Резюме.Целью исследования явилось проведение корреляционных взаимосвязей между морфологическими, гистохимическими и биохимическими показателями нефротоксичности у крыс с сулемовой нефропатией без лечения и получавших тауцин.Эксперимент проведен на 24 беспородных крысах-самцах массой 200-250 г, разделенных на 3 группы (n=8).Первая группа -контроль; вторая -опыт 1 (животные получали сулему, внутрибрюшинно в дозе 0,1 мг/кг/день); третья -опыт 2 (животные получали сулему, внутрибрюшинно в дозе 0,1 мг/кг/день и комбинацию таурина с цинка диаспартатом (тауцин) в дозе 500 мг/кг/день -внутрижелудочно).Анализ корреляционных взаимосвязей у крыс с сулемовой нефропатией свидетельствует о том, что резкое возрастание в плазме и синхронное снижение в моче маркерных показателей нефропатии (содержание мочевины и креатинина, клиренс последнего) в значительной степени ассоциируются с поражением митохондрий эпителиоцитов проксимадьных извитых канальцев корковых нефронов, степенью «сморщивания» почечного тельца и выраженностью внутриканальцевого гидронефроза.Под влиянием тауцина характер взаимосвязей изменяется не однозначно.Исчезает их большая половина и появляются отсутствующие новые.Совокупность этих изменений свидетельствует о его нефрозащитном действии, обусловленном в большей степени доминирующим компонентом -таурином и усиленным цинка диаспартатом.Эти результаты дополняют и углубляют ранее полученные нами данные о его нефрозащитном действии.На их основании

Изучено нефрозащитное действие комбинации таурина с цинка диаспартатом (тауцин) у крыс с контраст-индуцированной нефропатией. Установлено дозозависимое нефрозащитное действие комбинации таурина (20 г/моль в смеси) с цинка диаспартатом (1 г/моль в смеси), вводимых в желудок (250 и 500 мг/кг) в течение 14 дней у крыс с контраст-индуцированной (амидотризоат натрия и меглюмина, внутрибрюшинно 800 мг/кг/день, 14 дней) нефропатией.

A combination of taurine (20g/mole, 2.5 g) with zinc diaspartate (1 g/mole, 0.35g) named “taucine”, administrated in the rat stomach at doses of 250 mg/kg and 500 mg/kg over 14 days has a dose-dependent nephro-protective action in rats with sublimate nephropathy ( intraabdominally 0.1 mg/kg over 14 days) . It manifests in an increased volume of the primary urine in cortical nephrons glomerales because of a weakened compression of their capsule by hydropic fluid, in reduction of the inner diameter of cortical nephrons proximal convoluted tubules as consequence of a less pronounced «inner tubular» hydronephrosis and increased height of lining epithelial cells. A detailed analysis of the latter shows that they are less damaged by sublimate: the percentage of undamaged cells increases because of decrease with destruction of apical sections and increase of cells height by ½ as well.

A new approach to identification of the factors, responsible for predisposition to ethanol-induced liver damage, was developed. It is based on the examination of the liver in the same animals both before (biochemistry) and after (histology, blood markers of liver damage) chronic alcohol administration and comparison the biochemical and histological sets of data, using the methods of multiple stepwise regression, correlation, canonical analyses and ANOVA. The experiments were carried out in 118 male Wistar rats (250-300 g). In 94 animals the central and left lateral hepatic lobes (~65-70% of the liver weight) were removed under anaesthesia with a ligation of the lobar bases. Two months later, after liver recovery (confirmed by biochemistry and histology), they were administered ethanol (30% water solution, 5 g/kg, intragastrically, once a day, for 57 days). Control animals after the same hepatectomy operation received the same volumes of water instead ofethanol. It wasfound that animals with initially higher activity of alcohol dehydrogenase and lipid peroxidation system and lower contents of reduced glutathione, retinols and cytochrome b, lower activity of UDP-glucuronyl-, glutathione-S-transferases and rate of NADH oxidation in the liver had higher ethanol-induces liver damage indicated by histology and increased alanine and aspartate aminotransferase activities in blood. Those rats were also more sensitive to the hypnotic effect of ethanol. The proposed animal model and approach can be used in the finding of other biomarkers of the sensitivity to the hepatotoxic effect of ethanol (predisposition to the alcohol-induced liver damage) as well as biomarkers of the sensitivity to other hepatotoxins.

The nephroprotective properties of a combination of taurine with zinc diaspartate (taucin) in rats with contrast-induced nephropathy have been estimated. It is established that the combination of taurine with zinc diaspartate (20 and 1 g/mol, respectively, ingested in doses 250 and 500 mg/kg in the stomach during 14 days) produces a dose-dependent nephroprotective action on rats with contrast-induced (sodium and meglumin amidotrizoates, 800 mg/kg/day intraperitoneally, 14 days) nephropathy.

