Publications by authors named "N I Krutetskaia"

The involvement of Arp2/3 complex, which causes actin filament branching, in the effect of drugs glutoxim and molixan was investigated. Using Fura-2AM microfluorimetry it was shown for the first time that Arp2/3 complex inhibitor CK-0944666 almost completely prevents the increase in intracellular Ca2+ concentration, induced by glutoxim or molixan in macrophages. The data suggest the involvement of Arp2/3 complex in the glutoxim and molixan effect on the Ca2+ signalling processes in macrophages.

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Glutoxim and molixan belong to a new generation of disulfide-containing drugs with immunomodulatory, hepatoprotective and hemopoetic effect. Using Fura-2AM microfluorimetry, the possible involvement of the cyclooxygenase and lipoxygenase pathways of arachidonic acid oxidation in the effect of glutoxim and molixan on the intracellular Ca2+ concentration in rat peritoneal macrophages has been investigated. We have shown for the first time that preincubation of the cells with the cyclooxygenase inhibitors, indomethacin and aspirin, or lipoxygenase inhibitors, nordihydroguaiaretic acid, caffeic acid and baicalein, almost completely prevents the intracellular Ca2+ concentration increase induced by glutoxim or molixan.

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Using voltage-clamp technique, the possible role of the cytoskeleton in the effect of pharmacological analogue of oxidized glutathione (GSSG), drug glutoxim, on Na+ transport in the frog Rana temporaria skin was investigated. It was shown for the first time that preincibation of the skin with the microtubular disrupter, nocodazole, actin filament disrupter, cytochalasin D or protein phosphatase PP1/PP2A inhibitor, calyculin A, significantly decrease the stimulatory effect of glutoxim on Na+ transport. The data suggest the involvement of microtubules and microfilaments in the regulatory effect of glutoxim on Na+ transport in frog skin and that reorganization of actin filaments or microtubules leads to inhibition of stimulatory effect of glutoxim on Na+ transport in frog skin epithelia.

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Glutoxim and molixan belong to new generation of disulfide-containing drugs with immunomodulatory, hepatoprotective and hemopoetic effect on cells. Using Fura-2AM microfluorimetry, two structurally distinct actin filament disrupters, latrunculin B and cytochalasin D, and calyculin A, which causes actin filaments condensation under plasmalemma, we have shown the involvement of actin cytoskeleton in the intracellular Ca(2+)-concentration increase induced by glutoxim or molixan in rat peritoneal macrophages. Morphological data obtained with the use of rhodamine-phalloidine have demonstrated that glutoxim and molixan cause the actin cytoskeleton reorganization in rat peritoneal macrophages.

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Effects of arachidonic and other fatty acids on the intracellular Ca2+ concentration ([Ca2+]i) in rat peritoneal macrophages was investigated. It has been shown that cis-polyunsaturated arachidonic and linoleic induce a significant and dose-dependent increase in [Ca2+]i, which is due to depletion of thapsigargin-sensitive Ca2+ store and to stimulation of Ca2+ entry from the extracellular medium. Pharmacological characteristics of Ca2+ entry induced by arachidonic acid appeared to be similar to those of store-dependent Ca2+ entry activated by thapsigargin or cyclopiazonic acid; Ca2+ entry is attenuated by the same Ca2+ channel inhibitors, by tyrosine kinase inhibitor genistein and epoxygenase inhibitor proadifen.

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