[Effect of ischemic damage factors on lipid peroxidation in rat brain synaptosomes]. / Vliianie faktorov ishemicheskogo povrezhdeniia na perekisnoe okislenie lipidov v sinaptosomakh mozga krys.

Accumulation of TBA-reactive substances after a 40 min incubation of rat brain synaptosomes at 37 degrees C was analysed. A lowering of pH to 6.5-5.5 or arachidonic acid (0.1-1.0 mM) increased lipid peroxidation which was blocked by antioxidants. Acidosis (pH 6.0) and arachidonic acid used in combination had a strong synergic effect. Depolarisation of plasma membranes or intrasynaptosomal mitochondria were without influence on lipid peroxidation at neutral or acid pH. The results support a leading role of acidosis and phospholipases in stimulation of peroxidation under ischaemia.

[Effect of acidosis on membrane potential and calcium transport in rat brain synaptosomes]. / Vliianie atsidoza na membrannyi potentsial i transport kal'tsiia v sinaptosomakh mozga krys.

The influence of acidosis on the transmembrane potential, sodium pump and membranous systems of calcium transport was studied on isolated presynaptic nerve terminals (synaptosomes) from rat brain. It is established that acidic shift causes a decrease of membrane potential, a large inhibition of the sodium pump (by three times at pH 6.0). All the systems controlling both inward- and outward-directed calcium fluxes are partially blocked by low pH. At pH 6.0 the basal influx and calcium pump are reduced two-fold while the voltage-sensitive calcium channels and Na+/Ca2+ exchanger are inhibited by three and four to five times, respectively. We have no found any evidence of acidosis-induced net flux of calcium directed inwards.

Effect of gamma-irradiated carbohydrates on isolated synaptic membranes.

The effect of gamma-irradiated solutions of carbohydrates, mainly glucose, upon Na+, K(+)-ATPase and lipid peroxidation in rat brain synaptosomal membranes was studied. The membrane damage by irradiated glucose was enhanced in the presence of Fe2+ and was diminished when a free-radical scavenger (BHT) or metal chelators (EDTA, EGTA) were present. It is suggested that a key element in the free-radical membrane damage by irradiated carbohydrates is an Fe(2+)-complex of some species of the radiolysis products. Participation of radiotoxins of carbohydrate origin in radiobiological effects is discussed.

Sensitivity of the brain synaptosomal membrane Mg(2+)-ATPase activity to arachidonic acid is under control of the Na+,K(+)-ATPase state.

Evidence is presented for the sensitivity of the synaptosomal plasma membrane Mg(2+)-ATPase activity to arachidonic acid being dependent on the functional state of Na+,K(+)-ATPase. An "Inversion effect" was observed at arachidonic acid concentrations exceeding 80 mumol/l when the Mg(2+)-ATPase activity (after ouabain addition) is higher than the total ATPase activity (without ouabain). The "Inversion effect" is reduced by cyclooxygenase inhibitor indomethacin or acetylsalicylic acid and restored by prostaglandin PGA2 or PGD2.

[The coupling of Na,K-ATPase with the sodium channels in the plasma membranes of the brain synaptosomes of rats]. / Sopriazhenie Na,K-ATFazy s natrievymi kanalami v plazmaticheskikh membranakh sinaptosom mozga krys.

Effect of neurotoxins veratrine (100 micrograms/ml) and tetrodotoxin (1 microM) on the binding of 3H-ouabain (10(-8) M) with Na,K-ATPase of intact synaptosomes and isolated synaptic membranes was studied. The persistent opening of sodium channels in synaptosomes by veratrine results in an increase of specific binding of the labeled ligand by 20%. A similar effect was caused by Na/H exchanger monensin. Destruction of microtubules with vinblastine and colchicine has no influence on veratrine action, while depolymerization of microfilaments with cytochalasin B reverses the neurotoxin effect. In isolated synaptic membranes veratrine and tetrodotoxin stimulate ouabain binding, the absolute veratrine-induced increment being several times higher in the presence of ATP than in its absence. Since the closed vesicles of any type are not permeable to ATP and ouabain, it means that in the isolated membranes an interaction between sodium channels and Na,K-ATPase molecules takes place. In intact nerve endings such a mechanism may be operative along with the known ways of control of sodium pump and its ouabain-binding site.

[Effect of cross-linking agents on electron transport and proton transfer in the mitochondrial respiratory chain]. / Vliianie sshivaiushchikh agentov na transport élektronov i perenos protonov v dykhatel'noi tsepi mitokhondrii.

The effect of protein cross-linkage on proton translocation and electron transport in mitochondria respiratory chain was studied. Dimethylsuberimidate (1 mM) or dicyclohexyl carbodiimide (50 g/ml) inhibit proton translocation with concomitant stimulation of respiration. It is concluded that the definite level of dynamic mobility of proteins is needed for proton translocation.

