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S Ia Proskuriakov

Publications and source records attributed to S Ia Proskuriakov.

At least 19 recordsLinked to original sources
PubMed2004

[Ageing and necrotic form of "unwanted" cells].

Collecting experimental data testify that cellular necrosis is the same component of "unwanted" cell system elimination in a metaphyte, as well as apoptosis. The essential role of the last in definition of rates of ageing is expressed, in particular, in secretion by phagocytes of the factors overwhelming inflammatory reactions which are rather characteristic for such illnesses as an atherosclerosis, a diabetes and others. Apparently, infringement of balance between necrotic and apoptotic forms "unwanted" cell elimination from an organism can be the important factor of ageing and the reason of reduction of life expectancy as a result of supression of renewal processes in an organism, occurrence and weights of development of some senile illness.

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PubMed1996

[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↗
PubMed1989

[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↗
PubMed1979

[Effect of a DNA-rubomycin complex on the molecular mass, radiosensitivity and reparation of gamma-induced single-stranded breaks in the DNA of sarcoma 180 cells].

The use of the DNA-rubomycin complex resulted in appearance of one-thread breaks (OB) in DNA and markedly increased the number of the DNA OB determined immediately after irradiation. The DNA-rubomycin complex decreased the volume of the repaired OB and induced postreparation degradation of the one-bond DNA (oDNA) in the sarcoma 180 cells. The effect of the decrease in the molecular mass of the oDNA 6 hours after the irradiation to the level of the initial damage is probably in favour of the fact that degradation takes place in the areas of the repaired breaks. The data indicated that the viscosimetric method for the analysis of the OB in DNA may be promising in estimation of the efficacy of radiation and chemotherapy of solid tumors.

Animals↗
PubMed1979

[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.

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PubMedDate not supplied

[NO-inhibiting activity of radioprotectors].

The effect of radioprotectors of different structure on the syntheses of nitric oxide induced by endotoxin in mice was studied. Using ESR-spectroscopy and spin trap techniques, it was shown that compounds of different chemical structure, such as aminothiols, isothiuronium derivatives, thiazolines, indolylalkylamines and others, suppressed the nitric oxide production in a whole body. The analysis of the relevant literature has confirmed the phenomenon described by the authors: radioprotectors show NO-inhibiting activity.

Animals↗
PubMedDate not supplied

[Distribution of beta-carotene in the rat upon its intraperitoneal administration in water soluble and oil forms].

Accumulation and excretion of beta-carotene in rat liver tissue were studied when the carotinoid was intraperitoneally administered as olive oil as suspension and a water liposomal suspension. Single injection of the liposomal form of beta-carotene caused an increase in its content in liver tissue. If beta-carotene was administered at a dose of 10 mg/kg its maximal content 44 mg/g of the tissue was observed within one day, and at a dose of 50 mg/kg, its maximal content constituted 178 mg/g within two days. Administration of beta-carotene as an oil suspension at a dose of 50 mg/kg led to a considerably slight accumulation in rat liver tissue with the maximal value of 12 mg/kg of the tissue within two days. Possible use of beta-carotene various forms, as well as experimental models for study their biological activity are discussed.

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PubMedDate not supplied

[The inhibition by the tumor necrosis factor of the death and DNA fragmentation of lymphoid cells in irradiated rats].

The influence of a tumor necrosis factor, administered 16 h before irradiation of rats, on the radiation response of thymus and bone marrow cells has been investigated. Three and 6 h after irradiation the following indices were analyzed: the number of apoptotic cells in the thymus; the accumulation of polydeoxyribonucleotides and the appearance of single-strand breaks in DNA of bone marrow and thymus cells; and the electrophoretic properties of thymocyte DNA. The injection of a tumor necrosis factor reduced the number of polydeoxyribonucleotides, inhibited internucleosome DNA fragmentation, and did not influence the formation of single-strand breaks in DNA.

Animals↗
PubMedDate not supplied

[The estimation of the nitric oxide role in the aggravation of combined radiation-thermal injuries].

The influence of specific inhibitor of inducible NO synthase S-ethil-isothiourea (as "Difetur" preparation) on liver NO production level, and 30-days survival, mean survival time and probability of mortality within animals under combined radiation/thermal injury (CRTI) were evaluated. Experiments were carrying out on mice (whole body gamma-irradiation at the dose of 7 Gy + 10% body surface full-thickness thermal burn). It was shown, that CRTI induce 2-fold statistical significant increase of NO production in liver of experimental animals. Mice pretreatment with Difetur preparation lead to practically full inhibition of NO production. In the group of animals, with Difetur administration during first two days after CRTI 60% mice survived as compared 15% survive in control group. In pair with data on probability of mortality it was suggested that growth of NO production in the early period of CRTI increase sensitivity of animals to pathological processes leading to death on 10-12 days.

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PubMedDate not supplied

["Ischemia/reperfusion" for stem cells of two "critical" cell renewal systems of organism].

In this article is presented the result of the experiments on mice-hybrids F1(CBA x C57B1/6), which indicates the presence of the reaction of "ischemia/reperfusion" for stem cells of two "critical" cell renewal systems of organism (bone marrow and intestinal epithelium) during the irradiation under the conditions of hypoxic radioprotector application. The additional injection of the source of nitric oxide radicals-sodum nitroprusside (SNT) to the mice right after the irradiation under the conditions of hypoxic protection by serotonin, resulted the substantial increase of the survival rate of hematopoietic stem cells (registered by the methods of endogenous and exogenous colony forming in spleen) and stem cells of intestinal epithelium (registered by the method of intestinal "microcolonies"). The similar radioprotective effect was also registered during the test of survival rate of mice under tests of "bone marrow" and "intestinal" forms of radiation lethality that is evidence of the importance of the realization of phenomenon "ischemia/reperfusion" in the reaction of whole organism on the acute radiation injury. As SNP weakens the manifestation apoptosis and necrosis through competition with active forms of oxygen (AFO) during the period of "reperfusion" on basis of the found out phenomenon experimental model for studying mechanisms of stem cells damage in vivo induced by AFO and for the search of the modifiers weakening or strengthening such damage can be developed.

Animals↗
PubMedDate not supplied

[Enhancement by metronidazole of the antitumor effect of cyclophosphane].

In experiments on mouse tumors (sarcoma-180, Ehrlich ascites tumor and hemoblastosis La) the ability of metronidazole to enhance the antitumor chemotherapeutic action of cyclophosphane was investigated. It was shown that metronidazole (1000 mg/kg) injected 60 min before cyclophosphane administration can elicit an almost two-fold increase in its radioprotective efficiency. The chemosensitizing effect of metronidazole depends on the drug concentration and the tumor type.

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