[Effect of vitamin E from by-products of cotton oil processing on the glutathione peroxidase system in rats]. / Vliianie vitamina E iz otkhodov pererabotki khlopkovogo masla na glutationperoksidaznuiu sistemu krys.

The activities of glucose-6-phosphate dehydrogenase, glutathione reductase and glutathione peroxidase from liver, skeletal muscles and erythrocytes of rats fed a vitamin E-deficient, or supplemented, diet were studied. Vitamin E was added in the diet either as a pure pharmacy form of alpha-tocopherol or as a tocopherol mixture derived from oil wastes. The deficiency of vitamin E caused an increase in the activity of the above mentioned enzymes. Both alpha-tocopherol and the tocopherol mixture were found to influence the glutathione peroxidase system. The dose-dependent response of the glutathione peroxidase system was revealed. Possible mechanisms of the changes in the antioxidizing enzymes induced by vitamin E are discussed.

[Anti-oxidant activity and tissue accumulation of tocopherols from a new source]. / Antioksidantnaia aktivnost' i nakoplenie tkaniami tokoferolov iz novogo prirodnogo istochnika.

Properties of a tocopherol concentrate, obtained from side products of cotton oil treatment containing alpha-tocopherol and other isomers of vitamin E and carotinoids at high concentrations, were studied in vivo and in vitro. The concentrate exhibited higher antioxidative activity in reaction with 2,2'-diphenyl-1-picrylhydrazine and inhibited lipid peroxidation in liver microsomes similarly to synthetic alpha-tocopherol. After addition of the concentrate to rat ration at a dose of 100 IU of vitamin E per 100 g of food the animals accumulated tocopherol from this source in the same way as it was observed for the synthetic preparation (liver, heart, lung) or at the higher level (kidney, brain, fatty tissue). Consumption of the concentrate was decreased after its emulsification. Contribution of gamma-tocopherol to antiradical effect of the tocopherol concentrate and to stabilization of the membrane lipid moiety is discussed.

[Effects of different types of nutritional imbalance on lipid peroxidation and viscosity of membrane lipids]. / Vliianie razlichnykh vidov alimentarnogo disbalansa na stepen' perekisnogo okisleniia i viazkost' membrannykh lipidov.

For 90 days male August rats were kept on 5 diets: (I) balanced semisynthetic, (II) with amino acid unbalance, (III) with excess polyunsaturated fatty acids (PUFA), (IV) with vitamin E deficiency, and (V) polyunbalanced (amino acid unbalance, excess PUFA, vitamin E deficiency). In liver microsomes, the authors studied the kinetics of malonic dialdehyde accumulation in the course of NADPH-dependent lipid peroxidation (LP) and microviscosity of the lipid phase of microsomal membranes according to eximerization of the pyrene fluorescent hydrophobic probe. The microsomes of the animals fed diets I, III and IV showed on the average a 50 to 55% increase in the rate of MDA formation, whereas those of rats on diet V a 78% increase as compared with appropriate characteristics in the animals fed diet I. A good correlation was established between the decrease in the pyrene eximerization rate and accumulation of lipid peroxides: r = 0.09 (P less than 0.05). The possibility of affecting LP in the membranes by the goal oriented modification of the diet is discussed. The participation of proteins, lipids and tocopherol in the maintenance of the membrane structure is described.

[Action of pro-oxidant diets on the enzymatic system of Ca2+ transport in the sarcoplasmic reticulum]. / Deistvie prooksidantnykh ratsionov na fermentnuiu sistemu transporta Ca2+ v sarkoplazmaticheskom retikulume.

August male rats were kept for 90 days on one of the following diets: balanced semisynthetic diet with casein as a source of protein (group 1), amino acid balanced diet with casein replaced by gluten (group 2), a diet with excess of polyunsaturated fatty acids (group 3), with vitamin E deficiency (group 4), and polyunbalanced diet, comprising a combination of amino acid imbalance, excess of polyunsaturated acids, and vitamin E deficiency (group 5). Structural and functional parameters of Ca2+ transport (Ca2+ accumulation rate, activity of Ca2+-ATPase, Ca/ATP ratio), content of lipid fractions and accumulation of malonic dialdehyde were studied in sarcoplasmatic reticulum (SR) fragments from rat hind limb muscles in the course of ascorbate-dependent lipid peroxidation. Reduction of Ca2+ absorption rate, Ca2+-ATPase, and Ca/ATP ratio in SR membranes were observed in groups 2-5. In parallel, decreased phospholipid and triglyceride levels and increased content of free fatty acids and cholesterol in SR membranes were established.

[Mechanisms of stabilizing effect of vitamin E against lipid peroxidation in biological membranes]. / Stabiliziruiushchee deistvie vitamina E na biologicheskie membrany pri perekisnom okislenii lipidov.

Mechanisms of the inhibitory effect of vitamin E on the process of lipid peroxidation (LPO) in biological membranes are studied. Both alpha-tocopherol and its derivatives (a-tocopherylacetate, o- and p-tocopherylquinones possess no radical scavenging activity) inhibit non-enzymatic (Fe2+ + ascorbate)-induced LPO and prevent LPO-dependent inhibition of Ca2+ transport in sarcoplasmic reticulum membranes from skeletal muscles. The protective effect of alpha-tocopherylacetate, tocopherilquinones and partially of alpha-tocopherol is due to a stabilizing effect of these compounds on sarcoplasmic reticulum membranes, registered by a decrease of fluidity of membrane lipid bilayer (probed by nitroxile radical TEMPO) and by a decrease of its passive permeability for Ca2+. Under the enzymatic NADPH-dependent LPO induction in rat liver microsomal fraction a strong inhibitory effect of tocopherylquinones is similar to the effect of other electron acceptors (methylnaphtoquinone, TEMPO) and is due to their ability to compete with LPO reaction for reducing equivalents in NADPH-dependent electron carriers wich results in the formation of hydroxy-derivatives having pronounced radical scavenging activity.