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Oxidative processes and lipid metabolism in young (3-4 months) and old (25-28 months) were studied. The increase of the rate of reactions of free radical oxidation of lipids (hydroperoxides, and malondialdehyde) and the accumulation of products of oxidative modification of proteins was recorded in mitochondrial fraction of rat brain. The accumulation of nitric oxide in the mitochondria and the oxidation products leads to the development of oxidative stress. Investigation of the lipid spectrum in old rat brains showed that aging was accompanied by a change in the qualitative and quantitative content of phospholipids. A change in the metabolism of neutral glycolipids leads to a decrease in the content of cerebrosides and sulfoserobrosides. At the same time an increase in sphingosine (a product of hidrolytic decomposition of neutral glycolipids) was observed. The key role of lipid metabolism in age pathologies was noticed.

The antioxidant activity of a newly synthesized compound, cysteine lithium salt, was discovered using methyl oleate oxidation model of dopaminergic system disorder. Experimental data show that injection of the synthesized compound in animals with experimentally induced L-DOPA brings to normalization effect conditioned by inhibiting free radical reactions in the nuclear and mitochondrial fractions of brain cells. Antioxidant effect of the synthesized compound is related to its chemical structure that contains cysteine--an agent involved in the biosynthesis of glutathione, which is a component of glutathione peroxidase and glutathione reductase enzymes participating in the antiradical protection system.

The content of lipid peroxidation products and the metabolism of gangliosides and galactosylceramides in brain tissue were studied in the presence of ischemia and when an agent containing nicotinic acid and cysteine is administered. The above agent was found to have an antioxidative effect that was evident in the lower levels of lipid peroxides and in the normalized qualitative and quantitative content of galactosylceramides and gangliosides.

The authors have displayed that ischemic insults are accompanied by the significant intensification of free radical peroxidation processes both in erytrocyte membranes and in blood plasma. The changes mentioned are characterized by the simultaneous decrease of erytrocites resistance to peroxide hemolysis, as well as by the parallel lowering of alpha-tocopherol concentration in blood plasma.

Changes in the concentrations of antioxidant (Cu, Zn superoxide dismutase catalase, ceruloplasmin, and transferrin) and recently discovered pro-oxidant (cytochrome B-558 I-IV and suprol, a superoxide producing lipoprotein) metalloproteins and cytochrome B-5 were assessed in the blood of anesthesized and control rats. The concentrations of antioxidant and pro-oxidant metalloproteins varied. They were not changed during anesthesia, except suprol. As for the qualitative changes, phospholipid composition was altered, superoxide production decreased, and lipid peroxidation of suprol increased during anesthesia. The authors propose using antioxidant metalloproteins for decrease of the undesirable consequences of halothane anesthesia in experimental medicine.

Alterations in content of phospholipids as well as dynamics of lipid free-radical oxidation were studied in the hepatocytes of the rats poisoned with various doses of the toxic agent ucrinol within 1.3 and 6 months. Low concentrations of the toxin (1.5 mg/kg) did not cause any detectable alterations of the patterns studied. However, higher concentrations of ucrinol (15-150 mg/kg) produced markedly pronounced destructions which were dose- and time-dependent.

The effect of R-plasmid on the qualitative and quantitative compositions of phospholipids and their fatty acids in bacterial (S. derby) cells has been studied. It has been found that the lack of R-plasmid in bacterial cells leads to a sharp decrease in the phospholipid content, in the phosphatidylcholine content in particular, and causes an increase in the per cent content of lysophosphatidylcholines. The per cent content of saturated and nonsaturated fatty acids of phospholipids in plasmid-free cells does not change appreciably. In the plasmid-free strain of S. derby the intensity of lipid peroxidation is associated with a relatively high content of alpha-tocopherol.

The enhancement of the sum of phospholipids in seizure period was observed during initially generalized corazol seizure in white rats' cerebral cortex. This sum fell in an hour after epileptic fit. It is noted that the maintenance of lysophosphatidylcholines and phosphatidylserines enhanced during the fit, and the maintenance of phosphatidylcholines and phosphatidylethanolamines fell either in cerebral cortex, or in cerebellum. At the same time the enhancement of the mixed fraction of sphingomyelin and phosphatidylinositide level and cardiolipins-1 in the cerebral cortex was observed. The maintenance of the latter in cerebellum fell during an hour after the attack. The quantity of cardiolipins-2 in cerebellum enhanced during the attack. It is suggested that the effect of corazol seizure leads to the enhancement of lisoforms at the expense of the intensification of disintegration of other fractions of lisoforms.

