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Showing papers in "Fiziolohichnyĭ zhurnal in 2008"


Journal Article
TL;DR: There is evidence to suggest that microglia is capable of secreting neurotrophic or neuron survival factors upon activation during inflammation or injury, and the current status of knowledge on origin, morphology and functional features of microglial cells is reviewed.
Abstract: Microglia, one of three types of glial cells in the central nervous system (CNS), plays an important role as resident immunocompetent and phagocytic cells in CNS in the event of injury and disease. It was del Rio Hortego who in 1927 determined that microglia belong a distinct glial cell type apart from astrocytes and oligodendrocytes. Since 1970s there has been wide recognition that microglial cells are immune effectors in the CNS that respond to pathological conditions and participate in initiation and progression of neurological disorders including Alzheimer's disease, Parkinson's disease, multiple sclerosis, and acquired immune deficiency syndrome dementia complex by releasing potentially cytotoxic molecules such as proinflammatory cytokine, reactive oxygen intermediates, proteinases and complement proteins. There is also evidence to suggest that microglia is capable of secreting neurotrophic or neuron survival factors upon activation during inflammation or injury. It is thus timely to review the current status of knowledge on origin, morphology and functional features of microglial cells.

16 citations


Journal Article
TL;DR: It is shown that upon PTP opening, isolated mitochondria release adenosine, inosine and 3'-ribosyl uric acid monophosphate (3-RUAMP), and that perfused hearts subject to IPC release inosines and 3-UUAMP derivatives, and that these events were inhibited by the PTP blockers cyclosporin A and sanglifehrin A.
Abstract: Both mitochondrial permeability transition pore (PTP) opening and purine signaling are implicated in cardioprotection via ischemic preconditioning (IPC). The PTP opening is accomponied by release ofintramitochondrial solutes, and therefore we hypothesized that purine release from mitochondria during PTP opening may by required for IPC signaling. Herein we show that upon PTP opening, isolated mitochondria release adenosine, inosine and 3'-ribosyl uric acid monophosphate (3-RUAMP), and that perfused hearts subject to IPC release inosine and 3-RUAMP derivatives. Both these events were inhibited by the PTP blockers cyclosporin A and sanglifehrin A. Implications for cardioprotective signaling by purines and the PTP are discussed.

8 citations


Journal Article
TL;DR: The new mechanism of iNOS activation, prostaglandine and tetrahydrobiopterin synthesis stimulation by ecdysterone has been proposed, due to stimulating enzymatic degradation of sphingosine-1-phosphate as effective regulator ofiNOS, COX and GTP-cyclohydrolase in cardio-vascular system.
Abstract: Streptozotocine (STZ) administration (5 mg/100 g) up regulates oxidative (lipid peroxidation as a marker) and nitrosative (protein nitrosilation as a marker) stresses as well as ROS (O(2-), H2O2, OH) generation in heart and aorta in rats after 60 days of STZ action. The level of oxydative stress was higher in aorta. Xanthine oxidase (XO) activation (uric acid as marker), but not lipoxygenase (LTC4 as marker) or cyclooxygenase (TxB2 as marker) are the main oxydases that generate O(2-) as calculated by correlation analysis. STZ administration led to sphingosine pools up regulation in heart and aorta, but pools of polyamines in this organ was down regulated. C27-phytosteroid hormone ecdysterone (100 ng/100 g, per os, 60 days) mimics the action of its structural analog C27-steroid hormone calcitriol (1alpha,25-dihydroxyvitamin D,) and protects rise of ROS generation (by XO inhibition), lipid peroxidation, protein nitrosilation, polyamine degradation in heart and aorta of rats after STZ administration. The new mechanism of iNOS activation, prostaglandine and tetrahydrobiopterin synthesis stimulation by ecdysterone has been proposed. It was due to stimulating enzymatic degradation of sphingosine-1-phosphate as effective regulator of iNOS, COX and GTP-cyclohydrolase in cardio-vascular system: sphingomyelin > ceramide > sphingosine > S-I-P > phosphoethanolamine > ethanolamine.

