PubMed Health⌕ Search

Biomedical subjects

M Kh Levitman

Publications and source records attributed to M Kh Levitman.

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↗
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↗
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↗
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↗
PubMed1983

[Change in cerebral microcirculation at long-term periods following irradiation with protection by gammaphos].

A study was made of the influence of prophylactic administration of gammaphos (300 mg/kg) on radiation alterations in the system of cerebral microcirculation of rats in a long-term period following local irradiation of doses of 40-60 Gy. It has been shown that the number of animals with severe vascular injuries and the degree of these injuries lessen. A computerized analysis has shown that gammaphos administration weakens a decrease in the mean number of vessels and an increase in their average size caused by irradiation.

Amifostine↗