PubMed Health⌕ Search

Biomedical subjects

N V Gulyaeva

Publications and source records attributed to N V Gulyaeva.

14 recordsLinked to original sources
PubMed2000

Role of nitric oxide in the ethylcholine aziridinium model of delayed apoptotic neurodegeneration in vivo and in vitro.

The involvement of nitric oxide in neurodegenerative processes still remains incompletely characterized. Although nitric oxide has been reported to be an important mediator in neuronal degeneration in different models of cell death involving NMDA-receptor activation, increasing evidence for protective mechanisms has been obtained. In this study the role of nitric oxide was investigated in a model of NMDA-independent, delayed apoptotic cell death, induced by the neurotoxin ethylcholine aziridinium ethylcholine aziridinium both in vivo and in vitro. For the in vivo evaluation rats received bilateral intracerebroventricular injections of ethylcholine aziridinium (2nmol/ventricle) or vehicle. In the hippocampus a transient decrease in nitric oxide synthase activity occurred, reaching its lowest levels three days after ethylcholine aziridinium treatment (51.7+/-9.8% of controls). The decrease coincided with the maximal reduction in choline acetyltransferase activity as marker for the extent of cholinergic lesion. The effect of pharmacological inhibition of nitric oxide synthase was tested by application of various nitric oxide synthase inhibitors with different selectivity for the nitric oxide synthase-isoforms. Unspecific nitric oxide synthase inhibition resulted in a significant potentiation of the loss of choline acetyltransferase activity in the hippocampus measured seven days after ethylcholine aziridinium application, whereas the specific inhibition of neuronal or inducible nitric oxide synthase was ineffective. These pharmacological data are suggestive for a neuroprotective role of nitric oxide generated by endothelial nitric oxide synthase. In vitro experiments were performed using serum-free primary neuronal cell cultures from hippocampus, cortex and septum of E15-17 Wistar rat embryos. Ethylcholine aziridinium-application in a range of 5-80microM resulted in delayed apoptotic neurodegeneration with a maximum after three days as confirmed by morphological criteria, life-death assays and DNA laddering. Nitric oxide synthase activity in harvested cells decreased in a dose- and time-dependent manner. Nitric oxide production as determined by measurement of the accumulated metabolite nitrite in the medium was equally low in controls and in ethylcholine aziridinium treated cells (range 0.77-1.86microM nitrite). An expression of inducible nitric oxide synthase messenger RNA could not be detected by semiquantitative RT-PCR 13h after ethylcholine aziridinium application. The present data indicate that in a model of delayed apoptotic neurodegeneration as induced by ethylcholine aziridinium neuronal cell death in vitro and in vivo is independent of the cytotoxic potential of nitric oxide. This is confirmed by a decrease in nitric oxide synthase activity, absence of nitric oxide production and absence of inducible nitric oxide synthase expression. In contrast, evidence for a neuroprotective role of nitric oxide was obtained in vivo as indicated by the exaggeration of the cholinergic lesion after unspecific nitric oxide synthase inhibition by N-nitro-L-arginine methylester.

Animals↗
PubMed2000

A radiometric analysis of nitric oxide synthase activity in Hymenolepis diminuta.

The free radical nitric oxide (NO) is a neuronal messenger which is synthesized from L-arginine and O2 by nitric oxide synthase (NOS). In the synthesis NO and L-citrulline are produced in a stoichiometric 1:1 relation. The activity of NOS was analysed in homogenates of the rat tapeworm Hymenolepis diminuta by measuring the formation of L-[3H]citrulline after incubation with L-[3H]arginine. The nature of NOS in H. diminuta was determined by studying the effect of 3 types of NOS inhibitors: (1) L-NAME, (2) EGTA, (3) 7-nitro-indazole. All inhibitors caused a significant but not complete reduction in the formation of L-[3H]citrulline. The results are discussed against the background of nerve cells and fibres positive for NADPH-diaphorase staining in H. diminuta.

Animals↗
PubMed1997

Prophylaxis of encephalopathies and risk factors of atherogenesis development in the postresuscitation period in rats by means of succinic acid.