7 citations


Journal Article
TL;DR: In experiments on isolated Langendorff perfused hearts of guinea pig with modeling of ischemia and reperfusion the cardioprotective effects of flokalin were shown and mitochondrial as well as sarcolemmal K(ATP) channels play role in the recovery of ischemic myocardium functions.
Abstract: In experiments on isolated Langendorff perfused hearts of guinea pig with modeling of ischemia (20 min) and reperfusion (40 min) the cardioprotective effects of flokalin were shown. Preliminary preischemic perfusion of isolated heart with flokalin (5 mM) for 5 minutes has significantly improved the recovery of contractive function ofischemic myocardium at repcrfusion. Particularly, recovery of systolic and developed pressure was improved and the increasing of end-diastolic pressure in left ventricle was prevented. The vasoconstriction of coronary vessels was prevented and number of extrasystols at reperfusion of ischemic heart was decreased. Morphological studies have shown that flokalin prevents the significant damage of myocardial structure and the development of hypercontraction of myofibrils at ischemia-reperfusion of myocardium. It also preserves the intact sarcolemma and intracellular organelles. The intact structure of mitochondria also was saved by flokalin that maintains the energy potential of myocardium. Using the selective blocker of mitochondrial K(ATP) channels 5-hydroxydecanoate (200 mM) allows to determine the relative role of sarcolemmal and mitochondrial K(ATP) channels activation in these effects. It was shown that mitochondrial as well as sarcolemmal K(ATP) channels play role in the recovery of ischemic myocardium functions: first are responsible for recovery of contractive function and second are responsible for coronary blood flow recovery.

5 citations


Journal Article
TL;DR: The testing of the levels of NO and superoxide generation in mitochondria simultaneously with cyclosporine A-sensitive MPTP opening by Ca2+ and phenylarsine oxide to determine whether downregulation of both NO and O2(-) generation in heart mitochondria by potent steroid antioxidant and free radical scavenger ecdysterone may protectHeart mitochondria of aging rats again tissue damage is suggested.
Abstract: Nitric oxide reacts rapidly with superoxide to produce the potent oxidant peroxynitrite. In vivo mitochondria produce superoxide as well as NO. In heart mitochondria of aging rats the amount of NO and O2(-) are increased thus the levels of peroxynitrite produced may be increased too, in this reason mitochondria may be a major site of peroxynitrite formation. Oxidative stress induces cyclosporine A-sensitive mitochondrial efflux of calcium and proapoptotic factors through MPTP (mitochondrial permeability transition pore) opening in heart mitochondria which may contribute to tissue damage and mitochondrial dysfunction in aging rats. We tested the levels of NO and superoxide generation in mitochondria simultaneously with cyclosporine A-sensitive MPTP opening by Ca2+ and phenylarsine oxide (PAO) to determine whether downregulation of both NO and O2(-) generation in heart mitochondria by potent steroid antioxidant and free radical scavenger ecdysterone may protect heart mitochondria of aging rats again tissue damage. C27-phytosteroid hormone ecdysterone (10 mkg/100g, per os, 2 weeks) mimics action of its structural analog C27- steroid hormone calcitriol (1alpha,25-dihydroxyvitamin D3) and exert its cardio protection in aging heart mitochondria by inhibition of MPTP opening with effectivity of action of hormone melatonine (150 mkg/100g, 2 weeks [ V.F. Sagach et al. Fyziol. J (Ukr), 2006, 52(2), 3-15]). MPTP inhibition is dependent on paradoxycally high activation by ecdusterone of oxidative degradation of L-arginine by mtcNOS in mitochondria, by downregulation of superoxide generation and L-arginine degradation by arginase II and NO generation by mtiNOS in de novo and by NADP-dependent mtNR (nitrate reductase) in salvage pathways. These results suggest that MPTP opening may be directly influenced by ecdysterone signaling in mitochondria. The signaling pathway by which ecdysterone may coregulate the O2(-) and NO generation in heart mitochondria of aging rats may involve an outer mitochondrial membrane estrogen receptor coupled to mitochondrial PI3K/Akt/PKB activation results in superactivation and constitutive NO synthesis by mtcNOS.

