[The effect of cyclooxygenase and lipoxygenase inhibitors on Ca(2+)-responses induced by glutoxim and molixan in macrophages].

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.

[The involvement of actin cytoskeleton in glutoxim and molixan effect on intracellular Ca(2+)-concentration in macrophages].

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.

[Superfamily of voltage dependent K+ channels: structure, functions and pathology].

In this review the recent studies related to the voltage dependent K+ channels are discussed. During the last 15 years the molecular cloning revealed a large number of alpha-subunits of voltage dependent K+ channels. This approach enabled to elucidate the properties of different types of channels and, in particular, characteristics of such structural elements as auxiliary subunits.

[The effect of oxidized glutathione and its pharmacological analogue, glutoxim, on intracellular Ca2+ concentration in macrophages].

The effect of oxidized glutathione (GSSG) and its pharmacological analogue, glutoxim, on intracellular Ca2+ concentration in rat peritoneal macrophages was investigated using Fura-2AM microfluorimetry. It was shown that both GSSG and glutoxim increased intracellular Ca2+ concentration inducing Ca(2+)-mobilization from thapsigargin-sensitive Ca(2+)-stores and subsequent Ca2+ entry into macrophages from external medium. Dithiothreitol, which reduces S-S-bonds in proteins, completely prevented or reversed the increase in the intracellular Ca2+ concentration induced by GSSG or glutoxim.

[The effect of phosphatidylinositol kinase inhibitors on store-dependent Ca2(+)-transport in macrophages].

Using Fura-2AM microfluorimetry the role of phosphatidylinositol kinases in the regulation of Ca2+ signals induced by purinergic agonist ATP and endoplasmic Ca2(+)-ATPase inhibitor thapsigargin in rat peritoneal macrophages was investigated. It was shown that two structurally distinct phosphatidylinositol 3- and phosphatidylinositol-4-kinases inhibitors wortmannin and LY294002 showed a dose- dependent effect on store-dependent Ca2(+)-entry, induced by thapsigargin or ATP. The data suggest that phosphatidylinositol 3- and phosphatidylinositol-4-kinases play an important role in the activation of store-dependent Ca2(+)-entry in macrophages and that their effect might be mediated by their influence on actin cytoskeleton.

[Effect of latrunculin B, jasplakinolide and brefeldin A on the store-dependent Ca2+ entry in macrophages].

Using Fura-2AM microfluorimetry, effect of actin filament modifiers and vesicular trafficking inhibitor on the store-dependent Ca2+ entry induced by purinergic agonists (ATP, UTP) and endoplasmic Ca2+-ATPase inhibitors (thapsigargin, cyclopiazonic acid) in rat peritoneal macrophages was investigated. It was shown that inhibition of actin polymerization by latrunculin B had a biphasic time-dependent effect on Ca2+ entry, showing an initial potentiation followed by inhibition of Ca2+ entry. Moreover, addition of latrunculin B after induction of store-dependent Ca2+ entry inhibited the Ca2+ influx.

[Effect of arachidonic and other fatty acids on the intracellular calcium concentration and calcium signaling in peritoneal macrophages].

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.

[The role of cytoskeleton structures in regulation of Ca2+ responses in macrophages].

The role of the cytoskeleton in regulation of purinergic agonist- and endoplasmic Ca(2+)-ATPase inhibitors-induced Ca2+ signals in rat peritoneal macrophages was investigated. It has been shown that in cells pretreated with agents that disrupt microtubules (vinblastine, colchicine, colcemid) or actin microfilaments (cytochalasins, phalloidin), the ability of thapsigargin or cyclopiazonic acid to empty Ca2+ stores and activate store-dependent Ca2+ influx was significantly attenuated. On the contrary, microfilaments and microtubule disrupters did not affect ATP- or UTP-induced Ca2+ mobilization, indicating that release of Ca2+ from intracellular stores through the inositol phosphate pathway was intact.

[The rhythmicity of physiologic changes in the functional state of the visual and skin temperature analyzers in man].

Considering significance of the light and the temperature factors for the rhythmic activity of the organism, the maximum of the day's functional activity of the thermoreceptor system was noted at 5 p.m. and the minimum--at 1 a.

[Reflex interaction between the visual and skin temperature analyzers in focal lesions at the level of the optic thalamus and brain stem].

The authors convened a clinico-physiological study of the interaction of the visual and skin temperature analyzers in patients with disturbed circulation in the deep branches of the posterior cerebral artery (the first group) and in patients with disturbed circulation in the vertebro-basillar system (the second group). Inasmuch as in the first group there was an involvement of thalamic structures, the significant disorders connected with disturbances of reflectory interaction in the visual and skin-temperature analyzers are presumably related to these structures. An insignificant change in the continuing of the visual and skin temperature analyzers in disturbances of the brain stem indicate to the limited importance of nonspecific structures of this area in the reflectory interaction of these analyzers.