[Pro- and antioxidant status of patient with postradiation encephalopathy and its correction].

During the clinical research we found disorders in peroxidation--oxidizing activity in blood of people who were under the influence of small doses of long radiating irradiation and this was one of the main reasons of postradiation encephalopathy development in people injured during Chernobyl accident. Formerly it was shown that the adaptation to the mountain hypoxia conditions in Prielbrusie or the use of normobaric hypoxytherapy normatized pro- oxidant status inpatients with postradiation encephalopathy after the course of hypoxytherapy. Symptomatology of disease essentially smoothed, blood formula and behavioral reactions improved and the rehabilitation proceeded more intensively.

[Prooxidant-antioxidant condition under increased convulsive activity].

During the clinical-biochemical research it was found that the trand's manner of epileptic disease in general is determined by the oxidative-antioxidant balance condition in the sick organism. The experimental research, made on rats, which were under bemegrid kindling confirmed the supposition that the pro-antioxidant brain balance disruption is one of the major factors in the increased convulsive activity development and probably plays the key role in the genesis and clinical revelation of epilepsy.

[The clinico-laboratory criteria of brain death in neurosurgical patients].

With the purpose of developing scientifically substantiated criteria for brain death complex of clinical and physiological, biochemical, physicochemical, and morphological studies was initiated in 55 patients in a critical state because of a dangerous craniocerebral injury, tumours, and vascular affections of the brain. Generalized in the paper are well-known parameters characterizing irreversibility of changes. The following items are to be regarded as the principal criteria for brain death at the present stage of development of medicine: death of truncus cerebri and irreversibility of metabolic disturbances in brain activity.

[The activity of free-radical lipid-peroxidative reactions in the acute and late periods of severe craniocerebral trauma].

Severe craniocerebral injury is shown to result in intensification of processes of lipid peroxidation (LPO), decline in activity of the antioxidant system, which facts lead to further damage to the injured brain caused by products of LPO processes. Activity of LPO processes is recordable as is decline in activity of the antioxidant system after the treatment administered and in 12 and 24 months following the injury sustained as well. The authors recommend that natural and synthetic antioxidants be included into a complex of measures designed to treat severe craniocerebral injury.

[Free-radical perodixative reactions in the acute period of craniocerebral trauma].

The condition is analyzed of the pro-oxidant-antioxidant balance in patients in the acute phase of craniocerebral injury. The higher the degree of craniocerebral injury, the more enhanced are lipid peroxidation processes, the more apparent is the decline in the function of the bodily antioxidant system. Changes in metabolic processes were at their greatest in patients beyond forty four years of age, especially in women with severe craniocerebral injury.

[Free-radical and neuroimmune processes in primary and repeated craniocerebral trauma (in an experiment)].

The impact of primary and repeated brain injury (BI) (moderate contusion of the brain) on changes of pro- and antioxidative processes in the brain and blood, as well as on the body's neuroimmune responses during 30 days following injury were studied in an experiment on albino rats. The changes in the rate of lipid peroxidation (LPO) were shown to be significantly higher in repeated BI than in primary one. There was no correlation between the changes in the rate of LPO in the blood and in the brain tissue.

[The effect of low doses of long-term internal irradiation on the ultrastructure and intensity of lipid peroxidation in rat brain and blood].

Rats were administered with the mixture of 137Cs and 85Sr for 30, 56 and 90 days. Dynamic of ultrastructural changes of lipid peroxidation has been studied in cerebrum and blood. Maximum biochemical changes have been detected after radionuclide administration for 30 days (increase in spontaneous chemiluminescence intensity and quantity of TBA-active products).

[Effect of ionizing radiation on central nervous system].

Main properties of ionizing radiation as a factor affecting the organism are described. Data on molecular and cellular mechanisms of the radiation injury of the central nervous system, impacts of the radioactive irradiation on the vascular system of the brain adn on a hematoencephalitic barrier, a system effect of radiation on the brain are discussed.

[Correction of lipid peroxidation disorders of patients in the acute period after craniocerebral trauma].

In sufferers at the acute period of mild and severe craniocerebral trauma, the processes of peroxide oxidation of lipids become essentially more active. The antioxidative function of an organism decreases. Changes in the metabolic processes are the most pronounced in patients under 44 years and in women of different age in severe craniocerebral trauma.

[Hyperbaric oxygenation in the comprehensive therapy of young and middle age patients in the acute period after mild craniocerebral trauma].

