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1.
Georgian Med News ; (192): 87-92, 2011 Mar.
Article in Russian | MEDLINE | ID: mdl-21525545

ABSTRACT

The aim of our study was the investigation of toxicity of denture prosthetic appliance Prothyl Hot on the model system of Jurkat cell culture. As a result of our study it was revealed that denture prosthetic appliance Prothyl Hot: - hadn't manifested toxic effects the viability Jurkat cells (that reviled by stability of activity of mitochondrial dehydrogenises and mean of mitochondrial membrane potential; - didn't influence on the balance of pro-and antyinflammatory cytokines, expressed by Jurkat cells; - induces intensification of oxidative metabolism in Jurkat cells, which may be considered as compensatory reaction developing in the cells.


Subject(s)
Dental Materials/adverse effects , Dentures/adverse effects , Apoptosis/drug effects , Catalase/metabolism , Cytokines/metabolism , Glutathione Reductase/metabolism , Humans , Jurkat Cells , Membrane Potential, Mitochondrial/drug effects , Oxidative Stress , Superoxide Dismutase/metabolism , T-Lymphocytes/drug effects
2.
Georgian Med News ; (159): 58-61, 2008 Jun.
Article in Russian | MEDLINE | ID: mdl-18633154

ABSTRACT

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.


Subject(s)
Apoptosis/radiation effects , Gamma Rays , Jurkat Cells/pathology , Radiation Injuries/pathology , Dose-Response Relationship, Radiation , Humans , Jurkat Cells/radiation effects
3.
Patol Fiziol Eksp Ter ; (1): 11-2, 1991.
Article in Russian | MEDLINE | ID: mdl-2057219

ABSTRACT

The authors studied the mechanisms of disorders of energy provision of myocardial contractility in rabbits in hemorrhagic shock and appraised the efficacy of a new Soviet-produced agent dalargin possessing an antiadrenergic property. It is shown that dalargin exerts a significant effect on the condition of the cardiovascular system and the function of the myocardial mitochondria (MC). The effect differed depending on the time of the injection and the condition of the organism. Increase of the heart contractive function, improvement of MC function, and prolonged survival of the animals were encountered only in rabbits who received dalargin 30 minutes after blood loss. The mechanisms of the effects of dalargin in acute blood loss are discussed.


Subject(s)
Energy Metabolism/drug effects , Enkephalin, Leucine-2-Alanine/analogs & derivatives , Hemorrhage/drug therapy , Myocardial Contraction/drug effects , Sympatholytics/pharmacology , Acute Disease , Animals , Enkephalin, Leucine-2-Alanine/pharmacology , Rabbits
4.
Biokhimiia ; 52(1): 37-41, 1987 Jan.
Article in Russian | MEDLINE | ID: mdl-3814652

ABSTRACT

The changes in the oxidative metabolism of rabbit myocardium in hemorrhagic shock were studied. The external pathway of NADH oxidation was shown to be activated, while the rates of glutamate oxidation in the presence of an uncoupler were diminished as compared to control values. These changes are probably due to the activation of phospholipase A2 and lipid peroxidation, since their inhibitors eliminate with the same efficiency the activation of the external pathway of NADH oxidation both in normal and damaged myocardium.


Subject(s)
Mitochondria, Heart/metabolism , NAD/metabolism , Shock, Hemorrhagic/metabolism , Animals , Energy Metabolism , Lipid Peroxides/metabolism , Male , Oxidation-Reduction , Phospholipases A/antagonists & inhibitors , Phospholipases A/metabolism , Phospholipases A2 , Rabbits
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