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Earlier, we demonstrated for the first time that the natural antioxidant α tocopherol in a wide concentra tion range can modify the structure of different lipid regions in the endoplasmic reticulum and plasma membranes of hepatocytes in experiments in vitro [1,2]. Despite the biochemical and functional differences between endoplasmic reticulum and plasma mem branes, they are characterized by similar polymodal non linear dose dependences of the effects of α toco pherol on the rigidity of superficial (~8 Å) and micro viscosity of buried (~20 Å) lipid bilayer regions. Such patterns are typical for biologically active substances, showing an effect over a wide concentration range, including ultralow doses [1,2]. The polymodality of dose dependences is associated with the statistically significant effects of α tocopherol in three concentra tion ranges. It is assumed that three possible mecha nisms of action may underlie the effect of this com pound depending on its concentration: insertion into the membrane, interaction with specific binding sites, and the information transfer through the layers of water with special physical and chemical properties [1][2][3]. It is known that the main physicochemical characteristic of antioxidants is their ability to inhibit lipid peroxidation (LPO) both in vitro and in vivo, the regulatory system of which includes the microviscosity of lipids [4].In view of above, a question arises as to what are the common and distinctive features of the effects of nat ural and synthetic agents at ultralow doses and whether the relationship between the ability of antiox idants to inhibit LPO and modify the structure of bio logical membranes is retained when they are used at ultralow doses. To answer this question, we assessed the effect of potassium salt of β (4 hydroxy 3,5 diter tbutylphenyl) propionic acid (potassium phenosan), a synthetic antioxidant, in a wide concentration range on the lipid microviscosity of EPR and PM of hepato cytes.The study was performed with 100 F 1 mice (C 57 BL × DBA 2 ). Potassium phenosan solutions were prepared by successive tenfold dilutions of the initial solution (10 -3 M) with distilled water followed by shaking on a shaker for 1 min. Plasma membrane and endoplasmic reticulum were isolated from mouse hepatocytes by centrifugation by the method of Loten [5]. Mice were sacrificed by decapitation. Protein concentration was determined by the method of Lowry [6]. The parameters characterizing the struc ture of membranes were calculated from the spectra obtained at 293 K on a Bruker 200D EPR spectrome ter (Germany) by the spin probe method [7]. The microviscosity of buried lipid bilayer regions (~20 Å) was estimated using 16 doxylstearic acid (С 16 ). The membrane microviscosity near the С 16 probe was eval uated on the basis of the rotational correlation time of the probe τ С1 and τ С2 , which was determined by the formulas for rapid anisotropic rotation of radicals [7]. The absolute values of parameters τ С1 and τ С2 in the control and after the treatment with potass...

This paper discloses for the first time the effects of the gas phase (GP) and the tar of cigarette smoke on lipid peroxidation (LPO) and on the structure of different lipid regions in liposomes. The LPO development was analysed in terms of the total unsaturation of lipids (double-bond, DB, content) and the formation of dienic conjugates (DC), ketodienes (KD), and malonic dialdehyde (MDA). As expected, the exposure of liposomes to either the GP or the tar led to a significant decrease in the DB content. However, the formation of oxidation products revealed different dynamics: MDA generation was inhibited, while the formation of DC and KD increased during the first few hours of the LPO development followed by its inhibition. The smoke constituents exhibited opposite effects on the structure of the lipid bilayer of liposomes: the GP markedly enhanced the microviscosity of liposomal membranes, whereas the tar caused a drastic lowering of microviscosity.

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