[Free radical oxidation in children with severe craniocerebral injury].

Changes in the products of lipid peroxidation (LPO) and the antioxidative system (AOS) were studied in 94 children aged 3 to 15 years with severe brain injury (BI) on days 1, 3-5, and 7-10. The contents of dienic conjugates and malonic dialdehyde and the level of induced peroxide hemolysis and peroxide resistance of red blood cells in the plasma were determined. Children with severe BI were found to have activated LPO processes and decreased AOS activity, the most significant changes occurring within 24 hours of injury. The increased activity of peroxide processes was attended by reverse AOS changes. In children, the time course of changes in the parameters of LPO and AOS differs from that in adults since there is no phase of excessive LPO activation due to the exhaustion of AOS reserves.

[The unknown physiological role of carbon dioxide]. / O neizvestnoi fiziologicheskoi roli uglekisloty.

In rats adapted to hypoxia, in gradual increase of CO and decrease in monosialogangliosides, were shown as well as insufficient accumulation of the lipid peroxidation products. The data suggests that carbon dioxide is a natural element of the organism antioxidant defence system.

[Rat brain gangliosides under the combined effect of hypercapnia, hypoxia and hypothermia]. / Gangliozidy golovnogo mozga krys pri sochetannom vozdeistvii giperkapnii, gipoksii i gipotermii.

The paper deals with the content and composition of brain gangliosides under two forms of acute hypoxia, hypoxic and hemic ones which develop as a result of the effect of gradually increasing concentration of CO2, decreasing concentration of O2 and external cooling (1st form) and parenteral introduction of sodium nitrite (2nd form). The increase of a sum of polysialogangliosides and decrease of monosialogangliosides under the 1st and 2nd forms of acute hypoxia, respectively, is shown. The increase of the content of unsaturated fatty acids and fatty acids with the great number of carbon atoms as well as the products of lipids peroxidation is more expressed under the 2nd form of hypoxia. The decrease of antioxidative power of blood is also noticed. It is supposed that polysialogangliosides possess antiperoxide effect and preserve neuronal membranes for destruction under acute form of hypoxia.

[Protective action of 5-hydroxy-6-methyluracil and ferrocenes in nitrite-ion poisoning]. / Zashchitnoe deistvie 5-oksi-6-metiluratsila i ferrotsenov pri intoksikatsii nitrit-ionom.

It is shown that ferrocenes and 5-oxy-6-methyluracil efficiently inhibit methemoglobin-formation in experiments in vitro and in vivo. Preliminary administration of ferrocene or 5-oxy-6-methyluracil to laboratory animals essentially increases life time in case of sodium nitrite intoxication. Ferrocene protection from sodium nitrite intoxication normalizes the level of methemoglobin and lipoperoxidation in erythrocytes as well as activity of superoxide dismutase of erythrocytes. Activity of catalase, glutathione reductase and dehydrogenases of the pentosephosphate way were not normalized during ferrocene protection from sodium nitrite intoxication. In case of ferrocene protection the catalase activity during sodium nitrite intoxication remains lowered, while activity of glutathione reductase and dehydrogenases of the pentosephosphate pathway grows sharply.

[Protective effect of sodium bicarbonate in nitrite ion poisoning]. / Zashchitnoe deistvie bikarbonata natriia pri intoksikatsii nitrit-ionom.

It is shown that sodium bicarbonate effectively protects the organism from toxical action of sodium nitrite. Administration of this drug promotes the increase of the lifetime of animals under intoxication with lethal doses of sodium nitrite. The preliminary administration of sodium bicarbonate permits one to decrease the level of methemoglobin in the blood under intoxication with sublethal doses of sodium nitrite, to normalize activity of the basic enzymes of antioxidant protection--superoxide dismutase, catalase glutathione reductase as well as the total activity of dehydrogenases of pentose phosphate way. Under the protection with sodium bicarbonate the level of lipid peroxidation in erythrocytes decreases, the increment of content of the restored glutathione in response to sodium nitrite intoxication decreases.

[Effect of nitrobenzenes on methemoglobin formation and activity of antioxidative enzymes in mouse erythrocytes]. / Vliianie nitrobenzolov na metgemoglobinoobrazovanie i aktivnost' antiokislitel'nykh fermentov éritrotsitov myshi.

The mice intoxication with intraperitoneal introduction of 1,3,5-trinitrobenzene and 2,4,6-trinitrotoluene causes an increase of methemoglobin and a decrease of glutathione level. But intoxication by polynitrobenzenes exerts no effect on the total level of SH-groups. A small increase in total activity of dehydrogenases of the pentose phosphate way in response to 2,4,6-trinitrotoluene intoxication is also revealed. The level of both lipid peroxidation, superoxide dismutase and catalase activity is not influenced by 2,4,6-trinitrotoluene and 1,3,5-trinitrobenzene.

[Effect of alpha-halogen-alpha-nitroalkanes on methemoglobin formation and activity of antioxidant enzymes in mouse erythrocytes]. / Vliianie alpha-galogen-alpha-nitroalkanov na methemoglobinoobrazovanie i aktivnost' antiokislitel'nykh fermentov éritrotsitov myshi.

It is shown that 1-chlorine, 1-bromine and 1-iodine-nitroethanes intensify methemoglobin formation in vivo. Such an effect was not revealed for 1-fluorine-1-nitroethane. Change of biochemical parameters of erythrocytes under intoxication by alpha-halogen nitroalkanes in a dose LD50 with the exception for 1-fluorine-1-nitroethane is rather identical with that under the intoxication by soda nitrite which is connected with the generality of reaction mechanism of soda nitrite and alpha-halogen-alpha-nitroalkanes with hemoglobin. Thus the administration of alpha-halogen-alpha-nitroalkanes to laboratory animals leads to the increase of the total activity of dehydrogenases of pentose phosphate way and glutathione reductase of erythrocytes (on the example of 1-iodine-1-nitroethane), the increase of lipoperoxidation (on the example of 1-bromine-1-nitroethane), the decrease of catalase activity. Absence of the inhibition of superoxide dismutase activity was found under the intoxication by all the mentioned drugs. The increase of activity of glutathione reductase of erythrocytes (on the example of (1-iodine-1-nitroethane) under intoxication with alpha-halogen-alpha-alkanes in contrast to intoxication by soda nitrite is explained by some differences of mechanisms of hemoglobin interaction with soda nitrite and alpha-halogen-alpha-nitroalkanes.

[Effect of sodium nitrite poisoning on the activity of enzymes of anti-oxidant protection and peroxidation processes in mouse erythrocytes]. / Vliianie intoksikatsii nitritom natriia na aktivnost' fermentov antioksidantnoi zashchity i protsessy peroksidatsii v éritrotsitakh myshi.

The intoxication of white mice with sodium nitrite results in the decrease of red cell superoxide dismutase (SOD) and catalase activity. The glutathione peroxidase activity is the same as in the control group. The level of red cell lipid peroxidation in the group of mice that receive sodium nitrite is higher as compared to the control group. After the intoxication the total activity of glucose-6-phosphate dehydrogenase and dehydrogenase of 6-phosphogluconate as well as the activity of glutathione reductase are higher than in the control group. The level of SH-groups and reduced glutathione is higher in the group of mice that receive sodium nitrite in comparison with the control group.