[Specificity of cellular response to various occupational toxicants].

The article covers study concerning influence of coal rock dust and high fluorine concentrations on energy metabolism and oxidation-reduction reactions in blood WBC of experimental rats. The authors demonstrated that the cells vary in response to long action of coal rock dust and high fluorine concentrations.

[Clinical and experimental studies of metabolic response to chronic exposure to coal dust].

In miners anthracosilicosis is caused by chronic exposure to coal dust and is characterized by progressive development of the inflammatory process, the expressed disorders of lipid metabolism, and immunodeficiency. In the experiment we revealed the stages of anthracosilicosis development according to which adequate measures of prevention and correction of the disorders caused by long exposure of an organism to coal dust are recommended.

[Tissue morphological changes in experimental anthrasilicosis].

Anthrasilicosis was experimentally stimulated by inhaled inoculation. Various degrees of morphological changes were detected depending on the time of inoculation and the stage of the pathological process: the changes were early observed in the lung and liver, which became worse by week 12 of inoculation; from week 6 these were in the heart and kidney, which was indicative of systemic disorders in response to dust exposure.

[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.

[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.