5 citations


Journal Article
TL;DR: The article describes the types of synaptic interaction of the autonomic nervous system neurons by the example of sympathetic neurons of the superior cervical ganglion and plasticity of the neurons of this ganglia grown in culture conditions in relation to the expression ofrenergic and cholinergic properties as well as the role of the calcium ions in regulation of cellular processes.
Abstract: As a result of intensive research performed in different laboratories recent years in the field of autonomic nervous system physiology, considerable experimental material was collected and some new and interesting hypotheses were proposed. This review is a short sketch about the progress in the study of autonomic transmission mechanisms. Since the sixties of the last century non-adrenergic non-cholinergic nerves were opened, and it was the later recognition of a multiplicity of neurotransmitter substances in autonomic nerves. The concept of cotransmission proposed in the late seventies was found for sympathetic, parasympathetic and enteric nerves. The idea of presynaptic receptors gave impetus to recognition of neuromodulation, and the existence of nonsynaptic interaction between neurons became an obvious fact for the last forty years after its discovery. The article describes the types of synaptic interaction of the autonomic nervous system neurons by the example of sympathetic neurons of the superior cervical ganglion and plasticity of the neurons of this ganglia grown in culture conditions in relation to the expression ofadrenergic and cholinergic properties as well as the role of the calcium ions in regulation of cellular processes. Studies of the last few decades have given impetus for elaboration of new concepts of autonomic nervous system function, part of which is represented in this review. The prospects for further investigations are described.

5 citations


Journal Article
TL;DR: It was established that influence of MP electromagnetic emission results in adverse movement by cerebral blood flow and regulatory systems of organism.
Abstract: It was investigated in experiment on volunteers the influence of mobile phone (MP) electromagnetic emission on brain blood supply rheoencephalographic parameters, and on status of neurohumoral regulation using the heart rate variability analysis. It was established that influence of MP electromagnetic emission results in adverse movement by cerebral blood flow and regulatory systems of organism.

5 citations


Journal Article
TL;DR: It was shown that additional acute hypoxic influence and acute hemorrhage accompanied with less significant structural violations in lung tissue and myocardium of animals, which were adapted to hypobaric hypoxia.
Abstract: Priority of effect of oxygen concentration and/or atmospheric pressure changes on morphofunctional state of lung tissue and myocardium under exasperate influence on the organism, which lead to the development of different hypoxic states, was investigated. It was shown, that the intermittent hypoxia without barometric pressure lowering influence on ultrastructure of tissues less traumatically, then hypobaric hypoxia. Additional acute hypoxic influence and acute hemorrhage accompanied with less significant structural violations in lung tissue and myocardium of animals, which were adapted to hypobaric hypoxia. Stress exchanges were less considerable after normobaric hypoxic trainings.

4 citations


Journal Article
TL;DR: It is found that isoflurane in clinically relevant concentrations effectively stops hippocampal seizures and suggests that the mechanism by which seizures are terminated differ from the mechanism responsible for preventing of the initiation of seizures.
Abstract: In the present study we examined the effect of isoflurane on seizure-like activity at hippocampal CA3 pyramidal region of immature rats in vivo. We found that isoflurane in clinically relevant concentrations effectively stops hippocampal seizures. When animal was under isoflurane anesthesia seizure-like activity still can be evoked by application of proconvulstant agents, but this activity was qualitatively different from that obtained in nonanesthetized rats. This observation suggests that the mechanism by which seizures are terminated differ from the mechanism responsible for preventing of the initiation of seizures.

4 citations


Journal Article
TL;DR: Review of last 15 years literature and own experimental data on role of reactive oxygen species (ROS) and redox signalization in induction of cell protective systems and development of adaptive resistance and concept of ROS involvement in non-specific component of increase resistance is introduced.
Abstract: Review of last 15 years literature and own experimental data on role of reactive oxygen species (ROS) and redox signalization in induction of cell protective systems and development of adaptive resistance. Modem ideas of ROS involvement in redox signalization, induction of transcription factors and protective proteins, ways of cell response to ROS, essential limitations of exogenic antioxidants are shown. Concept of ROS involvement in non-specific component of increase resistance is introduced. Peculiarities of author's method of adaptation to change oxygen level are discussed. Experimental data on efficacy of adaptation to periodic hypoxiahyperoxia from ROS-induced stresses are presented.

