using spectrophotometric and viscosimetric techniques, the effects of cycloheximide on the activity of alkaline and acid DNAses in the homogenate cells of thymus, mesenterial lymphatic node, spleen, liver and in blood serum of the rat were studied. Using these two methods, it was demonstrated that cycloheximide inhibits the activity of alkaline DNAase in the spleen, lymphatic node and liver cells by 70% without changing that of acid DNAase in all the organs tested but has no inhibiting effect on the activity of alkaline endonuclease in the thymocytes. Cycloheximide inhibits the activity of alkaline DNAase in rat blood serum by 85%. It can thus be concluded that in the spleen, lymphatic node and liver cells there occurs a practically constant synthesis of alkaline DNAase, the bulk of which is released into the blood stream.

Animals

[Increase in the resistance of a liposome-incorporated rubomycin-DNA complex to the action of DNAses].

When DNA and the rubomycin-DNA complex were incorporated into liposomes containing stearylamine, about 90 per cent of their amounts associated with the liposomes, incubation of such liposomes for an hour at 25-50 degrees C being not accompanied by liberation of DNA and its complex. Only about 10 per cent of DNA associated with the liposomes was destroyed by DNase I. The liposomal DNA was more stable to ultrasound than free DNA. The molecular mass of DNA associated with the liposomes on treatment with ultrasound decreased 1.9 times, whereas that of free DNA decreased by more than 3 times. With an increase in the weight ratio of lipid/DNA the level of DNA degradation lowered. This is evidence of the fact that liposomes increase resistance of DNA and its complex to chemical and physical factors.

Chemical Phenomena

[Comparative analysis of the destroying effects of prednisolone and irradiation of lymphoid cells].

The hormone-induced and post-irradiation changes in the molecular weight of a single-stranded DNA (SSDNA) in alkaline nuclear lysates and the activities of DNAses and pyknotic nuclei from rat thymocytes were studied. It was shown that 1 hr after injection of prednisolone (1 mg per 100 g of body weight) the molecular weight of SSDNA in the lymphoid organs is decreased with a subsequent increase by the 6th hour. The hormone-induced degradation of DNA is not accompanied by any marked increase in the activities of DNAses or by an appearance of pykotic nuclei in the thymocytes. The irradiation of the animals at a dose of 900 R leads to an irreversible decrease of the molecular weight of SSDNA in the lymphoid organs, to a steady increase of the DNAse activity and a sharp increase of the amount of pyknotic nuclei in the thymocytes. Studies on the mechanism of post-hormonal degradation of DNA in rat thymocytes in vitro demonstrated that prednisolone exerts its effects on the early and late stages of DNA degradation.

Animals

[Mechanism of the formation of single-stranded DNA breaks under the effect of prednisolone on rat liver thymocytes].

Rat liver thymocytes were incubated in vitro with prednisolon, and molecular weight of single-stranded DNA was estimated in alkaline lysates of nuclei by viscosity methods. The number of single-stranded breaks was estimated, which originate in DNA after 3 hours of incubation with prednisolon at a concentration of 3-10(-9) M--3-10(-4) M. Maximal hormone effect was produced within 30 min., and it remained constant for the rest 3 hours of the incubation. Cycloheximide prevented hormone-induced DNA depolymerization, and actinomycin D only slightly inhibited the formation of single-stranded DNA breaks, originated after 30 min. incubation of thymocytes with prednisolon, were repaired after their washing and reincubation in the fresh medium for 1 hour at 37 degrees C. The washing of thymocytes and their reincubation for 3 hours resulted in the decrease of the molecular weight of single-stranded DNA. Possible mechanism of the formation of single-stranded DNA breaks in prednisolon-induced thymocytes is discussed.

Animals