[Role of phospholipase A2 and epoxygenase in inhibition of respiration burst in neutrophils by low intensity radiation of extremely high frequency]. / Rol' fosfolipazy A2 i époksigenazy v ingibirovanii respiratornogo vzryva neitrofilov nizkointensivnym élektromagnitnym izlucheniem kraine vysokoi chastoty.

The role of some components of the phospholipid metabolism in the activation of neutrophil respiratory burst and its inhibition by electromagnetic radiation (EMR) of extremely high frequencies (EHF) was studied. It was shown that EHF EMR has effect on cells with a high sensitivity to the inhibitor of phospholipase A2 4-bromophenacyl bromide. However, againsts the background of the inhibitor, the effect of EHF EMR was not observed on cells with either high or low sensitivity to the inhibitor. EHF EMR was also inefficient with cells pretreated with proadifen, an inhibitor of epoxygenase (cytochrome P-450). The results obtained suggest that the effect of EHF EMR manifests itself in cells with a high activity of phospholipase A2 and is realized with the participation of epoxygenase metabolites of arachidonic acid.

[Viscumin modulates neutrophil respiratory burst, caused by a chemotactic peptide]. / Viskumin moduliruet respiratornyi vzryv v neitrofilakh, vyzvannyi khemotaksicheskim peptidom.

The ability of viscum at different concentrations to modulate the respiratory burst in neutrophils, induced by the chemotactic peptide N-formyl-methionyl-leucyl-phenylalanine was studied. This does not exclude the possibility that viscum can interact with the receptor of this peptide. The analysis of the primary structure of viscum revealed elements structurally analogous to the chemotactic peptide. It is assumed that viscum can exhibit the properties an antagonist of the receptor of N-formyl-methionyl-leucyl-phenylalanine, and the mechanism of action of viscum depends on its concentration.

[Features of the modulating effect of complexes of ribosome-inactivating proteins type II with sugars on respiratory burst of neturophils, caused by a chemotactic peptide]. / Osobennosti moduliruiushchego deistviia kompleksov ribosom-inaktiviruiushchikh belkov II tipa s sakharami na respiratornyi vzryv neitrofilov, vyzvannyi khemotaksicheskim peptidom.

It was shown that agents inducing phagocytosis (zymosan, lectins) cause changes in the number of receptors responsible for fast neutrophil reaction (chemotaxis or respiratory burst) or inhibit the binding of the agonist to its receptor. Among lectins are ribosome-inactivating proteins of type II ricin and agglutinin ricin, which penetrate the cell by binding to mannose and galactose receptors. It was shown that ribosome-inactivating proteins of type II can exhibit the properties of the antagonist of the receptor N-formylmethionylleucylphenylalanine. Ricin is more effective in modulating the respiratory burst induced by the chemotactic peptide than agglutinin ricin. The modulating effect of ribosome-inactivating proteins of type II on neutrophils is likely to be mediated by their interaction with galactose rather than mannose receptors. Presumably, the affinity of ribosome-inactivating proteins to galactose receptors increases with increasing amount of saccharides bound to the protein molecule. The modulating effect of ribosome-inactivating proteins of type II on the respiratory burst of neutrophils induced the chemotactic peptide is due to the structural peculiarities of these proteins.

[Millemetre waves inhibit the synergistic effect of calcium ionophore A23187 and phorbol ester in neutrophil respiratory burst]. / Millimetrovye volny ingibiruiut sinergicheskii effekt kal'tsievogo ionofora A23187 i forbolovogo efira v aktivatsii respiratornogo vzryva neitrofilov.

The effect of extremely high frequency electromagnetic field (mm-waves) on respiratory burst of neutrophils was studied. The peritoneal evoked neutrophils of the mice (NMRI line) were used. The production of reactive oxygen species was estimated by luminol-dependent chemiluminescence technique. Cells were irradiated by the mm-waves of 41. 95 GHz in the far field zone of the channel radiator during 20 min. Absorbed energy flux density was 150 microW/cm2. The irradiation was carried out at different concentrations of calcium ionophore A23187 and then neutrophils were stimulated by phorbol 12-myristate 13-acetate (PMA) 1 microM, activator of PKC. At irradiation of neutrophils the synergistic action of A23187 and PMA was not changed at low concentration of ionophore 10 nM-0.5 microM and was suppressed at high concentrations 0.5-10 microM. The largest inhibition of about 60% was obtained at the concentration of A23187 20 microM. The effect of mm-waves was not found under exposure in Ca(2+)-free medium for all used A23187 concentrations. We suggest that the mm-wave effect on the production of reactive oxygen species by neutrophils is determined by the influx of extracellular Ca2+ and PKC.

[Perfluorocarbon emulsions and other corpuscular systems influence on neutrophil activity]. / Deistvie emul'sii perftororganicheskikh soedinenii i drugikh korpuskuliarnykh sred na aktivnost' neitrofilov.

Influence of perfluorodecalin, perfluoromethilcyclohexylpiperidine, perfluorotributylamine emulsions on active oxygen form (AOF) generation by neutrophils has been studied. All investigated emulsions stabilized both proxanol 268 and egg yolk phospholipids inhibited PMA-stimulated neutrophil activity. Castor oil emulsion also inhibited the neutrophil activity. Neutrophil response for chemotactic peptide, was unchanged in the presence of all tested emulsions. We suppose that fast hydrophobic attachment of inert submicrone emulsion particles to cell surface provokes alteration of neutrophil plasma membrane function resulting in a decrease of AOF generation.