4 citations


Journal Article
TL;DR: A large number of structural associations between labeled cells and vessels in the temporal and insular cortex indicate that NADPH-d-reactive interneurons can contribute to regulation of the cerebral regional blood flow in these areas.
Abstract: The distribution of NADPH-diaphorase-reactive (NADPH-dr) neurons and neuronal processes in the cerebral cortex and basal forebrain and their association with parenchymal vessels were studied in normal adult rats using NADPH-d histochemical protocol. The intensely stained cortical interneurons and reactive subcortically originating afferents, and stained microvessels were examined through a light microscope at law (x250) and high (x630) magnifications. NADPH-dr interneurons were concentrated in layers 2-6 of the M1 and M2 areas. However, clear predominance in their concentration (14 +/- 0.8 P GI (18.0%, n = 640) > S1 (13.3%, n = 720) > M1 (6.3%, n = 1360). A large number of structural associations between labeled cells and vessels in the temporal and insular cortex indicate that NADPH-d-reactive interneurons can contribute to regulation of the cerebral regional blood flow in these areas.

Journal Article
TL;DR: The data indicate the important role of ER stress in processes of cardiomyocytes death at anoxia-reoxygenation and inhibition of proteasomal and autophagic proteolysis and propose that it unconditionally should cause necrotic cell death.
Abstract: At modeling of endoplasmatic reticulum (ER) stress by it classic inducer thapsigargin, anoxia-reoxygenation and simultaneous inhibition ofproteasomal proteolysis, autophagy and apoptosis a diversity of ultrastructural peculiarities was shown. Their comparison allows to make a conclusion that changes in these groups of experiments are similar and typical for ER stress. Thapsigargin application was shown to result in accumulation of giant mitochondria in perinuclear zone of cardiomyocytes. Some of these mitochondria had destroyed and high condensed matrix. The structure of ER was normal but in some regions of cells the dilation of ER cisterns occurred that, to our opinion, is an essential sign of ER stress. In another group of cells thapsigargin caused dehydratation and osmiophilia of cytoplasm, significant dilation of ER cisterns, partial or complete degranulation of these organelles that often formed vacuoles with high electron density material. Also, the significant decrease of the number and size of mitochondria that had partially destroyed and condensed matrix was observed in these cells. The accumulation of lipofuscin and myophilament destruction at preservation of sarcoplasmic membrane integrity was detected. However, in conditions of simultaneous inhibition ofproteasomal proteolysis, aytophagy and apoptosis the loss of membrane integrity was shown, and we propose that it unconditionally should cause necrotic cell death. That was confirmed by use of fluorogenic dyes to detect necrosis and apoptosis. Our data indicate the important role of ER stress in processes of cardiomyocytes death at anoxia-reoxygenation and inhibition of proteasomal and autophagic proteolysis.

Journal Article
TL;DR: After injection ofaminoguanidine in animals under diabetes the efficiency of both pathways in leucocytes decreases, which may be the basis of reconstitution of physiological pool to the relatively essential amino acid L-arginine.
Abstract: In experimental streptozotocin-induced diabetes, the activity of enzymes which have common substrate (L-arginine) changes in leucocytes of peripheral blood. It leads to misbalance between different pathways of arginine metabolism: NO-synthase (oxidative) pathway is activated, whereas arginase (nonoxidative) one is depressed. The injection of L-arginine under diabetes activated nonoxidative pathway, which can be seen in possible decrease in NO-synthase activity with unchanged arginase activity. After injection ofaminoguanidine in animals under diabetes the efficiency of both pathways in leucocytes decreases, which may be the basis of reconstitution of physiological pool to the relatively essential amino acid L-arginine.

Journal Article
TL;DR: Examining of cultured autologous MSC as effective activators of bone resorption, inflammation and some immunological reactions in the process of altered osteoreparation allows examining the immunoregulatory role of transplanted autologueous cells in inflammation and own bone reparation processes during posttraumatic bone fracture healing.
Abstract: Bone marrow contains mesenchymal stem cells (MSC) including osteoblast progenitor cells. When culturedunder conditions promoting an osteoblastic phenotype,MSC proliferate to form colonies that produce alkaline phosphatase and, subsequently, a mature osteoblastic phenotype. Transplantation of cultured autologous MSC to patients with non-healing bone fractures gives a good result leading to complete bone fracture consolidation. The aim of the study is to determine a quantitative production of IL-1beta, IL-2, IL-4, IL-6, IL-8 and TNF-alpha by cultured uncommitted and committed osteogenic MSC. The results showed that the cytokine profile consisting of IL-1beta, IL-2, IL-4, IL-6, IL-8 and TNF-alpha is secreted by cultured MSC. The secretion of IL-1beta and IL-2 by cultured MSC together with hyper production of IL-6 (up to 276.5 pg/ml, p<0.05) and IL-8 (up to 106.6 ng/ml, p<0.05) by osteoinducted MSC are firstly shown. The immunoregulatory role of transplanted autologous cells in inflammation and own bone reparation processes during posttraumatic bone fracture healing is highlighted. In conclusion, the data obtained allow examining of cultured autologous MSC as effective activators of bone resorption, inflammation and some immunological reactions in the process of altered osteoreparation.

