[The transfer of genes for Brown Rust resistance from Aegilops umbellulata Eig. to wheat (Triticum aestivum L.) genome]. / Perenos genoc ustoichivosti k buroi listovoi rzhavchine ot Aegilops umbellulata Eig. v genom pshenitsy (Triticum arstivum L.).

The potential of a genome-substituted form Avrolata (AABBUU) as a genetic system in genomic and chromosome manipulations for gene transfer from the wild species Aegilops umbellulata Eig. (UU) to cultivated wheat was studied. It was shown that plants combining resistance to leaf brown rust with high productivity may be produced from this form by classical hybridization procedures. The resistance gene introduced to line R-12 is dominant and probably identical to the Lr9 gene. By N-banding, chromosome staining technique and gliadin electrophoresis, the structural changes in chromosomes 1A, 2A, 4B, 6B, 7B, 1D, and 2D of the resistant line R-12 were revealed.

Anti-oxidant capacity of spinal cord and erythrocytes of guinea pigs in case of experimental allergic encephalomyelitis and after disease suppression.

In the lumbar spinal cord of EAE guinea pigs a significant increase in SOD activity, lipid hydroperoxides content (more than 60%) and Fe2(+)-ascorbate-induced lipid peroxidation was observed. Multiple injections of cytochrome C-vitamin B2-vitamin PP (CV-combination) during the disease latent period resulted in suppression of EAE development. Supplementation with vitamin C, vitamin B12 or ATP eliminated this suppressive effect. Upon treatment with CV-combination beginning on the day of the first EAE clinical signs a half of the sick animals recovered. In their erythrocytes the ratio between SOD and catalase activities was normalized, though on a higher level. In the lumbar spinal cord the concentration of lipid hydroperoxides was decreased to the control one. Oxidative damage of the central nervous system is one of the mechanisms underlying the pathogenesis of lethal EAE.

[Regulating and disturbing effects of alpha-tocopherol on lipid bilayers]. / Uporiadochivaiushchee i razuporiadyvaiushchee deistvie alpha-tokoferola na lipidnye bisloi.

Using the high resolution 1H-NMR spectroscopy and spin-probes the influence of alpha-tocopherol on lipid bilayer microviscosity has been studied. It has been established that alpha-tocopherol shows the cholesterol-like action on the physical state of lipid bilayer: alpha-tocopherol increase microviscosity of unsaturated bilayers and decrease microviscosity of saturated bilayers. The character of alpha-tocopherol action is determined by the fatty acidic lipid composition but does not depend on the polar group structure of phospholipid molecule as cholesterol-like action of alpha-tocopherol is found itself in liposomes prepared both from phosphatidylcholine and phosphatidylethanolamine. Analog of alpha-tocopherol without phytol chain 2,2,5,7,8-penthamethyl-6-oxychroman does not show the cholesterol-like action as it is not able to disorder the saturated bilayers.

Effect of chronic copper loading on the activity of rat liver antioxidative enzymes.

The activity of antioxidative enzymes SOD, catalase, glutathione peroxidase and the related glutathione reductase, glucose-6-phosphate dehydrogenase and NADPH-isocitrate dehydrogenase was examined in liver cytosol and large granule fraction (mitochondria) from control and copper-loaded rats. An increase of SOD activity (more than 100%) and a decrease of both catalase (by 60%) and glutathione peroxidase activity (by 30%) in large granule fraction were observed after copper loading. The cytosolic glutathione peroxidase activity was also markedly decreased: glutathione peroxidase I (EC 1.11.1.9)--by 35% and glutathione peroxidase II (EC 2.5.1.18)--by 75%. Cytosolic catalase activity and the glutathione reductase, glucose-6-phosphate dehydrogenase and NADPH-isocitrate dehydrogenase activities in cytosol and in mitochondria of copper-loaded rats were unchanged. It is concluded that under chronic copper loading the primary mechanisms of copper toxicity are accompanied by disturbances of the antioxidative enzyme function.

Inhibition of phospholipid hydrolysis by soluble phospholipase A2 in biological membranes of different origin after lipid peroxidation.

