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Biomedical subjects

V V Shaposhnikova

Publications and source records attributed to V V Shaposhnikova.

At least 19 recordsLinked to original sources
PubMed2004

[Antitumor effect of natural avermectins].

The effects of the natural avermectin complex, aversectin C and individual avermectin B1 on the growth of ascitic and solid transplantable tumors in animals were studied. The results showed for the first time that both aversectin C and avermectin B1 possessed marked antitumor activity. In subtoxic doses aversectin C significantly inhibited the growth of P388 lymphoid leukemia and Ehrlich carcinoma, both ascitic and solid ones. In some administration regimens aversectin C inhibited the tumor growth by 70 to 80%. The highest effect of aversectin C was observed after its intraperitoneal administration. Avermectin B1 inhibited the growth of solid Ehrlich carcinoma and carcinoma 755.

Administration, Oral↗
PubMed2004

[Modification of antitumor effect of vincristine by natural avermectins].

The effect of avermectins (aversectin C, aversectin C1 and avermectin B1) on the vincristine antitumor action with respect to murine transplantable tumors was studied. It was shown that both the natural avermectins mixtures and the individual avermectin B1 potentiated the antitumor action of vincristine on Ehrlich carcinoma, melanoma B16 and P388 lymphoid leukemia, including the vincristine resistant strain P388. Such an effect of the avermectins was observed only when they were administered after vincristine.

Animals↗
PubMed2003

Combined action of doxorubicin and gestagens on doxorubicin-sensitive and doxorubicin-resistant MCF-7 cells.

The combined cytostatic effect of doxorubicin and gestagens progesterone, medroxyprogesterone acetate, mecigestone, and butagest on doxorubicin-resistant and doxorubicin-sensitive human breast cancer MCF-7 cells was studied by the MTT assay. On the 6th day of incubation progesterone, medroxyprogesterone acetate, mecigestone, and butagest in high concentrations (10(-5) M) potentiated the cytostatic action of doxorubicin in sensitive and resistant cells by 30-50%. Potentiation of the cytostatic effect produced by doxorubicin in sensitive cells is related to intrinsic cytotoxic activity of gestagens. In resistant cells these changes are associated with potentiation of the effect of doxorubicin.

Antibiotics, Antineoplastic↗
PubMed2000

[Cytotoxic and cytostatic effect of avermectines on tumor cells in vitro].

Effect of natural avermectin complex (aversectin C) and separate avermectins A1, A2, B1 and B2 in the cell culture of murine myeloma Ns/o, Erlich carcinoma ascites and human larynx carcinoma Hep-2 was investigated. It was shown that aversectin C within the concentrations of 0.1 to 1.0 mcg/ml inhibited proliferation of tumor cells and induced their death. Proliferation inhibition was due to the delay of the cells cycle start (lag-phase prolongation) and blocking of mitotic cycle. Ns/o cells death had apoptosis signs: chromatin condensation and fragmentation, DNA fragmentation. It was demonstrated that only avermectin A1 has cytotoxic activity within the concentrations used, avermectins A2 and B2 had cytostatic activity, avermectin B1 showed no activity under the experimental conditions.

Animals↗
PubMed1999

[Action of avermectins on lymphoid leukemia P-388 cells in vitro].

Avermectins are final products in the fermentation process with Streptomyces avermitilis. They have parasitocidic activity and are used as the main substances of insectoacaronematocides. The study of the activity of the natural avermectin complex (aversectin C) and separate avermectins A1, A2, B1 and B2 in the cell culture of lymphoid leukemia P-388 showed that within the concentrations of 0.1 to 1.0 microgram/ml aversectin C inhibited the growth of the tumor cells and induced their death. The inhibition was due to blocking the cell mitosis. The cell death was accompanied by internucleosomal degradation of the DNA nuclei i.e. the death was of the apoptosis type. The sensitivity of the cells to aversectin C was directly proportional to their initial proliferative activity. As for the separate avermectins only avermectin A1 had the cytotoxic activity within the concentrations used, avermectin A2 had the cytostatic activity and avermectins B1 showed no activity under the experimental conditions.

Animals↗
PubMed1998

The effect of inhibitors of arachidonic acid metabolism on proliferation and death of tumor cells.

The effect of inhibitors of arachidonic acid metabolism on proliferation and death of tumor P-388 cells in a broad concentration range was studied. Cell proliferation was estimated by the metaphase frequency and the proportion of cells in S phase; cell death was determined from lysis, staining of cells with trypan blue, nuclear damage, percentage of cells with subdiploid DNA and the type of DNA fragmentation. It was shown that low concentrations of phospholipase A2 and lipoxygenase inhibitors stimulated the proliferation of P-388 cells. At higher concentrations, the inhibitors suppressed cell proliferation by blocking the G1-S transition and induced cell death of the apoptosis type. Indomethacin, an inhibitor of cyclooxygenase, did not initiate cell death, nor did it affect the proliferation of P-388 cells at concentrations of up to 10 microM.