Journal Article
TL;DR: Alimentary deprivation and intermittent hypoxia have positive effects on the physiological remodelling of bone tissue and registered significant increasing of serum acid phosphatase activity in animals, which have breathed hypoxic gas mixture.
Abstract: Influencing of 28-days alimentary deprivation and intermittent hypoxia to 3 months Wistar male rats (n = 30) bone tissue physiological remodelling is studied. We investigated 3 groups of animals, I group was control, II--food limitation mode (-40% in relation to the normal ration) and III--animals, which breathed hypoxic gas mixture with 13% O2 in nitrogen (HGM) during 4 hours in the intermittent mode (10 min of deoxygenation and 10 min of reoxygenation). It is showed significant increasing of melatonin and glicozaminoglikans levels in the rats II and III gr. serum. Activity of alkaline phosphatase in the bone tissue of III gr. rats increased and in the bone tissue and serum of II gr. rats for 1.2 and 1.4 time accordingly. We registered significant increasing of serum acid phosphatase activity in animals, which have breathed hypoxic gas mixture. The IGF-I gene expression level did not change practically in both experimental groups. We conclude, that alimentary deprivation and intermittent hypoxia have positive effects on the physiological remodelling of bone tissue.

Journal Article
TL;DR: Experimental and clinical researches on studying biological effects of ozonetherapy and offers on prospects of development ozone technologies in biomedicine were stated.
Abstract: The results of experimental and clinical researches on studying biological effects of ozonetherapy were observed. Modem ozonetherapy methods and ways, indications and contra-indications the use of this method of oxidizing therapy were described. The ozonetherapy problems were analysed and offers on prospects of development ozone technologies in biomedicine were stated.

Journal Article
TL;DR: HPA hormone secretion mediates alterations of programming of brain development induced by prenatal stress, and was tested in this study with dexamethasone (Dex) used for suppression of HIPA stress responses.
Abstract: The hypothesis on the mediating role of hypothalamic-pituitary-adrenocortical (HPA) hormone secretion in neuroendocrine, neurochemical and behavioral alterations generated by prenatal stress in male rat offspring was tested in this study with dexamethasone (Dex) used for suppression of HIPA stress responses. Pregnant dams were being restrained daily for 1 h over the last week of gestation. In male offspring this resulted in attenuation of sex-specific pattern of the protein fractions (on the 5th postnatal day), steroid aromatase activity (on the 10th postnatal day) in the brain preoptic area, and in a decrease of male copulatory behavior, hypothalamic noradrenaline and plasma corticosterone responses to an acute stress, an increase in HPA responses to noradrenergic stimulation and other effects in adulthood. All those changes were prevented with prenatal Dex in a dose of 0.1 mg/kg b.w. injected 30 min prior to restraining pregnant dams. As such, HPA hormone secretion mediates alterations of programming of brain development induced by prenatal stress.

Journal Article
TL;DR: It is shown that systematic physical exercises (volley-ball game) cause substantial positive changes in endothelium-dependent physiological indexes.
Abstract: Experimental data regarding the features of the functional state of vascular endothelium in girls of 18-20 years old with a different level of physical activity are presented in the article. It is shown that systematic physical exercises (volley-ball game) cause substantial positive changes in endothelium-dependent physiological indexes.