[Structural and functional changes in the synaptic membranes of the brain during aging]. / Strukturno-funktsional'nye izmeneniia sinapticheskikh membran mozga pri starenii.

Below 37 degrees the mobility of lipids in rat brain synaptic membranes evaluated by the spin probe method is higher in old (24-26 months) than in young (5-6 months) animals. The number of ouabain receptors in membranes increases with age, while maximum rate and Km values are not changed. The relation between structural state of membrane and properties of ouabain binding centers is discussed.

[Muscarinic cholinoreceptors of brain synaptic membranes from animals of various ages]. / Issledovanie muskarinovykh kholinoretseptorov sinapticheskikh membran mozga zhivotnykh raznogo vozrasta.

In old rats in contrast to young and mature ones the treatment of synaptic membranes with SH-reagent N-ethylmaleimide, cholinergic agonist carbamylcholine or both of them decreases the specific binding of labeled muscarinic antagonist 3H-quinuclidinylbenzylate. The age related change of receptor conformation with exposure of thiol groups responsible for antagonist binding is suggested.

[Sites responsible for stimulation of brain Na,K-ATPase by serotonin]. / O prirode tsentrov, otvetstvennykh za stimuliatsiiu serotoninom Na,K-ATPazy mozga.

Serotonin (10(-6)-10(-3) M) stimulates Na,K-ATPase in the rat brain cortex homogenate with a maximal effect at 10(-4) M. Deseril (10(-5) M), antagonist of serotonin receptors, removes the stimulating effect. Deseril has no influence on noradrenaline-induced ATPase activation; the alpha-adrenergic blocker phentolamine does not affect serotonin activation. The effects of the two transmitters are additive. It is assumed that the mediators interact with different membrane sites, serotonin activation being initiated via the serotonin receptors.

[Membrane regulation of brain Na,K-ATPase inhibition by calcium ions]. / Membrannaia reguliatsiia ingibirovaniia Na, K-ATPazy mozga ionami kal'tsiia.

In contrast to the purified enzyme. Na, K-ATPase from intact synaptic membranes is inhibited by Ca2+ according to a biphase pattern at Ca2+ concentrations of 10(-6) to 10(-3) M. The membrane damage after three washings with bidistilled water results in elimination of low cocentration phase. Recombination of the sediment and the supernatant restores the initial shape of the inhibition curve. Dithiothreitol greatly increases the inhibition by low Ca concentrations. This effect is absent in the purified enzyme preparation and is considerably reduced after the membrane damage. Recombination restores the dithiothreitol effect. It is suggested that the sensitivity of membrane Na,K-ATPase to low concentrations of Ca2+ is controlled by the components (most likely, peripheral proteins), which are loosely bound to the membrane, this process being dependent on the degree of the SH-group reduction.

[Mechanism of brain Na,K-ATPase activation by adrenaline]. / Issledovanie mekhanizma aktivatsii Na,K-ATPazy mozga noradrenalinom.

Norepinephrine stimulates Na, K-ATPase from rat brain homogenates at concentrations of 10(-4)--10(-5) and 10(-7)--10(-8) M. A low concentration maximum is observed after 48 hrs of incubation at -20 degrees C and is not changed by the addition of alpha-tocopherol, glycerol and MAO inhibitor ipraside. The maximum observed at the mediator concentration equal to 10(-4)--10(-5) M is eliminated after treatment with EGTA. At all concentrations of norepinephrine the enzyme stimulation is removed by the alpha-adrenoblocker phentolamine. The activated enzyme reveals lower sensitivity to Ca2+ induced inhibition. The role of Ca2+ and conformational state of the membranes in the realization of the remote effect on the adrenoreceptor-Na, K-ATPase system is discussed.

[Structural rearrangements in membranes induced by anesthetics]. / Strukturnye perestroiki membran, indutsiruemye anestetikami

Studies were carried out on the effects of anesthetics on the stability of membranes to sodium dodecylsulfate and trypsin. The initial rate of membrane desintegration by detergent evaluated by light scattering with stopped flow method was increased in the presence of ethanol, propanol, benzyl alcohol, procain-amide (erthrocyte membrane) and chlorpromazine (rat brain synaptosomes). Concentrations of anesthetics which correspond to half of the maximum effect were very close to that of blocking the action potential and inducing 50%--antihemolysis. Alcohols and procaine at anesthetic concentrations inhibited proteolysis of isolated erythrocyte membranes but were without effect on their ultrasonic fragments. Increase of membrane desintegtation rate is interpreted as structural rearrangements of membranes with the weakening of detergent sensitive intermolecular interactions. Proteolysis inhibition of ghosts but not the gragments indicates against the participation of the basic func of proteins in the structural membrane rearrangements.