Pathomorphological Changes in the Brain in Dynamics of Long-Term Dust Exposure.

Histological and morphometric studies of brain autopsy material showed that the development of hypoxic changes in miners starts at the early stages of working in the dusty atmosphere. Edema of the pericellular and perivascular zones and the pia mater, degenerative changes in some nerve cells and even their loss and formation of gliosis foci were identified. The revealed changes in neurons progressed with increasing the duration of working under hazardous conditions.

Participation of Free-Radical Processes in Structural and Metabolic Disturbances in the Lung Tissues Caused by Exposure to Coal-Rock Dust and their Adaptogenic Correction.

Adaptive correction of structural and metabolic disturbances in the lungs caused by longterm exposure to coal-rock dust were studied in experiments on rats. It was shown that the complex antioxidant preparation containing dihydroquercetin compensated disturbances in the redox balance in the lung tissue, prevented the formation of dust granulomas, and reduced the severity of degenerative changes in the bronchopulmonary system.

Specificity of morphologic changes in target organs, associated with exposure to coal rock dust and fluorine compounds.

The studies revealed specificity of morphologic changes in target organs, depending on acting occupational hazard. Evidences are that inhalation of coal rock dust causes irreversible sclerotic and degenerative changes mostly in lungs and bronchi even on 6th week of the experiment. In liver, changes in parenchyma and stroma are controlled by reparative processes by 9th week. Accumulation of sodium fluoride in the body causes irreversible necrotic changes mostly in liver, on 6th week of the intoxication. With that, morphologic changes in lungs and bronchi are minor, characterized by immune inflammation with degenerative changes only after the 9th week. Irrespective of the acting hazard, vascular changes are characterized by media and intima hypertrophy with endothelial dystrophy and hyalinosis since the 6th week of the experiment.

Experimental studies of intracellular liver protective mechanisms in development of chronic fluorine intoxication.

The authors studied intracellular liver protective mechanisms in development of chronic fluorine intoxication. Findings are that synthesis of protective proteins HIF-1α, HOx-1, HOx-2 and HSP72, restricting free radical oxidation in hepatocytes increased in liver at early stages (1-3 weeks) of exposure to fluorine. At late terms of chronic fluorine intoxication (6-12 weeks), damaging effects of fluorine result from its genotixicity - ability to suppress synthesis of intracellular protective proteins and enzymes of main metabolic cycles in liver.

Experimental Study of the Mechanisms of Intracellular Defense in Cardiomyocytes Associated with Stages of Anthracosilicosis Development.

Mechanisms of intracellular defense of rat cardiomyocytes were studied in dynamics of anthracosilicosis development induced by long-term inhalation of coal and rock dust. It was shown that synthesis of transcription factor HIF-1α and protective proteins increased in the heart at the early stages of coal and rock dust inhalation (1-3 weeks), and these changes limited the development of free radical oxidation and activated metabolism of glucose and fatty acids. Exposure to coal and rock dust for 6-12 weeks activated free radical oxidation and decreased basal metabolism in cardiomyocytes.

Mechanisms of intracellular defense and activity of free radical oxidation in rat myocardium in the dynamics of chronic fluorine intoxication.

The mechanisms of intracellular defense and activity of free radical oxidation in the myocardium were studied in the dynamics of chronic fluorine intoxication. At the early stages of fluorine intoxication (day 3-week 3), the concentrations of defense proteins HIF-1α, HSC73, and HOx-2 and activity of the main metabolic enzymes increased, which promoted maintenance of cardiomyocyte structure and function at the normal physiological level. At late stages of fluorine intoxication (weeks 6 and 9), metabolic changes in the myocardium attest to high strain of the adaptive mechanisms.

[The experimental search of immunological criteria for identifying stages of development of chronic fluoride intoxication].

The experiment has shown the staging of the development of immune response to the chronic fluoride intoxication. Diagnostic criteria of the initial compensation stage are: leukocytosis against the background of reduced number of lymphocytes and increased one of monocytes; high levels of ceruloplasmin in blood plasma, a progressive increase in TNFalpha and cytokine IL-10. At the decompensation stage there are: leukocytosis with increased number of neutrophils; low levels of ceruloplasmin and the cytokines IL-1beta, IL-4 and the high level of TNFalpha, IL-6, IL-10. At the stage of exhaustion there are: leukopenia against the background of lymphocytosis, a high level of Hp, the low values of the level of IgM, IgG.

[Experimental studies of pathogenesis of chronic fluoride intoxication].