In peroxidized rat liver microsomal membranes phospholipid hydrolysis catalyzed by porcine pancreas phospholipase A2 was found to be inhibited. The extent of inhibition depended on the amount of lipid peroxidation products (MDA) accumulated in the membrane. This effect was not due to the direct action of lipid peroxidation products on the enzyme but to membrane modification. The same inhibitory effect was also found with other membranes--rabbit skeletal muscle sarcoplasmic reticulum, bovine retina rod outer segments and rat brain synaptosomes--differing in phospholipid and fatty acid composition. The inhibition of phospholipase reaction by lipid peroxidation depended at least on three factors: decrease in the amount of phosphatidylethanolamine; decrease in the level of phospholipids, containing polyunsaturated fatty acid residues and occurrence of membrane structural rearrangements resulting in unavailability of phospholipid substrates for phospholipase A2 attack. Membrane destruction with anionic detergent--sodium cholate--led to a sharp increase of phospholipase hydrolysis rate.

The influence of starvation on some characteristics of the Ca2+ transport system and lipid content in rat liver mitochondria.

The effects of 48-hour starvation on some characteristics of the Ca2+ transport system as well as on lipid content and free fatty acids composition in rat liver mitochondria were determined. The ion fluxes in mitochondria in steady state and oscillations were measured using Ca2+, Sr2+ and H+ sensitive electrodes. The Ca2+ uptake in liver mitochondria was changed after starvation. In the case of equal amounts of endogenous mitochondrial Ca2+ the capability of liver mitochondria to accumulate and store exogenous Ca2+ was decreased after starvation. After inhibition of the energy dependent (active) Ca2+ transport by ruthenium-red (RR) the rate of the passive Ca2+ efflux was activated and this could be explained by the induction of the electroneutral 2H+/Me2+ exchange after starvation. The disproportion in the amounts of linoleic and docosahexaenoic acids in mitochondrial phospholipids after starvation is considered to be the possible cause of the changes in the structure and permeability of the mitochondrial membrane.

[Inhibition of phospholipid hydrolysis by phospholipase A2 in microsomal and mitochondrial membranes subjected to lipid peroxidation]. / Ingibirovanie gidroliza fosfolipidov fosfolipaznoi A2 v membranakh mikrosom i mitokhondrii, podvergshikhsia perekisnomu okisleniiu lipidov.

The rate of phospholipid hydrolysis in rat liver microsomal and mitochondrial membranes catalyzed by phospholipase A2 was shown to decrease after ascorbate + Fe2+-induced lipid peroxidation. The degree of inhibition was linearly dependent on the amount of lipid peroxidation products (malonyl dialdehyde) accumulated in the membrane. The decreased phospholipid hydrolysis rate in membranes after lipid peroxidation was registered using phospholipases A2 from two sources: porcine pancreas and bee venom. It was established that the inhibitory action of phospholipid peroxidation products was not linked with a direct effect on the enzyme and was not caused by depletion of phospholipase reaction substrates (as a result of lipid peroxidation). A possible role of lateral separation of oxidized and non-oxidized lipid phases in the mechanisms of inhibition of phospholipid hydrolysis by phospholipase A2 is discussed.

Lipid peroxidation in liver mitochondria from copper-loaded rats.

The amount of phospholipids in liver mitochondria decreased after chronic alimentary copper-loading of rats (40 mg CuSO4 per rat per day in the course of two weeks), while 24 hours after a single intraperitoneal injection of copper (20 mg CuSO4 per kg body weight) it remained unchanged, notwithstanding that both copper treatments highly increased the copper level in mitochondria. Alimentary copper-loading led to a decrease in the relative proportions of the majority of unsaturated fatty acids in mitochondrial phospholipids. Both the spontaneous and Fe2+-induced formation of malonaldehyde were more enhanced in the mitochondria from the two experimental groups as compared to the controls.

Copper deficiency-induced changes in the fatty acid composition of mitochondrial and microsomal membranes of rat liver.

