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Experiments on random-bred white male rats have demonstrated the activation of induced lipid peroxidation in red cell membranes, elevation on the basal level of plasma lipid peroxides, a decrease in the content of alpha-tocopherol in plasma and red blood cell membranes, considerable shifts in the content of esterified and free cholesterol in plasma and red blood cell membranes under prolonged acoustic stress (91 dB). Administration of alpha-tocopheryl acetate in a dose of 1 mg/kg exerted a beneficial effect on the test parameters under prolonged acoustic stress.

Using clinico-biochemical and EEG examinations, the authors have studied over time 30 epileptic patients who along with anticonvulsants received lithium carbonate orally and vitamin E in injections. Before the administration of the above drugs epileptic patients with a progressive course of the disease showed intensified lipid peroxidation, low levels of total and free cholesterol of erythrocyte membranes, elevated concentrations of vitamin E and a decreased activity of superoxide dismutase (SOD) in the blood. The use of lithium carbonate and vitamin E leads to a considerable decrease in lipid peroxidation, an elevation in the content of total and free cholesterol of red cell membranes and an increased SOD activity in the blood. There was also a considerable improvement in EEG parameters. The above positive changes in paraclinical indices were accompanied by a reduction in the frequency of epileptic attacks and affective calming of patients. The authors believe that the obtained results can be explained by the normalization of the cell membrane permeability and recommend that lithium carbonate and vitamin E be included into the array of anticonvulsive drugs.

Studies of the lipid peroxides and phospholipid content in the rat brain in different periods after burns showed that the total phospholipid content in all the periods is decreased. The daily intraperitoneal administration of alpha-tocopherol in a dose of 100 mg/kg against a background of the burn decreases sharply the phospholipid content. alpha-Tocopherol in a dose of 1 mg/kg, administered immediately after the trauma and then 3, 7, 12 and 17 days after burns restores the phospholipid content to normal. The described changes were connected mainly with the lecithin and phosphatidylethanolamine fractions.

The membrane conductivity for K+ and Ca+2 ions was studied on bilayer phospholipid membranes formed by phospholipids extracted from the rat liver 1 hour, 1, 3, 7, and 15 days after burning. A pronounced increase in the membrane conductivity was noted. The most potent effects were seen by the 1t, 3d and 7th day of the experiment and the conductivity value varied depending on the medium pH. The process was accompanied by lipid peroxidation increase. Intraperitoneal administration of alpha-tocopherol at 1 mg/kg dose immediately after burning, followed by injections on the 3d, 7th and 12th day, normalized the characteristics studied. Bilayer membranes formed by healthy rat liver phospholipids previously added with an appropriate amount of methyl oleate or cumylhydroperoxide demonstrated higher conductivity as compared to the normal.

Burns affected the content of L-alpha-glycerophosphate /L-alpha-GP/ in rats; its level was reduced within 15 days after burns. Phasic changes in L-alpha-glycerophosphate dehydrogenase and glycerokinase activities in liver and brain tissues and phospholipase A in blood were also observed. Intraperitoneal administration of alpha-tocopheryl acetate into rats subjected to burns abolished the decrease in content of L-alpha-GP although the activity of the drug varied within this 15 day period. In brain the activity of these enzymes was increased 2-3-fold. The data obtained are in good agreement with those published previously and indicating loss of phospholipids in liver and brain tissus following burns.

The contents of Cu, Zn-superoxide dismutase and catalase isolated and purified from the rat liver at the terminal stages of alloxan diabetes were decreased by 40% and 15%, respectively, as compared to the control. It can be concluded that the decrease in superoxide dismutase and catalase activity in experimental alloxan diabetes is mainly connected with the decline in the content of these proteins at the terminal stages of the disease, this, probably, being the result of DNA degradation and RNA transport disturbances under the effect of oxygen active forms.