Journal Article
TL;DR: The data obtained indicate that mitochondrial factor might serve as an effective way of diagnostics of oxidative stress in injured tissues at ischemia/ reperfusion in the lower extremities.
Abstract: The study was conducted within a group of 17 patients suffering from thrombosis in the femoral artery to identify a mitochondrial factor release into the blood at ischemia/reperfusion in the lower extremities. To test the mitochondrial factor as a possible marker of the mitochondrial permeability transition pore opening under oxidative stress we determined the rates ofoxidative stress (malonic dyaldehyde, MDA), oxidative protection (catalase) and mitochondrial factor release under ischemia/ reperfusion induced by surgical operation. It has been shown that the parameters of pro- and antioxidant systems changed in a way characteristic of oxidative stress: content of MDA in the blood at reperfusion increased, but activity of catalase decreased. We were the first to record the mitochondrial factor release into the blood of the femoral artery on the wave length of 245 nm using spectrophotometry. The data obtained indicate that mitochondrial factor might serve as an effective way of diagnostics of oxidative stress in injured tissues at ischemia/ reperfusion in the lower extremities.

Journal Article
TL;DR: Investigation of pattern of lipid and lipoprotein metabolism disturbances in patients with manifested clinical signs of coronary atherosclerosis concluded that hypertrigliceridemia is the factor which can initiate the proatherogenic systemic disturbances which include changes in lipid,lipoprotein and glucose metabolism, the development of insulin resistance, systemic inflammation and oxidative stress.
Abstract: The aim of the study was to investigate the pattern of lipid and lipoprotein metabolism disturbances in patients with manifested clinical signs of coronary atherosclerosis. There was determined the significance of hypertrigliceridemia as the marker of these disturbances and its connection with other most important factors of atherogenesis such as insulin resistance, systemic inflammation, and oxidative stress, blood lipoprotein modification. The role of excessive alimentary lipid consumption as a factor, which initiates the hypertrigliceridemia development and accompanying activation of the other proatherogenic factors was determined with the use of acute lipid loading. It was established that hypertrigliceridemia is one of the most reliable signs ofatherosclerosis existence but it coincides as a rule with other signs of dislipidemia, a decrease in insulin sensitivity, systemic inflammation and lipid free radical oxidation development. The modification of blood lipoprotein and increase of blood atherogenic potentials were the integral effects of these factors. Significance of hypertrigliceridemia as the factor initiating all these disturbances both in normal volunteers and in examined patients was shown in conditions of acute lipid loading which was accompanied by the development of the whole complex of proatherogenic disturbances. It was established that the development of atherosclerosis is connected with the decrease of lipid tolerance and as a result the same lipid loading was accompanied with proportional increase of both hypertrigliceridemia and connected with it proatherogenic disturbances. The obtained data allowed concluding that hypertrigliceridemia is the factor which can initiate the proatherogenic systemic disturbances which include changes in lipid, lipoprotein and glucose metabolism, the development of insulin resistance, systemic inflammation and oxidative stress. These changes are pathogenically interconnected, capable to amplify one another and induce blood lipoprotein modification with appearance of both proatherogenic and autoantigenic propertries, which stipulate the role of hypertrigliceridemia in atherogenesis.

Journal Article
TL;DR: The aim of this work was to study the influence of organic seenium in comparison with inorganic selenium on the factors of unspecific resistance and state of humoral immunity of chicken-broilers.
Abstract: The deficit of selenium is related to immunity worsening. Selenium improves an immune answer and raises disease resistance. The aim of our work was to study the influence of organic selenium in comparison with inorganic selenium on the factors of unspecific resistance and state of humoral immunity of chicken-broilers.

Journal Article
TL;DR: In case of T-cell mediated liver injury, the balance between cell proliferation and cell death in mononuclear liver cells was shifted toward the significant increase of apoptotic and necrotic cell death, particularly Fas-mediated apoptosis, while immune processes activation and cell proliferation were more pronounced in the case of antibodies-mediated injury.
Abstract: Two types of experimental liver failure in mice were investigated to study the immune mechanisms of liver disease: 1) T-cell-mediated injury induced by administration of concanavalin A (ConA) and 2) antibody-mediated injury induced by administration of anti-liver antibodies (ALA, gamma-globulin fraction of sera from rabbits immunized with liver tissue). It was established, that both types of liver injury were accompanied by the activation of immune processes in the liver, as shown by the increase of liver mononuclear cell proliferation, estimated using IPO-38 monoclonal antibodies. In contrast to ConA treatment, the immune activation under ALA-treatment was also associated with the increase in the percentage of plasma cells and small lymphocytes in liver mononuclear cells. At the same time, an increase in apoptotic and necrotic mononuclear cell death was more pronounced under ConA-treatment. This was accompanied by enhanced Fas receptor expression in these cells. Thus, it was shown that in case of T-cell mediated liver injury, the balance between cell proliferation and cell death in mononuclear liver cells was shifted toward the significant increase of apoptotic and necrotic cell death, particularly Fas-mediated apoptosis, while immune processes activation and cell proliferation were more pronounced in the case of antibodies-mediated injury.