Total content of phospholipids and their individual components were distinctly increased in microsomal, mitochondrial fractions and in inner mitochondrial membrane of rat hepatocytes under conditions of alloxan diabetes. The concentrations of these substances were decreased in outer mitochondrial membrane. Activation of lipid free-radical oxidation was found in all the membrane structures studied. In microsomal fraction of hepatocytes the rate of hydroxylation reaction was decreased, accompanied by a decrease in content of cytochromes b5 and P-450.

Quantitative and qualitative composition of gangliosides, sulfatides and cerebrosides were studied in normal state and in experimental brain edema by means of thin-layer chromatography. In the experimental edema content of mono- and disialogangliosides was decreased while tri- and tetrasialogangliosides were unaltered. Statistically distinct increase in content of sulfocerebrosides (sulfatide 1.2) was also detected in brain edema as compared with controls. At the same time, amount of cerebroside 2 was decreased, whereas increase in cerebroside I concentration was detected.

It was shown that introduction of ethanolamine, phosphoethanolamine and phosphatidylethanolamine in a concentration of 0.05 mumol into the fraction of the brain mitochondria increased the endogenous respiration and the P/O value. In insulin hypoglycemia introduction of the mentioned substances led to a proportional increase in the level of respiration and nonorganic phosphorus; due to this energy provision remained at the level of the intact rat indices.

The authors investigated the cardiotonic effect of monoethanolamine (MEA) and its influence on experimental cardiac hypertrophy in albino rats. In isolated hearts, myocardial cells, and glycerinized fibres as well as in the whole organism of the animals, a distinct cardiotonic effect on MEA was observed, which was most marked in pathological states of the organism. In rats with experimental coarctation of the aorta, MEA dosed 10 mg/kg stimulated, and dosed 60 mg/kg, inhibited the development of myocardial hypertrophy, while the myocardial contractility remained sufficiently preserved. The mechanism of cardiotonic action and the inhibitory effect on the development of myocardial hypertrophy at the dosage of 60 mg/kg are apparently connected with the participation of MEA in tissue metabolic processes contributing to a normalization of tissue respiration, oxidative phosphorylation, and activation of phosphatide-generating reactions, especially to the formation of phospholipids containing ethanolamine, which represent one of the most important membrane formations and components of numerous enzymic systems.

Peroxidation of lipids and alteration in antioxidative activity were studied in normal state and in experimental pancreatitis within 1, 3, 7, 14 and 30 days after the operation. Experimental pancreatitis was accompanied by increase in content of lipid peroxides and by decrease in antioxidative activity of lipids extracted from liver tissue. Administration of thiosulfate decreased slightly the lipid peroxides content and increased the level of antioxidants in pancreatitis. The data obtained suggest that thiosulfate is effective inhibitor of free radical oxidation; it may be used as therapeutic drug in acute pancreatitis.

The level of the neutral and acid phospholipids and thromboplastic activity of various portions of the rabbit brain were studied under normal conditions and following adrenaline stimulation. The level of total phospholipids, neutral phospholipids, and the ratio of neutral to acid phospholipids, thromboplastic activity and its increase following incubation of homogenates of the brain tissue of normal and adrenaline-treated animals were found to be distributed in the following descending order: the medulla oblongata, cerebellum, cerebral hemispheres. Adrenaline decreased the thromboplastic activity and induced changes in the neutral and acid phospholipid levels. The role of phospholipids in the biosynthesis of various components of the blood clotting and anticoagulant systems are discussed.

Quantitative and qualitative composition of phospholipids as well as lipid peroxidation were studied in outer and inner mitochondrial membranes and microsomal fraction from rat liver tissue under conditions of alloxane diabetes. In the diabetes amount of phospholipids, mainly cardiolipins and phosphatidylethanolamines, was increased in the inner and decreased in the outer mitochondrial membranes. Phosphatidylcholines and phosphatidylserines were increased in microsomal fraction. At the same time, lipid peroxidation was activated both in ascorbate- and NADPH-dependent systems of oxidation. These data suggest that lipid peroxidation affects the composition of mitochondrial membranes either by means of removing of the substances from membranes or via their redistribution between the subcellular fractions.

Alloxan diabetes was accompanied by an increase in ascorbate-NADPH-dependent lipid peroxidation with a simultaneous decrease in content of cytochrome P-450 and in the rate aniline hydroxylation in rat liver microsomal fraction. Activation of lipid peroxidation, which led to impairment of the endoplasmic reticulum integrity as well as to destruction of cytochrome P-450, may be important in pathogenesis of alloxan diabetes.