[MORPHOLOGICAL ALTERATIONS IN THE INTERNAL ORGANS OF RATS WITH ALLOXAN DIABETES].

The aim of our study was to assess morphological changes in internal organs in a redox-induced model of alloxan diabetes in rats.According to the results of the study, the blood glucose level in rats began to increase 24 hours after the of alloxan administration, reached the maximum level on the 15th day of observation, and decreased on the 25-35 day, to the control level. In parallel with the increase in blood glucose level, an increase in the malondialdehyde (MDA) content in the blood serum was observed.

CHANGES OF ENDOTHELIN-1 CONTENT AND BLOOD RHEOLOGICAL PROPERTIES IN CRUSH SYNDROME.

This study describes hematocrit values and quantitative changes in plasma endothelin-1 (ET-1) levels according to the severity of crush syndrome (CS) compression and decompression periods. The experiments were carried out on 50 randomly selected 200-250 gr mass Wistar rats with the use of the standard crush syndrome modeling method. The plasma level of ET-1 was determined by the immuneenzyme method with the use of ELISA REDEAR URIT 660.

CHANGES OF LIPOPEROXIDATION AND ANTIOXIDATIVE ENZYMES DURING CRUSH-SYNDROME MODELLING.

Crush-syndrome (CS) is characterized by numerous pathological deviations due to the soft tissue damage and their further reperfusion. The aim of the study was to investigate pro- and antioxidative processes during different regimens of crush syndrome. The experiment was carried out on randomly selected 200-250gr.

[The variants of changes in pro- and antioxidative processes in viral hepatitis and the necessity of differential approach in their antioxidative therapy].

There was investigated the changes in pro- and antioxidative processes in viral hepatitis of different etiology. It was revealed that the mechanisms mentioned above essentially differ from each other and for their treatment, accordingly, different groups of antioxidative drugs should be used. The data obtained indicates the impossibility of "universal" antioxidative therapy.

[The role of apoptosis in the development of virus hepatitis].

In present review hepatocyte apoptosis is presented as universal defensive reaction of liver, to the damages. Hepatocyte apoptosis may be caused by hepatotropic virus's direct affection, or by the immune reactions initiated by viruses. Apoptosis development caused by virus direct affection varies and contains at lest two mechanisms: production of specific proteins: B virus - X protein and C virus - core-protein; expression of the receptors leading the induction of this process on the hepatocyte membrane, for example, increasing of Fas-receptor and cell sensation to apoptosis stimulus.