Journal ArticleDOI
TL;DR: It has been demonstrated that in case of a suppressed activity of the pineal body the maximum number of melatonin receptors 1A in the neurons of the hypothalamic suprachiasmatic nuclei shifts and constitutes 0.35+/-0.012 conventional units (c.u.) of density, whereas a larger index is noticed at 20 hours making up 0.43+/- 0.015 c.u. of density.
Abstract: An immunohistochemical study of the density of melatonin receptors 1A in the neurons of the rat suprachiasmatic nuclei with diverse functional activity of the pineal gland has been carried out. The density of melatonin receptors 1A under conditions of the physiological function of the pineal gland was characterized by clear-cut diurnal variations. Simultaneously, a dysfunction of the gland results in their marked disturbance. In case of a hypofunction of the pineal body the density of the structures was reliably lower than in case of hyperfunction. It has been demonstrated that in case of a suppressed activity of the pineal body the maximum number of melatonin receptors 1A in the neurons of the hypothalamic suprachiasmatic nuclei shifts from 02.00 a.m. to 02.00 p.m. and constitutes 0.35+/-0.012 conventional units (c.u.) of density, whereas a larger index is noticed at 20 hours making up 0.43+/-0.015 c.u. of density when the gland is activated.

Journal Article
TL;DR: Expression of mRNA of 1 and 2 type (TRPVI and TRPV2) vanilloid receptors in the cultured hippocampal neurons was determined and found that these genes expression in different neurons is identical.
Abstract: Expression of mRNA of 1 and 2 type (TRPVI and TRPV2) vanilloid receptors in the cultured hippocampal neurons was determined. With the use of reverse transcription polymerase chain reaction (RT-PCR) of single neurons (single-cell RT-PCR), was shown the TRPV1 and TRPV2 receptors expression in both neurons and glia cell. With use of real-time (real-time PCR) we determined that the level of these genes expression in different neurons is identical. It was also shown that the level of mTRPVI in GABAergic neurons was considerably higher, than the level of mTRPV2, while expression of genes in the glutamatergic neurons did not differ. Findings about expression of TRPV 1 and TRPV2 allow to suppose that vanilloid receptors can play an important functional role in the hippocampal neurons.

Journal Article
TL;DR: Results demonstrate possible involvement of calcium signalling in pathogenesis of the disorders of HPA function in adult female rats, induced by neonatal androgenization.
Abstract: The effects of neonatal administration ofverapamil, a calcium L-type channel blocker, on the stress and noradrenergic responses of hypothalamo-pituitary-adrenal (HPA) axis in adult female rats with anovulatory syndrome induced by neonatal androgenization have been studied. There was no adrenocortical response to an acute stress nor noradrenaline infusion in the 3rd brain ventricle in females with persistent estrus. Verapamil pretreatment completely restored the adrenocortical responses to normal level. No changes were found in studied parameters following treatment with verapamil alone. These results demonstrate possible involvement of calcium signalling in pathogenesis of the disorders of HPA function in adult female rats, induced by neonatal androgenization.

Journal Article
TL;DR: It was demonstrated on the Wistar rats that in radiosensitive animals initial oxidative metabolism parameters were higher than in radioresistant ones, and prooxidant-antioxidant balance alteration after non-radiation stress were more evident and kept for a longer period.
Abstract: The data presented demonstrate possible personal radiosensitivity prognosis according to the immobilization stress response (animal model). It was demonstrated on the Wistar rats that in radiosensitive animals initial oxidative metabolism parameters were higher than in radioresistant ones, and prooxidant-antioxidant balance alteration after non-radiation stress were more evident and kept for a longer period. Those animals had had limphopenia and neutrophilosis. The differences in the response types between radiosensitive and radioresistant animals were due to the blood system reserve abilities, as well as the state of natural mature cells depot, and antioxidant defence enzymes.