The results of treatment of 107 young and middle aged sufferers with mild craniocerebral trauma have been analysed. The regimen for use of hyperbaric oxygenation contributing to normalization of general cerebral, focal disorders in high nervous and psychic activity, prevention of certain posttraumatic complications has been developed.

[The role of activation of lipid peroxidation of the tissues in response of the body to nociceptive stimuli].

Taking into consideration that activation of free radical processes is an indispensable consequence of any extreme action on man and animals and that lipid peroxidation (LPO) metabolites may play a role of original "primary mediators of stress", an attempt was made to define LPO participation in body response to nociceptive stimuli. Investigations carried out in patients belonging to different nosological groups, differing in the intensity of pain, established the presence of a direct relationship between the potency of painful action and LPO activation. LPO activation was also observed in experiments on animals exposed to painful tourniquetting of the limbs.

[Effect of extreme factors and adaptation to high-altitude conditions on peroxidation indices of serum lipids].

High and low temperatures, physical exercises and acute hypoxia are studied for their effect on indices of peroxide lipid oxidation in highly trained persons under alpine conditions (2100-5600 m). Temperature effects (-15 degrees C and +100 degrees C, for 30 minutes) as well as their combination with acute hypoxy cause an increase (by 10-30%) of malonic dialdehyde and a decrease (by 46-70%) of spontaneous chemoluminescence of blood serum in nonadapted people. Adaptation to alpine conditions in combination with physical exercises and low-caloric diet decreases shifts of these indices, considerably increasing the organism stability to the action of such extreme stress agents as high and low temperatures and acute hypoxy.

[Oxidative phosphorylation in the rat liver mitochondria under activation of lipid peroxidation].

The immobilization stress and oxygen effect under pressure of 0.8 atm (hyperbaric oxygenation) considerably activate lipid peroxidation both in the blood serum and rat liver mitochondria. Inhibition and partial separation of oxidative phosphorylation being more pronounced with intensification of lipid peroxidation are simultaneously observed.

[Effect of insulin and hydrocortisone on various indices of energy metabolism in rats irradiated with 6.0 MeV fast neutrons].

Neutron irradiation (1 Gy, 0.5 + 0.5 Gy) causes hypersecretion of glucocorticoids.

[Energy metabolism during stressful exposures (ionizing radiation), its self-regulation and correction].

Normal hormonal regulation of energy metabolism is mainly realized by glucocorticoids and insulin, their physiological antagonist. Under the effect of different extremal factors (including ionizing radiation) there arises non-specific stress, a syndrome the main component of which is the hyperfunction of glucocorticoids--the intermediate hormonal link in the stress reaction. Stimulation of hypercorticism by administering hydrocortisone to intact animals as well as its stimulation by administering this preparation to irradiated animals causes development and intensification of inhibition and uncoupling of the oxidative phosphorylation as well as disturbance in adenylic nucleotides metabolism.

[Participation of glucocorticoids and insulin in changes in energy metabolism in the spleen of irradiated rats].

Irradiation of rats with a fast neutron flow (0.5 Gy twice with a 7-day interval induces an increase in the content of 11-oxycorticosteroids and insulin in the blood plasma, the hormone ratio changing with glucocorticoids prevailing. Simultaneously oxidative phosphorylation is inhibited and the pool of adenylic nucleotides lowers in the spleen.

[Change in the level of acid-soluble adenine nucleotides in rat tissues in experimental hypo- and hypercorticism].

The level of free adenine nucleotides was studied in the rat tissues in deficiency and excess of the adrenal cortex hormones in the organism. Hypocorticism induced by adrenalectomy led to reduction of the concentration of total and individual adenine nucleotides in all the tissues examined, except ADP in the spleen and AMP in the myocardium. Single administration of hydrocortisone to intact rats caused an increase in the level of total and individual adenine nucleotides in the liver and reduction of their concentration in the spleen and the skeletal muscle.

[Effect of hydrocortisone and insulin on changes of oxidative phosphorylation after neutron irradiation].

Total double irradiation of rats with a fast neutron flow does not affect oxidative phosphorylation in the liver mitochondria but causes an essential decrease in the intensity of phosphorylation in mitochondria and chemoluminescence in blood serum of animals. Postradiation multiple administration of hydrocortisone intensifies the radiation inhibition of oxidation and phosphorylation of mitochondria and insulin administration stimulates phosphorylation in the liver mitochondria and the intensity of chemoluminescence in blood serum of rats. Hydrocortisone in combination with insulin has a less pronounced stimulating effect on phosphorylation than insulin, but the intensity of chemoluminescence in this case is higher than under the effect of each preparation separately.