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Oxidative stress may contribute to many pathophysiologic changes that occur after traumatic brain injury. In the current study, contemporary methods of detecting oxidative stress were used in a rodent model of traumatic brain injury. The level of the stable product derived from peroxidation of arachidonyl residues in phospholipids, 8-epi-prostaglandin(More)
The neurotoxic effect of exposure of rat cerebellar granule cells to glutamate (I00 μM) is to a large extent prevented by incubation of neurons not only with micromolar, but even with nanomolar concentrations of gangliosides GM1, GD1b, and GT1b. GM1 was also shown to decrease significantly the per cent of dead neurons in culture after induction of lipid(More)
The significant increase of free calcium concentration ([Ca2+]i) was found in rat cerebral cortex synaptosomes and hippocampal crude synaptosomal fraction after their exposure to glutamate. But no change of [Ca2+]i was revealed in cerebellar synaptosomes, the slight increase of [Ca2+]i in striatal synaptosomes was not significant. The presence of(More)
GM1 ganglioside was found to increase the survival of PC12 cells exposed to H2O2, its action was blocked by Trk tyrosine kinase inhibitor K-252a. Thus, the inhibition of H2O2 cytotoxic action by GM1 constituted 52.8 ± 4.3%, but in the presence of 1.0 μM K-252a it was only 11.7 ± 10.8%, i.e. the effect of GM1 became insignificant. Exposure to GM1 markedly(More)
To clarify the role of mitochondrial electron transport chain (mtETC) in heavy-metal-induced neurotoxicity, we studied action of Cd(2+), Hg(2+), and Cu(2+) on cell viability, intracellular reactive oxygen species formation, respiratory function, and mitochondrial membrane potential of rat cell line PC12. As found, the metals produced, although in a(More)
We compared 21- and 40-day old rat pups from rats subjected to emotional stress in trimester III and from intact females. The width of the parietal cortex and the size of layer V neuron cytoplasm and nuclei in the anterior parietal lobe and hippocampus were increased in 21-day-old test pups compared to age-matched controls. In 40-day-old test pups, neurons(More)
To elucidate mechanism of ganglioside neuroprotection, it is important to study their metabolic effects, specifically of action on Na+, K+ -ATPase. It has been shown that under effect of oxidative stress inductors and neurotoxins an oxidative inactivation of this enzyme takes place in PC12 cells and brain cortex synaptosomes, this inactivation being able to(More)
Ganglioside GM1 was shown to increase the viability of PC12 cells exposed to hydrogen peroxide or amyloid β-peptide (Aβ25–35). The PC12 cells transfected with mutant gene (expressing APPSW) were found to be more sensitive to oxidative stress than the cells transfected with wild type gene (expressing APPWT) or vector-transfected cells, GM1 being effective in(More)
The aim of this work was to compare protective and anti-apoptotic effects of α-tocopherol at nanomolar and micromolar concentrations against 0.2 mM H(2)O(2)-induced toxicity in the PC12 neuronal cell line and to reveal protein kinases that contribute to α-tocopherol protective action. The protection by 100 nM α-tocopherol against H(2)O(2)-induced PC12 cell(More)
Preincubation with 100 nM and 100 μM α-tocopherol for 18 h prevented long-term activation of extracellular signal-activated kinase (ERK1/2), induced by H2O2 in PC12 cells. α-Tocopherol significantly reduced H2O2-induced death of PC12 cell, but its protective effect was signifi cantly lower in the presence of ERK1/2 inhibitor. These data show that prevention(More)