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Biomedical subjects

M Kh Levitman

Publications and source records attributed to M Kh Levitman.

33 records · Page 2Linked to original sources
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[Growth inhibition and induction of tumor cell death by phospholipase A2 and lipoxygenase inhibitors].

We studied the effect of arachidonic acid metabolism inhibitors in a wide concentration range on the proliferation and death of lympholeukemia cells P-388. Proliferation of the cells was estimated by metaphase frequency and the proportion of cells in S phase; cellular death was determined by their lysis, trypan blue staining, damaged nuclei, the proportion of cells with subdiploid DNA content, and DNA fragmentation. Low concentrations of phospholipase A2 and lipoxygenase inhibitors were shown to stimulate cell division, while higher concentrations inhibited it by blocking G1-S transition and inducing apoptotic cellular death. Indomethacin, a cyclooxygenase inhibitor, had no effect on proliferation and induced no cell death at concentrations up to 10 microM. Inhibitors of phospholipase A2 and lipoxygenase also inhibited tumor growth in mice.

Acetophenones↗
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[Antitumor effect of combined treatment with ionizing radiation and vitamin B12-C complex].

The combined effect of ionizing radiation (0.5-4 Gy) and the vitamin B12-C complex on life-span of mice with Ehrlich carcinomas was studied. It was shown that antitumor effect of the combined treatment strictly depends on the sequence of the agent applying and on the time interval between them. For example, the combined treatment increased essentially the life-span of mice if the vitamins were used 24 h after irradiation but with the reverse order of influences, the antitumor effect was less than that of the vitamin complex only. It was supposed that the discovered regularities are due to tumor cell synchronization or division stimulation with the first influence.

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PubMedDate not supplied

[A study of the role of lipoxygenases in radiation-induced apoptosis of thymocytes. Inhibitory analysis].

The radiation-induced apoptosis of thymocytes is suppressed by the common inhibitor of lipoxygenases nordihydroguaiaretic acid but not the inhibitors of cyclooxygenases or cytochrome P-450, which indicates the key role of lipoxygenases in apoptosis. However, the specific inhibitors of 5-lipoxygenase (AA861) and of 12-lipoxygenase (baicalein) do not suppress apoptosis and even enhance it. This effect can be explained by an increase in the yield of the 15-lipoxygenase product upon inhibition of 5- and 12-lipoxygenases. Indeed, the addition of 15-hydroxyecosotetraenic acid, a product of 15-lipoxygenase, into the incubation medium induces apoptosis in thymocytes. The results obtained suggest that 15-lipoxygenase is one of the enzymes involved in radiation-induced apoptosis of thymocytes.

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[Analysis of 15-lipoxygenase activity in irradiated thymocytes].

We studied the effect of gamma-radiation on 15-lipoxygenase activity in rat thymocytes. The enzyme activity was determined as the rate of linoleic acid oxidation by the protein fraction isolated from the control and irradiated thymocytes under standard conditions. We demonstrate lipoxygenase activation immediately after irradiation of thymocytes. High lipoxygenase activity is observed in the cells for no more than an hour after irradiation. No high lipoxygenase activity later indicates that its synthesis is not directly induced by irradiation. Irradiation-induced generation of lipid peroxides can be the factor of lipoxygenase activation.

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[The early decrease in the endothelial cells of the cerebral vessels of rats after local irradiation].

Possible causes of diminution of endothelial cells of rat brain vessels immediately after local irradiation have been investigated. It has been shown that the diminution occurs during the first 24 h following irradiation, its value (-15%) being independent of radiation dose within a wide range (from 5 to 100 Gy), and the cellularity is not restored during the subsequent two weeks of observation. Interphase death of part of cells distinguished by high radiosensitivity seems to be the most probable reason for the population heterogeneity observed.

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[Use of gammaphos for protecting the brain from delayed radiation damage].

The influence of a radioprotector, gammaphos, on the development of delayed vascular changes and necrosis in rat brain following local brain irradiation with 25 Gy was investigated. The radioprotective effect was manifested by both the morphometric parameters of vessels and the survival rate and relative number of animals with gross vascular abnormalities and brain necrosis. There was a causative relationship between the development of gross vascular abnormalities and the occurrence of brain necrosis after exposure to moderate radiation doses.

Amifostine↗
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[Dynamics of changes in the cellularity of the vascular endothelium in the brain of rats following local irradiation].

Dynamics of changes in endothelium cellularity of rat brain vessels was studied during 12 months following local irradiation with a dose of 25 Gy that approximated the therapeutic one by its efficacy. A 15 per cent decrease in the endothelium cellularity was registered 24 h after irradiation followed by a slow 40 per cent depletion of the population at a constant rate up to the 6th month. By month 10 the cellularity was restored and after 12 months it dropped again drastically.

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PubMedDate not supplied

[Proliferation and death of thymocytes caused by phospholipase A2 activator--melittin].

The effects of mellitin, a component of bee venom activating phospholipase A2, on proliferation and death of the rat thymocytes were studied in a wide concentration range. Cell proliferation was estimated by the accumulation of colchicine metaphases, Necrosis was estimated by cell lysis and Trypan blue staining. Apoptosis was estimated by the type of DNA fragmentation, amount of fragmented DNA, and percentage of cells with hypodiploid DNA set. Low concentrations of mellitin (below 5 micrograms/ml) stimulated proliferation. At higher mellitin concentrations, the thymocytes die by the primary necrosis type. Mellitin did not induce apoptosis in the thymocytes within the concentration range used: on the contrary, at high concentrations, it inhibited apoptosis of the thymocytes in the control and after irradiation. Actinomycin D, inhibitor of RNA synthesis, exerted no effect on the thymocyte death in the presence of mellitin. It has been concluded that activation of phospholipase A2 may induce necrosis, rather than apoptosis, and consequently, activation of phospholipase A2 is not a necessary step in the signalling cascade that initiated apoptosis in the thymocytes.

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