The article presents the results of studies of occupational fluorosis pathogenesis on experimental model of chronic fluoride intoxication (CFI). In early fluoride intoxication, fluoride and calcium in the body are in compensatory relations. Later, they are disturbed. High reaction ability of fluoride in CFI is associated with hypocalciemia which triggers parathyroid hyperactivity. This results in hyperproduction of PHH which is unrelated with development of secondary hyperparathyrosis. CFI is accompanied also with elevated calcitonin having a hypocalciemic and hypophosphatemic action. The experiments showed double content of collagen fragments of bone tissue in urine of animals with fluoride intoxication which reflects resorption of bone tissue. Serum osteocalcin rose three-fold as it was unable to include in the bone tissue. There was also activation of lipid peroxidation in subnormal activity of respiratory enzymes.

[Monitoring and controlling risk of occupational morbidity on aluminium plant].

The authors specified and introduced a system monitoring occupational diseases (fluor intoxication) on aluminium plant. Clinical examination of workers in groups with various risk levels proved design values to be reliable. Suggestions included main principles of risk management to decrease probability of occupational diseases in aluminium production.

[Experimental development of atherosclerosis].

The article deals with influence of coal rock dust on biochemical and immunologic serum parameters in experiment. Findings are that 3-week impact of coal rock dust (22 mg/m3) causes stress reaction and metabolism activation. Double increase of the duration and the concentration induces hypoxia component, immune deficiency elements and inflammation start.

Disturbances in energy metabolism during traumatic shock and their pharmacological correction.

In compression traumatic shock caused by mechanical crushing of the lower limbs and eventuating in death of 80% animals, hemodynamic disorders by the end of day 1 lead to the development of energy deficiency most pronounced in skeletal muscles and less pronounced in the liver and kidneys. Energy production in the brain and heart was not impaired. Inhibition of ATP synthesis correlated with decreased SOD activity in organs, but not always with activation of lipid peroxidation, which can occur without concomitant disorders in energy metabolism (in the heart and brain). Therapy with succinate-containing hydroxypyridine derivative decreased animal mortality to 10%; this treatment did not modify hemodynamic parameters, but normalized energy metabolism in organs and activity of the antioxidant and prooxidant systems. These findings suggest that tissue (bioenergetic) hypoxia plays an important role in the pathogenesis of compression traumatic shock and that antihypoxic drugs are essential components of therapy of this condition.

[Effectiveness of the use of synthetic opioid peptide in rats with traumatic shock]. / Effektivnost' primeneniia sinteticheskogo opioidnogo peptida u krys s travmaticheskim shokom.

Experiments were conducted on 80 male Wistar rats. Traumatic shock was simulated by applying clamps to lower extremity soft tissue for 6 hours. After removing the clamps, experimental animals were intraperitoneally injected the synthetic leucine-enkephalin dalargin. The blood ionogram, the levels of urea, glucose, phosphorus, creatinine, lactic and pyruvic acids, blood plasma osmolarity, LDH activity were determined. In the animals untreated with dalargin, plasma concentrations of ions of potassium, phosphorus, creatinine, urea, osmolarity, LDH activity increased and the levels of glucose decreased when shock developed. At the same time the rat death rates were 70-80% 24 hours later. The administration of dalargin corrected the majority of the above-mentioned parameters and the death rates were decreased to 20%. It is concluded that dalargin has an early antishock effect.

[The effects of enkephalins on the water-salt metabolism of rats in ontogeny]. / Vliianie énkefalinov na vodno-solevoi obmen krys v ontogeneze.

The experiments were carried out in white Wistar rats of three ages: 25-30 days (Group 1, n = 102), 45-50 days (group 2, n = 62), over 180 days (group 3, n = 115). The water loading was given through a gastric tube in an amount of 5% of the body weight. A synthetic analogue of leu-enkephalin (SAE) was injected intraperitoneally in a dose of 100 mg/kg. The control animals received physiological saline. In the baby rats of group 1, administration of SAE slowed down the polyuric and ionouretic reactions in response to the water loading. In older rats of group 2 administration of SAE enhanced water elimination but with this the osmolarity of the blood plasma increased together with the content of potassium and sodium ions in it. In adult rats (group 3) injections of SAE produced a smooth diuretic reaction which retained constant ion levels in the blood plasma.

[Changes in carbohydrate metabolism during experimental alcoholic liver disease]. / Narusheniia metabolizma uglevodov pri alkogol'nom porazhenii pecheni v éksperimente.

Decrease in activities of alcohol dehydrogenase and catalase, inhibition of mitochondrial glycerophosphate-, lactate-, malate-, succinate dehydrogenases as well as a decrease in the pool of oxidized nicotinamide coenzymes were observed in liver tissue of rabbits after per oral administration of 30% ethanol within two months. Ratios of substrates of tricarboxylic acid cycle were altered: concentrations of malate and oxaloacetate were decreased and content of alpha-ketoglutarate exceeded distinctly the normal level. Content of glucose, pyruvic and lactic acids were also decreased in liver tissue.