The effect of oral administration of succinic acid was studied in 66 rats exposed to 10 min cardiac arrest with further resuscitation. A total of 30 mg/kg of the drug were administered daily for 5 days starting with day 3 up to day 7 after resuscitation. The experiments have revealed that treatment with succinic acid caused normalization of the orienting behavior in an 'open field' test, decrease of the intensity of response to electric shock, normalization of free radical formation in the brain and serum and reduced cerebral morphological changes. The succinic acid prevented the increase of cholesterol, triglyceride and low density lipoproteins in the blood. The data suggested that after additional trials the succinic acid could be used to prevent development of postresuscitation encephalopathies (3 months after reanimation).

Animals↗
PubMed1997

Postresuscitation changes in brain free radical-mediated processes and nitric oxide synthase activity in rats: effects of individual behavior in "emotional resonance" test.

Effects of 7-min cardiac arrest and individual behavior on free radical-mediated processes and nitric oxide synthase (NOS) activity was evaluated in brains of male Wistar rats one hour and one week after resuscitation. "Emotional resonance" test was used for the behavioral selection of rats. The test includes factors of significance for rats: the choice between large and lighted or small and dark space as well as signals of pain of another rat. Free radical generation (using chemiluminescence method), superoxide scavenging/generating activity, substances reacting with 2-thiobarbituric acid and NOS activity (by measuring mononitrosyl iron complex of NO with diethyl dithiocarbamate and endogenous brain Fe2+ by electron spin resonance spectroscopy) were determined in cerebral cortex, cerebellum and hippocampus. Cardiac arrest induced oxidative stress accompanied by the loss of NOS activity, as well as compensatory changes of free radical-mediated processes in cerebral cortex. Oxidative stress was also evident in cerebellum and, to a lesser extent, in hippocampus. Most of neurochemical differences between behavioral groups were induced by cardiac arrest. These differences were global, related to a specific brain region or became apparent in cerebral lateralization of biochemical indices.

Adaptation, Psychological↗
PubMed1996

Cardiac arrest induces decrease of nitric oxide synthase activity and increase of free radical generation in rat brain regions.

Rats were subjected to 15 min cardiac arrest and sacrificed 1 h or 15-20 days after resuscitation. Homogenates of brain regions were assayed for nitric oxide synthase (NOS) activity (by measuring the mononitrosyl iron complex of NO with diethyl dithiocarbamate and endogenous brain Fe2+ using electron spin resonance spectroscopy) and generation of free radicals (FRG; by measuring H2O2-induced, luminol-dependent chemiluminescence). Cardiac arrest induced marked decrease of NOS activity and the increase of FRG, most prominent in cerebellum and less marked in cerebral cortex. Two groups of rats were revealed 15-20 days after cardiac arrest: with NOS activity significantly lower than control and not different from control. Positive linear inter-regional cross-correlations of both NOS activity and FRG (except of the group 1 h after resuscitation) as well as negative correlations between NOS and FRG were demonstrated.

Animals↗
PubMed1996

Oxidative stress in the brain following intraventricular administration of ethylcholine aziridinium (AF64A).

AF64A is a toxic analog of choline that disrupts high affinity choline transport and produces a persistent presynaptic cholinergic hypofunction. The observed neuroprotectant effects of Vitamin E in the AF64A model suggested that oxidative stress contributed to the cholinotoxicity of AF64A. The studies presented here examined whether intraventricular injection of AF64A produces oxidative stress in the brain of male Wistar rats. Indices of oxidative stress including thiobarbituric acid reactive species (TBARS), free radical generation using hydrogen peroxide-induced, luminol-dependent chemiluminescence (CL) and superoxide scavenging/generating activity were measured in cerebral cortex, hippocampus and the rest of the brain, without cerebellum, 1, 3 or 5 days after bilateral intraventricular injection of 3 nmol of AF64A or artificial CSF (sham surgery). The sham operation itself induced oxidative stress throughout the brain (increased TBARS, CL and superoxide generation). In addition to the oxidative stress of the sham surgery AF64A increased basal TBARS on day 1 and Fe/ascorbate-induced TBARS on days 3 and 5 throughout the brain. AF64A produced compensatory 'antioxidative' changes as well with increased superoxide scavenging activity observed on day 3 and decreased basal TBARS on day 5. AF64A also induced specific changes in the hippocampus including a decrease of CL and an increase of superoxide scavenging activity on day 5. The increased superoxide scavenging activity persisted up to 126 days. The results of the present study provide the first direct evidence that AF64A induces oxidative stress following intraventricular injection.

