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Inflammatory granulomatous diseases are cha- racterized by a high concentration of granu- lomas in tissue interstitium in which phagocytic cells that produce active oxygen and nitrogen metabolites are accumulated. Because of their high reactivity, free radicals react with unsatu- rated fatty acids that are components of mem- brane phospholipids, activate lipid peroxidation processes (LPP), the products of which have a cytotoxic effect. The role of free radicals in the pathogenesis of diabetes and its complications has been proved. The purpose of the present work was to investigate the activity of lipid peroxidation processes in the liver of rats with silica-induced granulomatous inflammation, allo- xan diabetes and their combination. The expe- riment involved male albino rats divided into four main groups. The first group were rats with silica granulomatous inflammation (SL rats); the second group were alloxan diabetic rats (DB rats); and the third group were alloxan diabetic rats, in which silica granulomatous inflammation was induced 8 days after the disease onset (DB_SL rats), the fourth group were rats that were injected saline physiological solution into the tail vein (control rats). Rats were withdrawn from the experiment within different time pe- riods after the induction of pathological pro- cesses. LPP activity in liver homogenates was determined by the relative concentration of lipo- peroxides in the heptane-isopropanol system and the concentration of products of the reac- tion with 2-thiobarbituric acid-reactive substan- ces (TBARS). The severity of carbohydrate meta- bolism disorders was evaluated through the measurement of the blood level of glucose, daily urine volume and the relative weight of the kindneys. We found that silica administration activated LPP in the liver of SL rats; we ob- served the accumulation of primary products on day 1 after administration and later that of TBA- RS followed by normalization of their concen- tration by day 21 of the experiment. TBARS con- centration was higher in DB rats than in the control at all stages of the experiment indicating the maintenance of high LPP activity in the liver of DB rats. TBARS concentration in the liver of DB_SL rats decreased by 3 times by the end of the experiment compared to DB rats, at the same time, they displayed a decreased blood glucose concentration, reduced diuresis and relative weight of the kidneys caused by hyperglycemia and associated polyuria. We conclude that one of the possible mechanisms of the influence on silica granulomatous inflammation on the cour- se of alloxan diabetes can be 1) a reduced LPO activity in liver cells at the lates stages of gran- ulomagenesis process induced by a single dose of a suspension of silica microparticles and 2) a combined decrease in glucose production in the liver of alloxan diabetics rats.

Possibility of electron beam usage for immobilization of hydrazidum of an isonicotinic acid (HIA) on dextrane was studied to produce a drug for treatment of a tuberculosis. As a result of irradiation of dextrane the processes of oxidation and formation of polysaccharide occur due to carbonyl groups which are to link isoniasidum. The HIA immobilized on dextrane may be used as an effective medical preparation having prolonged action for action on endo and extracellular population of Micobacterium tuberculosis .

Highly pathogenic avian influenza H5N1 (HPAI H5N1) viruses can infect mammals, including humans, causing severe systemic disease with the inhibition of the immune system and a high mortality rate. In conditions of lymphoid tissue depletion, the liver plays an important role in host defence against viruses. The changes in mice liver infected with HPAI H5N1 virus A/goose/Krasnoozerskoye/627/05 have been studied. It has been shown that the virus persistence in the liver leads to the expression of proinflammatory cytokines (TNF-α, IL-6) and intracellular proteases (lysozyme, cathepsin D, and myeloperoxidase) by Kupffer cells. Defective antiviral response exacerbates destructive processes in the liver accelerating the development of liver failure.