[Post-receptor formation of active forms of oxygen in nonphagocytic cells]. / Postretseptornoe obrazovanie aktivnykh form kisloroda v kletakh, ne iavliaiushchikhsiia professional'nymi fagotsitami.

Generation of reactive oxygen species (ROS) in A431 cells, NIH3T3 fibroblasts expressing normal epidermal growth factor (EGF) receptor, L929 fibroblasts, and in mouse peritoneal macrophages (professionally phagocytic cells) upon the effect of different activators has been studied. It has been shown that ROS formation in A431 and NIH3T3 cells upon the effect of EGF is time- and dose-dependent process. A variety of stimuli were used to stimulate macrophage ROS production. However, the effect of only phorbol ester, opsonized zymozan, peptide fMLP, and platelet activating factor led to ROS generation, whereas tumor necrosis factor alpha, interferon gamma, and lipopolysaccharide did not stimulate macrophage oxidative burst. The literature data on ROS generation in a variety of cell types are presented. ROS formed in cells acted upon certain agents are considered as the molecules participating in intracellular signaling.

[Activation of astrocytes of by anaphylatoxins of the complement system]. / Aktivatsiia astrotsitov anafilatoksinami sistemy komplementa.

It has been shown that astrocytes (human glioblastoma U118 cell line) release reactive oxygen species (ROS), including superoxide O2.- and hydrogen peroxide H2O2 following the action of C5a complement component C5a (but not C3a). The effect of C5a (1 nM) is accompanied with hyperpolarization of the astrocyte plasma membrane. Component C3a (100 nM), which is not an inducer of ROS, caused a prolonged depolarization of astrocytes. However, both the agents induced a transient increase in intracellular Ca2+ concentration. The data obtained permit a conclusion that O2.- participates in the intracellular signal transduction, and is involved in the mechanism of hyperpolarization response of astrocytes to the effect of the inducer of ROS, complement component C5a.

[Mechanisms of hyperpolarization of plasma membrane of macrophages and astrocytes during activation]. / Mekhanizm giperpoliarizatsii plazmaticheskoi membrany makrofagov i astrotsitov pri aktivatsii.

The hyperpolarization response of macrophages and glial cells (astrocytes, U118 cell line) to the action of inducers of reactive oxygen species (ROS) has been studied. Macrophages were stimulated with chemotactic peptide fMLP and platelet activation factor (PAF). Astrocytes were affected by complement component--anaphylatoxin C5a. The hyperpolarization response of both cell types depends on intracellular Ca2+ concentration and extracellular K+ concentration. Depletion of K+ concentration in the medium (1 mM KCl) or chelation of intracellular Ca2+ with Quin-2 (50 microM) significantly decreased the hyperpolarization response or caused depolarization of plasma membrane. Moreover, inhibition of Ca(2+)-dependent K(+)-channels with quinidine (50 microM) induced only a prolonged depolarization of both cell types. The data obtained permit a suggestion that macrophage and astrocyte hyperpolarization response to stimulation with ROS inducers involves O2.- mediated activation of Ca(2+)-dependent K(+)-channels.

[NADPH oxidase--a specialized enzyme complex for the formation of active oxygen metabolites]. / NADFN-oksidaza--spetsializirovannyi fermentativnyi kompleks dlia obrazovaniia aktivnykh metabolitov kisloroda.

Generation of reactive oxygen species (ROS) by phagocytes play an important role in defence against infection. For this purpose, phagocytes possess superoxide-forming enzyme NADPH oxidase. NADPH oxidase is a complex, multicomponent enzymatic system which is assembled in plasma membrane upon activation. In recent years, it has been evident that other cells and tissues can also produce small amounts of ROS by NADPH oxidase-like enzyme. The growing list includes B-lymphocytes, fibroblasts, kidney mesangial cells, endothelial cells, osteoclasts. The physiological and pathophysiological relevance of this extra-phagocytic superoxide production has only recently begun to be addressed. Evidence is emerging that generation of ROS might be important factor in triggering variety of cellular functions (cell growth, development, locomotion). Here, we review numerous literature data concerning the structure, regulation and mechanisms of activation of NADPH oxidase of phagocytes and other mammalian cells.

[Hydrogen peroxide as a signal molecule]. / Perekis' vodoroda kak signal'naia molekula.

This review deals with numerous literature data on the action of small redox-active H2O2 biomolecule on the cellular activity. Evidence is provided on H2O2 sources in the cell, intracellular antioxidants and scavengers, and on the dependence of cellular response (cell damage or activation) on H2O2 concentration. Stimulation of cells by nontoxic doses of H2O2 and possible activation mechanisms are also discussed. The number of examples is given demonstrating H2O2 playing the role of a second messenger for the variety of agents that stimulate the cells.

[The effect of inhibitors of glucose utilization on the chemiluminescence and fluorescence of murine peritoneal macrophages]. / Vliianie ingibitorov utilizatsii gliukozii na khemiliuminestsentsiiu i fluorestsentsiiu myshinykh peritoneal'nykh makrofagov.

Using the inhibitors of glucose utilization and mitochondrial oxidation we found that the blue autofluorescence (AF) of murine peritoneal macrophages (MP) originates predominantly from the cytosolic NAD(P)H. AF intensity correlates with the changes in glycolytic enzymes activity. The luminol-dependent chemiluminescence (CL) intensity which characterizes the amount of O2- generating by MP upon the addition of formyl-methionyl-leucyl-phenylalanine (FMLP) is inhibited in the case of maximum activity of glycolytic enzymes. Incubation of MP with non-convertible analog of glucose, such as 2-deoxyglucose increases the CL intensity under the influence of FMLP. A conclusion is drawn that amount of O2- generating by MP depends on the intracellular concentration of sugars.