The aim of the study was to investigate the hepatoprotective action of taurine in combination with zinc diaspartate («taucin») in rats with predominant functional disturbances of liver, caused by paracetamol. We have established that «taucin» reduced the manifestation of paracetamol hepatotoxic action in the experiment on 50 male rats using morphological and histochemical studies of liver and biochemical studies of blood. It was manifested in the normalization of hepatotoxicity biochemical markers in plasma, the enzyme activity in hepatocytes (histochemical) and the structure of the liver.

The purpose of the study was to investigate the hepatoprotective action of a combination of taurine with zinc diaspartate («taucin») in rats with tetrachlormethane-induced hepatosohepatitis. During the experiment, conducted on 24 outbred male rats by morphological and histochemical studies of the liver and blood biochemical studies it was established that «taucin» weakens manifestation of tetrachlormethane-induced hepatosohepatitis.

It has been established that gentamycin-induced disturbances in nephron structure are associated with the inhibition of metabolism processes in them. According to the degree of interaction the indicators of matabolism are descending as follows: lactatdehydrogenase in proximal convoluted tubules (PCT) of cortical nephrons (CN) > alkaline phosphatase in PCT of CN = acid phosphatase in PCT of juxtamedullary nephrons > acid phosphatase in PCT of CN = ribonucleoproteins. The main gentamycin-induced metabolic disturbances in the kidneys are registered in PCT of CN and involve the inhibition of energetic exchange processes (according to the decrease in lactatdehydrogenase activity).

Gentamicin (60 mg/kg, i.p., once per day for 10 days) produces a nephrotoxic effect in rats, which is manifesting by the epithelium necrosis of proximal convoluted tubules (especially of cortical nephrons), decreasing creatinine clearance, and increasing protein in the urine. Acetylcysteine (40 mg/kg, i.p., once per day for 10 days) significantly decreases manifestations of the gentamicin nephrotoxicity. Acetylcysteine administration leads to the appearance of normal tubules (absent in rats treated by gentamicin), decreases the number of necrotized proximal convoluted tubules of cortical nephrons and reduces their internal diameter, and increases the height of paving epitheliocytes. The content of detrite in tubules of juxtamedullar nephrons decreases, while the activity of alkaline phosphatase in proximal convoluted tubules of cortical and juxtamedullar nephrons and the activity of lactatedehydrogenase in cortical nephrons increases.

The close interrelation has been established between the renal functional and structural indices in rats having gentamicin-induced nephropathy (60 mg/kg, intraperitoneally, once a day х 10). The positive interconnection between the increased plasma concentration of middle molecules, urea, creatinine and the percentage of severely damaged and lost proximal convoluted tubules (PCT) cortical nephrons (CN)) has been marked. The negative interconnection was found for the urea and the creatinine in the urine. Therefore, it is possible to predict the character and degree of the destruction of PCK CN on the basis of the results of plasma and urine examinations.

Gentamicin (60 mg/kg, i.p., once per day for 10 days) produces a nephrotoxic effect in rats, which is manifesting by the epithelium necrosis of proximal convoluted tubules (especially of cortical nephrons), decreasing creatinine clearance, and increasing protein in the urine. Acetylcysteine (40 mg/kg, i.p., once per day for 10 days) significantly decreases manifestations of the gentamicin nephrotoxicity. Acetylcysteine administration leads to the appearance of normal tubules (absent in rats treated by gentamicin), decreases the number of necrotized proximal convoluted tubules of cortical nephrons and reduces their internal diameter, and increases the height of paving epitheliocytes. The content of detrite in tubules of juxtamedullar nephrons decreases, while the activity of alkaline phosphatase in proximal convoluted tubules of cortical and juxtamedullar nephrons and the activity of lactatedehydrogenase in cortical nephrons increases.

A correlation between the individual features of the activity of renal enzymes and the expression of aminoglycoside (gentamicin) induced nephrotoxicity is established in hydronephrotic rabbits. The level of gentamicin-induced damage of the kidney is more significant in rabbits with initially (prior to gentamicin administration) increased activity of lactate dehydrogenase, decreased activity of succinate dehydrogenase and acid phosphatase, and low content of ribonucleoproteins.

The discussion of the article «The adaptation reaction to ethanol as a basis of alcoholism pathogenesis» was held. The problems of tissue hypoxia development in alcoholism and the adaptation reactions to this hypoxia as a factor of the alcoholism development were discussed.