Journal Article
TL;DR: The results indicate on specific bemitil action on scrotonin- and noradrenergetic neuromediator brain systems and dose-dependency of the effect of bemitsil is revealed.
Abstract: The study was carried out on brainstem noradrenergetic and serotoninergic neurons of cats and the effect of bemitil (100 mg/kg) introduction was investigated. The results indicate on specific bemitil action on scrotonin- and noradrenergetic neuromediator brain systems. Dose-dependency of the effect of bemitil is revealed.

Journal Article
TL;DR: It is concluded, that alimentary deprivation change the biochemical markers of bone tissue physiological remodeling for young animals, while the changes of physiological regeneration rates were insignificant for adult animals.
Abstract: We studied the influencing of designed during 28 days alimentary deprivation on the bone tissue physiological remodeling processes for 3- and 9-monthly Wistar rats-males (n=32). 4 groups of animals are probed: I, III - control, II, IV is the mode of calorie limitation (40% in relation to a valuable ration for every age group). It is shown, that alimentary deprivation increase the concentration of melatonin, glycosaminoglycans in blood serum and activity ofalkaline phosphatase in serum and bone tissue in 1,4 and 1,2 time accordingly at for young rats. For adult rats the reliable decline of activity of alkaline phosphatase is exposed in the blood serum after alimentary deprivation. Expression of gene ofinsulinlike growth factor-I for animals of both probed groups did not change practically. We conclude, that alimentary deprivation change the biochemical markers of bone tissue physiological remodeling for young animals, while the changes of physiological regeneration rates were insignificant for adult animals.

Journal Article
TL;DR: It was shown that the interrelation between these factors is the cause of blood lipoprotein proatherogenic and immunogenic modification, which is the main effector mechanism of atherosclerosis development and progression.
Abstract: The aim of the investigation was to determine the existence and describe interconnection between the lipid metabolism disturbances and development of systemic inflammation. The work was carried out on rabbits in two series of experiments: in the first one, the model of inflammation was reproduced by means of intravenous injection of bacterial lipopolysaccharide. In the second one, the model of lipid disturbances induced by lipids enriched diet was reproduced. In both series of experiments, the indexes of inflammation and oxidative stress intensity, metabolism of lipids and lipoproteins, insulin sensitivity, blood lipoprotein proatherogenic and immunogenic modification were determined. The data obtained confirmed the existence of distinct direct links between investigated influences: during the primary induced inflammation we observed pronounced disturbances in lipid and lipoprotein metabolism, while under the primary induction of lipid disturbances the systemic inflammation and oxidative stress were developed. The connection between the action of both influences was greatly mediated by their ability to induce insulin resistance. There was also shown that the interrelation between these factors is the cause of blood lipoprotein proatherogenic and immunogenic modification, which is the main effector mechanism of atherosclerosis development and progression.

Journal Article
TL;DR: Two approaches were used to activate synapses: a protocol of brief oxygen-glucose deprivation known to induce so-called anoxia-hypoglycemic long-term potentiation (LTP) as well as high frequency stimulation of Schaffer collaterals inducing LTP of evoked postsynaptic potentials in CA1 synapses, both of which caused a decrease in spatial clustering of SV.
Abstract: Prolonged activation of excitatory glutamatergic synapses causes modifications in their functioning and ultrastructural organization. While postsynaptic activity-induced changes have been relatively well studied, the data on spatial dynamics of synaptic vesicles (SV) under conditions of synaptic activation are still lacking. Using organotypic hippocampal slice cultures as a model system and electron microscopy as a technique, we analyzed changes in SV numbers and their spatial distribution in spine synapses ofhippocampal CA1 area. Two approaches were used to activate synapses: a protocol of brief oxygen-glucose deprivation known to induce so-called anoxia-hypoglycemic long-term potentiation (LTP), as well as high frequency stimulation of Schaffer collaterals inducing LTP of evoked postsynaptic potentials in CA1 synapses. Observations during the first hour after stimulation (30 and 60 min time-points) have shown that in both cases active functioning of synapses leaded to decrease in the total SV number as well as to depletion of the readily releasable SV pool. Both experimental protocols caused a decrease in spatial clustering of SV which was more pronounced after anoxia-hypoglycemic LTP. Possible mechanisms and functional consequences of these phenomena are discussed.