Acetophenones↗
PubMed1998

Tissue transplantation as a compensation for deleterious effects of ageing, radiation, diabetes, and craniocerebral trauma.

The presence of blood-brain and blood-ocular barriers allows the transplantation of various biological tissues into the brain and the anterior eye chamber without acute immune rejection. Tissue grafting into the immuno-privileged areas (brain, anterior eye chamber) allows its long-term functioning without immuno-suppression. This method was shown to be effective in compensating for the deleterious effects of ageing, radiation, diabetes, and craniocerebral trauma.

Aging↗
PubMed1997

The effect of melittin on proliferation and death of thymocytes.

The effect of melittin, an activator of phospholipase A2, on proliferation and death of rat thymocytes in a broad concentration range was studied. Cell proliferation was estimated by the accumulation of colchicin metaphases, necrotic death was determined from lysis and staining of cells with trypan blue, and apoptosis was assessed from the type of DNA fragmentation, the amount of fragmented DNA, and the percentage of cells with subdiploid DNA. It was shown that low melittin concentrations (below 5 microg/ml) stimulate thymocyte proliferation. At high melittin concentrations, thymocytes die by the primary necrosis type. Throughout the concentration range studied, melittin does not produce apoptosis in thymocytes. Conversely, high melittin concentrations even inhibit thymocyte apoptosis in the control and after irradiation. An inhibitor of RNA synthesis actinomycin D does not affect thymocyte death in the presence of melittin. It is concluded that the activation of phospholipase A2 can induce necrosis but not apoptosis and thus is not a necessary step in the signaling cascade that initiates apoptosis in thymocytes.

Animals↗
PubMed1996

Role of arachidonic acid metabolism in thymocyte apoptosis after irradiation.

The present study demonstrates that DNA fragmentation, nuclear pycnosis and trypan blue staining of irradiated thymocytes is prevented by inhibition of the lipoxygenase pathway of arachidonic acid metabolism and is not affected by cyclooxygenase inhibition. Exposed to irradiation [3H]arachidonic acid-labeled thymocytes release radioactive products to the external medium. The process is blocked by the lipoxygenase inhibitor, nordihydroguaiaretic acid. Thus, it can be concluded that irradiation activates arachidonic acid metabolism and that lipoxygenase metabolites play an important role in thymocyte apoptosis.

Animals↗
PubMed1995

Thymocyte proliferation and apoptosis induced by ionizing radiation.

Proliferation and apoptosis of rat and mouse thymocytes caused by ionizing radiation were studied. The percentage of proliferating cells was determined by the method of colchicine metaphases and the apoptosis was estimated as DNA fragmentation. In vitro irradiation with 0.05-0.2 Gy was found to stimulate thymocyte proliferation, the maximum was observed at 0.05 Gy for mouse thymocytes and at 0.1 Gy for rat thymocytes. These doses caused a slight decrease in DNA fragmentation, as compared to control. By raising the radiation dose, proliferation was reduced and DNA fragmentation was increased. The results obtained indicate that low radiation doses stimulate cell proliferation while higher doses trigger apoptosis of thymocytes.

Animals↗
PubMed1994

Dependence of thymocyte apoptosis on protein kinase C and phospholipase A2.

The effect of inhibitors and activators of protein kinase C and phospholipase A2 on radiation-induced apoptosis of rat and mouse thymocytes has been studied. It is shown that the apoptosis is prevented by the protein kinase C inhibitor 1-(5-isoquinolinylsulfonyl)-2-methylpiperasine dihydrochloride and is potentiated by protein kinase C activator phorbol 12-myristate 13-acetate, calcium ionophore A23187 and concanavalin A. The protein kinase C activators initiate apoptosis in mouse but not in rat thymocytes. The inhibitor of phospholipase A2 prevents apoptosis induced by all the factors. The results obtained indicate that both protein kinase C and phospholipase A2 are involved in the thymocyte apoptosis.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1993

On the role of intracellular concentration of Ca2+ and H+ in thymocyte death after irradiation.

The role of intracellular Ca2+ and H+ concentrations in radiation-induced interphase death of rat thymocytes has been studied. In response to concanavalin A treatment in the Ca(2+)-containing medium, or to the CaCl2 treatment in the Ca(2+)-free medium, the [Ca2+]i rise in irradiated cells was as in the non-treated cells. No changes in the level of [Ca2+]i and pHi were found within 1 h after irradiation of thymocytes with a dose of 6 Gy. 15 microM 5-(N-ethyl-N-isopropyl)-amiloride, an inhibitor of Na+/H+ exchange, did not affect the DNA fragmentation. The fragmentation was prevented by 2-4 microM (1-[bis(4-chlorophenyl)methyl]-3-[2-(2,4-dichlorophenyl)]-2-[(2,4- dichlorophenyl)-methoxy]-ethyl)-1-H-imidazolium chloride, an inhibitor of calmodulin. The above data indicate that triggering of interphase death in irradiated thymocytes is not mediated by changes in either [Ca2+]i or pHi. Such changes seem to be involved in intermediate steps of the interphase death process.