Animals↗
PubMed1994

NO synthase and free radical generation in brain regions of old rats: correlations with individual behaviour.

We have investigated the activity of NO synthase (NOS) and generation of free radicals (FRG) in selected brain regions of old male Wistar rats. Using the emotional resonance test, two groups of rats were selected for the experiment: passive, preferring dark space and active, preferring light space. Highest NOS activity and FRG were seen in cerebellum. As a rule, NOS activity was lower and FRG higher in the respective brain regions of active rats than in passive rats. Positive linear inter-regional cross-correlations of NOS activity as well as of FRG were found. When all rats were assessed as one group, negative correlations between NOS and FRG in cerebral cortex were revealed.

Aging↗
PubMed1987

Modulation of superoxide dismutase by electron donors and acceptors.

The competition between superoxide dismutase (SOD) and nitroblue tetrazolium (NBT) for O2- radicals in the presence of a number of physiologically active compounds was studied. The Na+ channel blockers, ajmaline, tetracaine, bipuvacaine, lidocaine and etmozine produced an increase in the amount of O2- reacting with SOD. Nitroprusside, ferricyanide, BAY K8644, levomycetin, cGMP, cAMP and GMP acted in the opposite way. All the SOD activtors had in common the property of being electron donors in the reactions with the light-induced free radicals of eosin whereas the SOD inhibitors behaved as electron acceptors. The electron activity of SOD modulators correlated qualitatively with their regulating efficacy.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1985

Mitochondrial membrane potential in lymphocytes as monitored by fluorescent cation diS-C3-(5).

A lipophilic fluorescent cation diS-C3-(5) and rotenone suppress the oxygen consumption rate of thymocytes in similar concentrations. Seventy percent inhibition corresponds to an inhibitor:cytochrome a molar ratio of about 1:1. Addition of uncouplers decreases the inhibition of respiration by diS-C3-(5) (but not rotenone). FCCP in similar concentrations increases O2 consumption in the absence of diS-C3-(5) and the diS-C3-(5) fluorescence intensity in the presence of TMPD in thymocyte suspensions. In most thymocyte preparations, oligomycin (0.05-0.1 microgram/mL) increases the fluorescence of diS-C3-(5) and further addition of TMPD (50-100 microM) decreases the fluorescence. Addition of NaCN (400 microM) after oligomycin leads to a fluorescence increase that is hardly affected by subsequent addition of 0.2 microM FCCP. Nigericin (10-50 nM) decreases the diS-C3-(5) fluorescence. The data indicate that the diS-C3-(5) fluorescence associated with mitochondrial transmembrane potential (delta psi m) may be an essential part of the diS-C3-(5) fluorescence in lymphocyte suspensions. The changes of the diS-C3-(5) fluorescence intensity in the presence of TMPD after FCCP addition reflect delta psi m.

Animals↗
PubMedDate not supplied

Biochemical correlates of individual behavior.

This article is a review of data (results of the authors' investigations and data from the literature) concerning neurochemical correlates of individual behavior in rats. The "emotional resonance" test was used for behavioral selection of rats. Individual behavior in this test is related to the differences in free radical-mediated processes, membrane lipid content, nitric oxide synthase activity, and cAMP pattern in cerebral macrostructures. Behavior-related differences may be revealed in intact animals; however, most of them are reactive (induced by significant external factors). These differences depend on age; they may be global, specific for selected brain regions, and/or related to interhemisphere lateralization of biochemical parameters.

Aging↗