[Effect of phenothiazines on the viscosity and electrical stability of model phospholipid membranes].

The effect of five phenothiazine derivatives on the viscosity of model phospholipid membranes (by eximerization of pyrene) and on their electrical stability has been studied All the phenothiazines tested (chlorpromazine, propazine, triftazin and nonachlazine), except for chloracyzine, considerably increase the viscosity of phospholipid liposome bilayer at a concentration of 10(-5)-10(-4) M. Phenothiazines have been also shown to decrease liposome break-down potential even at a concentration of 10(-7) M. No correlation between the magnitude of break-down potential and changes in liposome membrane viscosity has been revealed.

[Biochemical mechanisms of the effect of low molecular weight organochlorine aliphatic compounds on humans and animals (review)].

Data on the effects of 1,1,1-trichlorethane and tetrachlorethylene on human and animal organisms are reviewed. These compounds are used in industry and in homeservice. The review deals with some aspects of the action of these organic solvents at the subcellular level.

[Effect of the structure of liposomal membrane surface layer on the binding of phenothiazines].

By using a fluorescent 3-metoxybenzatrone probe the binding of the phenothiazine series drugs (chlorpromazine, triftazine, aethaperazine) with phospholipid vesicles--liposomes, was investigated. Cholesterol is shown not to affect the binding of these drugs with liposomes. The surface charge of liposomes influences only the combination with the chlorpromazine membranes.

[Oxidative phosphorylation in different regions of the rat brain following morphine administration].

The influence exercised by morphine in a dose of 20 mg/kg, introduced intraperitoneally, and also in concentrations of 10(-3) and 10(-5) "in vitro" on the parameters of oxidative phosphorylation of the brain cortex and stem of rats was studied. Morphine, used in a concentration of 10(-3), is shown to speed up the substrates oxidation rate. During the first days of its administration the narcotic analgetic inhibited oxidation of mitochondia released from the brain stem, and, once habituation to the narcotic had developed, the inhibition ceased to be effective.

[Effect of thiol-oxidizing agents on several enzymes in rat liver mitochondria].

The sulphydryl groups of nonprotein thiols and proteins of mitochondria, activity of enzymes, oxidative phosphorylation and swelling of these organellas were studied as affected by the thiol-oxidizing agents. Diamide and azoester are shown to oxidize SH-groups of mitochondria, inhibit isocytrate dehydrogenase and succinate: cytochrome oxidation and inhibits energy-dependent swelling of mitochondria. Under the effect of azoester the rate of oxygen consumption by mitochondria increases and there occurs their sharp swelling.