Nitric oxide dependent skin aging mechanism in postmenopasal women.

The goal of our study was to determine nitric oxide (NO)-dependent mechanisms of skin aging in post- and premenopausal women. 23 women (age 40-50 year) were investigated. Women were divided into 2 groups: I group - reproductive age women (10 patients); II group - menopause age women (13 patients). Patients were included in the menopausal group when they fulfill the following criteria: at least 12 month of amenorrhea. All patients are subjected to a standard diagnostic protocol. In each group we investigated estradiole, lipids and free NO content. Skin of postmenopausal women as a rule was pale, grayish, in some cases revealed pigmentation; skin around the eyes less flexible, wrinkled. Moderate hypercholesterolemia and reduced levels of nitric oxide and estradiole in the blood of studed postmenopausal women (in comparison reproductive aged women) was revealed. Decrease free NO content in blood may be due to the decrease of NO synthesis, as well as the oxidative degradation of NO in the oxidative stress conditions. N artcle the mechanism of dependence of NO-vasodilatative system activity on rhe level of hypercholesterolemia and estrogen content in blood are discussed. It was concluded that in menopausal women insufficiency of estrogen's content is the main factor, which stipulates insufficiency of of NO-dependent vasodilatative mechanism, and disorder of subcutaneous vasodilatation in aged (postmenopausal) women which contributes to violations of the oxidative processes in the skin and its rapid aging.

[Study of toxicity of denture prosthetic appliance prothyl hot on the Jurkat cell model system].

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.

[Contamination of some food products with Salmonella in Georgia].

Salmonella infections in Georgia are usually caused by S. enderitidis and S. typhimurium. Food products represent a leading vehicle in transmission of S. enderitidis, which predominates over other serotypes. The goal of our research was to study contamination of chickens and chicken eggs with S. enderitidis and S. typhimurium. Overall 90 chicken eggs, obtained from various poultries, 100 eggs, sold by peasant and 30 chicken and their excrements were tested. Cer Test Salmonella-immunchromatography one stage analysis were employed for detecting of salmonella microbe. Chickens and chicken eggs were contaminated with bacteria S. Enteritidis. The microbe isolation rate from eggs was 4.2±1.4%. It was 1.1 for eggs from poultries and 7.0±2.5 for eggs from peasant vendors. Chicken's contamination was found to be high--26.7±8.1%. The research data showed the prevalence of S. Enteritidis in etiology of salmonella infections in Georgia.

Treatment of experimental autoimmune encephalomyelitis by vitamin in animal model.

Study purposed to determine the effectiveness of vitamin treatment in experimental autoimmune encephalomyelitis (EAE) animal model of multiple sclerosis (MS) by comparing several blood serum inflammatory markers, neurological deficiency and histopathological changes in untreated and treated EAE animals. Eighteen, 9-13 week old, male Wistar rats were immunised by 100 µl MOG injection. Clinical signs of EAE scored by a masked investigator. After EAE exposition all rats were divided equally as untreated control and experimental group treated by vitamins (E, C, D3). Blood was obtained from all rats before and after immunization and on 7th day of treatment. ELISA method was used to detect the serum cytokine contents of IL-6, IFN-γ, IL-10. On 10th day of disease the rats were euthanized and transverse sections of spinal cord were divided in 16 areas with score of 1 for each area showing lymphocyte infiltration or demyelination. Mann-Whitney U-test was used for determining the level of significance of differences between sample means. On 7th day of treatment neurological deficiency stayed unchanged in control and was ameliorated in experimental group (p<0.05). Significant histopathological differences were found between control and experimental groups on 10th day of EAE. Serum levels of IFN-γ, IL-6 and IL-10 were elevated after exposition of EAE against healthy rats, while on 7th day of treatment the experimental group revealed the significant differences as compared to untreated control. Positive correlation was found between IL-6 and IFN-γ serum contents and neurological deficiency on 7th day of disease (r=+0.53, p<0.02 and r=+0.49; p<0.01).

[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.

[Composite herbal medicine paradon--modulator of apoptosis induced by nitrogen-oxygen stress].

Apoptosis is a mechanism that regulates the quantity and the quality of cells and provides the maintenance of body homeostasis. Disregularion of apoptosis may result in severe diseases. In this regard there is an urgent need in medicine, which modulates apoptosis. The purpose of the present research was to study the effect of composite herbal medicine Paradon on the intensity of apoptosis induced by nitrogen-oxygen stress. The research has been conducted on the intensively proliferating leukemia - transformed T cells (Jurkat cells). Medicinal preparation Paradon revealed proliferative - stimulating effect, antioxidant effect on Jurkat cells, incubated with oxygen and nitrogen free radical donors (hydrogen peroxide (Sigma) and sodium nitroprusside (Naniprus, Sopharma)). Paradon - through the recovery of energoproducing system activity reduces the intensity of necrosis, induced by nitrogen-oxygen stress, and replaces it with more mild mechanism of cell death - apoptosis.

[Role of NO and several mechanisms of plaferon lb action in the regulation of arterial blood pressure during hemorrhagic shock].

The present study aimed to establish the role of NO and mechanisms of plaferon LB (PLB) (USA patent N WO 02/12444 A2) effectiveness in the regulation of arterial blood pressure (ABP) during hemorrhagic shock (HS). As it follows from the results of our study and literary data analysis, stress-hormone mediated receptor-induced accumulation of Ca2+ ions in vascular cells occurs during experimental HS. At that, rapid release of large amount of NO due to Ca-dependent eNOS activation in endothelium results in the prevalence of NO-dependent relaxation mechanisms over Ca2+-dependent constriction in smooth muscle cells with subsequent abrupt decrease in ABP. In experimental HS, reproduced against preliminary administration of isoptine, blockage of Ca entry in endothelial cells prevents intensification of Ca-dependent synthesis of nitric oxide, and consequently, prevents activation of NO-dependent mechanisms of dilatation thereby facilitating ABP elevation. Preliminary administration of LNAME inhibits nitric oxide synthesis in blood vessel endothelium and consequently prevents activation of NO-dependent mechanisms of dilatation. Insignificant (by 17%) increase of Ca2+ levels in artery of animals of this experimental group is likely due to transitory hormone-induced entry of calcium through slow Ca channels, which at the inhibition of NO-dependent vasodilatation provides constriction of blood vessels and normalization of ABP. Given the ability of PLB to regulate nitric oxide synthesis at various pathological processes, we suggest that normalization of ABP by this preparation during HS is mainly due to NO-modulating activity of PLB. PLB maintains physiological concentrations of NO in blood vessels. Nitric oxide, in its turn, provides normalization of ABP in experimental animals due to the regulation of vascular smooth muscle tone through the modulation of Ca2+ levels. Thus, we can conclude that nitric oxide plays significant role in the regulation of the balance between constrictory and dilatatory mechanisms of vascular tone. PLB due to its NO modulating activity provides maintenance of physiological activity of nitric oxide, normalization of Ca2+ levels and ABP in blood vessels.

[Effect of dalargin on energy metabolism of heart contractile function in acute blood loss]. / Vliianie dalargina na énergoobespechenie sokratitel'noi funktsii serdtsa pri ostroi krovopotere.

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.

[Mechanism of activation of the external pathway of NADH oxidation in myocardial mitochondria during hemorrhagic shock]. / Mekhanizm aktivatsii vneshnego puti okisleniia NADH v mitokhondriiakh miokarda pri gemorragicheskom shoke.

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.