Amiloride↗
PubMed1993

Intercellular interactions in the interphase death of irradiated thymocytes.

The effect of the interaction of different types of cells on the interphase death and pycnosis of thymocytes irradiated in vitro was studied. When removed from the thymus suspension of cells with natural killer activity, medullary thymocytes and macrophages did not change the radiation-induced death of cortical thymocytes. On the other hand, postirradiation incubation of cortical thymocytes together with unirradiated thymocytes or with cells of certain other cell lines diminished thymocyte death. Mixing the cell suspensions and changing the incubation medium decreased thymocyte death. All of these results indicate that these cells produce soluble mediators that are toxic to the cells that secrete them. The possible nature of these autotoxic mediators has been studied using inhibitors of arachidonic acid metabolism. Inhibitors of phospholipase A2 or lipoxygenase reduced interphase death markedly, while an inhibitor of cyclooxygenase did not. These data suggest that some lipoxygenase products may serve as autotoxic mediators in the interphase death of thymocytes.

Animals↗
PubMed1991

[The role of changes in the cytoplasmic concentration of Ca2+ in dexamethasone-induced thymocyte death].

The putative role of changes in cytosolic Ca2+ concentration ([Ca2+]i) in the dexamethasone (DM) induced thymocyte death was investigated. Incubation of rat thymocytes with 10(-7) M DM for different time intervals from 0.1 to 8 h did not change the basal [Ca2+]i level ca 100 nM as measured with Ca(2+)-fluorescent probe Quin-2. Ca2+ influx measured by the rate of 45Ca2+ uptake was also just the same in DM treated and control cells. At the same time a 6-8 h incubation of cell suspension with 10(-7) M DM results in significant increase in DNA fragmentation and pyknosis, and a 24 h incubation is associated with the decrease in the percentage of cells not staining with Trypan blue. Thus, the results obtained indicate that 10(-7) M DM induces thymocyte death without any significant and constant [Ca2+]i rise during the first 8 h after hormone application.

Animals↗
PubMed1990

[Some quantitative parameters of the vascular system of transplanted brain tumors in experiments using rats].

A vascular system of several strains of brain tumors: neurinoma 46-1, gliomas: 11-9-2 and 101-8 were investigated by means of automatic analysis of microangiograms and histochemical-luminescent estimation of endothelial cells. It was shown that the mean quantity of vessels and their section-size in all strains of tumors are less than control independently of the rates of tumor development. The linear density of the endothelial cells appear less that in control vessels and is equal in different strains of tumors, though the inclination to hemorrhages in gliomas is higher than in neurinoma. The cause of this phenomenon is discussed.

Angiography↗
PubMed1990

[Age-related characteristics of cerebral blood vessels in the rat (morphometric study)].

Age changes in the vascular network density and transversal section of the vessels have been studied in the cerebral hemisphere cortex, corpus callosum, septum and nucleus caudatus of Wistar rats. Angiography has been performed by means of intracardiac injection of Indian ink, frontal colloidin slices of the brain 15 mcm thick have been prepared. Amount of vessels and section area of each vessel have been measured, using the automatic analysis. Each brain area studied has homogeneous vascularization density, however, they differ from each other by the amount of vessels. The vascular size in the areas does not differ. At the age of 2-20 months the average number of vessels in all the cerebral areas investigated does not change, while the vascular diameters demonstrate certain tendency to increase after 17 months of life.

Age Factors↗
PubMed1990

The mechanism of radiation-induced interphase death of lymphoid cells: a new hypothesis.

The interphase death of irradiated rat thymocytes depends on their concentration during postirradiation incubation. The kinetics of pycnosis and cell death determined with the trypan blue exclusion test in the samples with the highest cell concentration (1-2 x 10(7) cells/ml) is consistent with the data available in the literature, whereas the samples with the lowest concentration (2 x 10(5) cells/ml) undergo almost no pycnosis and death after irradiation with doses up to 50 Gy. On the basis of these results, we suggest a new mechanism of interphase death involving an interaction between irradiated thymocytes and the fraction of thymus cells possessing cytocidal activity. The observed correlation between the cytocidal activity and interphase death of thymocytes from animals of different ages favors our mechanism. It was found that the inhibitors which prevent the conjugation of killer cells and their targets do not influence interphase death, while the substances which block the secretion of cytotoxic factors or their action on the target membrane do protect from interphase death. Thus we suggest that the irradiation activates the killer cells to secrete some cytotoxic factors which induce pycnosis and interphase death of thymocytes.

Animals↗