The effects of copper deficiency on the fatty acid composition of mitochondrial and microsomal phospholipids in rat liver were studied. Copper deficiency was induced by a milk powder diet. To evaluate the effect of the milk diet on the fatty acid pattern of mitochondrial and microsomal phospholipids, one group of rats was fed Cusupplemented powdered milk. A decrease in the relative proportion of linoleic acid and an increase in the level of oleic and docosahexaenoic acids in membrane phospholipids were found in this group. However, no changes in the fatty acid pattern characteristic of essential fatty acid deficiency were observed. Dietary copper deficiency produced a significant decrease in the relative amounts of linoleic and arachidonic acids, as well as an increase in the docosahexaenoic acid content in both mitochondrial and microsomal membranes compared to the nondeficient controls. The disproportionate quantities of polyunsaturated fatty acids are discussed with a view to the disturbances of membrane function in copper deficiency.

Effect of total body X-irradiation on the hexobarbital oxidase activity in the rat liver.

It is established that the hexobarbital oxidase activity of 12,000 g rat liver supernatant does not change when examined at the 2nd h after whole body irradiation (700 R) but increases at longer postexposure periods (72 hours). Intraperitoneal injection of phenobarbital in daily doses of 80 mg/kg body wt for three days increases the hexobarbital oxidase activity of non-irradiated rats, the effect being much stronger in phenobarbital-treated rats at the 2nd h of postirradiation. The possible mechanisms of these effects are discussed, as well as their correlation with the increased lipid peroxidation and their significance for the radiation effect on the drug action.

X-irradiation effects on lipid peroxidation and superoxide dismutase and catalase activities in copper deficient and copper loaded rat liver.

The whole body X-irradiation was found to intensify the lipoperoxidative processes in rat liver mitochondria and microsomes, which resulted in a two-fold increase of hydroperoxides in the membrane lipids. The moderate copper-loading of the liver cell had a protective effect against X-ray induced lipid peroxidation. The X-ray influence on the superoxide dismutase (SOD) and catalase activity in normocupric state, copper deficiency and copper loading was also studied. The latter two states were used as models of altered enzyme activity. Copper deficiency decreased the specific SOD activity in both mitochondrial fraction and cytosol, while the increased copper cell content activated this enzyme in mitochondria and did not change it in cytosol. Irradiation inhibited SOD in all preparations studied, with the exception of cytosol upon copper deficiency. Whatever the cell level of copper, X-ray exposure resulted in a decrease of catalase activity in cytosol, while in the mitochondrial fraction, including peroxisomes, the irradiation effects were different. It was found that both SOD and catalase after whole-body irradiation exhibited a higher specific activity in mitochondrial fraction upon copper loading compared with normocupric state, which correlates with the delayed lipid peroxidation processes.

The effect of exhaustive swimming and chloramphenicol on the content of mitochondrial protein and cytochromes in rat liver and myocardium.

The content of mitochondrial protein and cytochromes aa3, b, c1 and c in rat liver and heart was determined in four groups of rats: controls, CAP-treated rats, exercised rats and CAP-treated exercised rats. Single swimming does not change the amount of mitochondrial protein in liver and myocardium as well as the content of cytochromes aa3, b, c1 and c in liver mitochondria. The content of cyt. c is lowered in heart mitochondria. CAP treatment of rats for three days decreases the amount of mitochondrial proteins and cyt. aa3, and b whereas no such changes are observed in heart mitochondria. The subsequent swimming on the background of the inhibitor does not affect additionally liver mitochondria, but lowers significantly the mitochondrial protein and the content of cyt. aa3, b, c1 and c in the myocardium. These data show that exhaustive muscular work alters the effect of CAP in heart mitochondria. Three hours of exhaustive swimming are not sufficient to change neither the amount of total mitochondrial protein, nor the cytochrome content. The lowered cyt. c content in heart mitochondria after swimming is explained by an intensified permeability of the outer membrane. Thus, the changes in the activity of some enzymes and the oxidative phosphorylation previously reported by us, are not due to alterations in the protein synthesis.