[Mechanisms of gamma-inducible death of Jurkat cells line].

Mechanisms of radio-inducible death of Jurkat cells were investigated. Human lymphoblastoid T-cell line Jurkat is widely established model for studying apoptosis mechanisms. The cell was radiated by "Teragam" (Czech Republic) by dose 2 g during 1 minute. After radiation cells were incubated at standard conditions during 24 hours. After gamma radiation in cell population amount of cells in gaplois (apoptotic G 0) stage was increased 8,2 folds, in diplois (G 0/G1) stage - by 17%, in synthetic (S) stage decreased by 35% and tetraploid (G2/M) stage by 73% in comparison to control group. It was revealed intensive production of free radicals of oxygen and nitric oxide and decreasing activity of antioxidant enzymes (superoxidismutasa, catalasa and glutathione peroxidase). Revealed dependence between intensification of apoptosis and radiation-induced arrest of cell cycle G2/M phase may be determined by excess amount of free oxygen and nitrogen radicals generated in Jurkat cells as a result of nondirect effects of low doses of gamma radiation.

[Plaferon LB in prevention of radiation-induced changes in lipid metabolism indices and erythrocyte deformability rate].

Oxidative damage of biological membranes plays critical role in the process of radiation-induced damages in tissues and cells. It involves reactive oxygen species generated under ionizing radiation. Development of radiation-induced oxidative stress facilitates the intensification of lipid peroxidation and fatty acid reorganization, which, in its turn, results in decreased lipid matrix fluidity, changes in biophysical properties of membranes, increased rigidity of membrane lipid-protein surface. Radiation-induced damage of cellular and subcellular membrane structures results in cellular metabolism disorder, which facilitates farther dysfunction of tissues and changes in homeostasis of whole organism. Hence, the search for effective protection is of actual interest of contemporary radiology. Our study aimed to determine membrane protective properties of Plaferon LB under radiation. On the basis of obtained results we can conclude that intensification of free radical oxidation, accompanying radiation damage, facilitates the activation of lipolysis in a body and functional and structural disorders of erythrocytes revealed by lowered deformability of erythrocytes and accumulation of methaemoglobin. Both vitamin C and Plaferon LB were found ineffective for correction of lipid metabolism at early stage of post radiation damage; although facilitating a decrease in oxidation intensity in blood, they provided retention of erythrocyte deformability and thereby, partial retention of rheological properties of blood. It should be mentioned that in contrast with vitamin C, Plaferon LB, apart from its ability to restrict reactive oxygen formation, revealed ability to stabilize erythrocyte membranes and thereby to prevent hemolysis.

[Plaferon lb as a protector of radioinducible disorder].

As it is known, p-53-dependent apoptosis is the cause of the radiosensitive cells' rapid death during the first ours after gamma-irradiation. It is considered, that short time suppression of the function of p-53 may decrease injury of normal tissue. The aim of our study was the determination of the effectiveness and possible mechanisms of radioprotective features of plaferon LB. It was found that plaferon LB provides correction of content and function of nitric oxide in hepatocytes during gamma-irradiation and that may be induced by its antioxidant capabilities. By the correction of oxidative metabolism plaferon LB decreases intensity of postradiation alterations. The restriction of intensification of nitric oxide synthesis after irradiation also results in decreasing of iNOS expression. Plaferon LB induces reduction of oxidative stress in the organism, also provides NO-modulatory activity. Increase of proapoptotic activity of p-53 is due to NO-stimulated DNA-dependent protein kinase and p-38 mitogen activated protein kinase. It may be concluded that during gamma-irradiation the preliminary influence of plaferon LB provides prevention of hyperproduction of nitric oxide and by this way promotes suppression of NO-inducible activation of p-53-induced apoptosis.