[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. In apoptosis induced by immune reaction T-lymphocytes could trigger off apoptosis in two principal ways: by releasing perporines that produce holes through hepatocyte membrane and according to this process granzyms are permetted inside the cells. By destroying of caspases by proteases that initiate apoptosis cascade. In this article molecular mechanisms of the processes mentioned above are also discussed.

[Molecular mechanisms of apoptosis].

Apoptosis is the vital issue of Biology and Medicine. Recent concept of molecular and cellular mechanisms of apoptosis--a well-controlled form of cell death was reviewed. The aim of a review was to broaden knowledge of apoptosis mechanism and to reveal molecular targets for the modulation of these processes. The data on the apoptosis was analyzed. The biological role of physiological cell death in normal state and in different human pathologies is described. The literature data showed that many molecular mechanisms of apoptosis are still unknown. Three mechanisms are actually known to be involved in the apoptotic process: a receptor-ligand mediated mechanism, a mitochondrial pathway and a mechanism in which the endoplasmic reticulum plays a central role. Morphological and biochemical definitions of poptosis are presented. An original scheme of apoptosis mechanisms is constructed. The term "mediators of poptosis" is introduced. Extra cellular and intracellular mechanisms of apoptosis are examined. The special attention is paid to mitochondrial factors of apoptosis, Ca(2+)-ions, and proteins (Bcl-2, Bax, p-53).

[The role of changes in tissue redox-status in mechanism of paraneoplasia].

To specify mechanisms of paraneoplastic alterations of redox-status of tissues in experimental malignant tumor growth, we investigated electronic paramagnetic centers of blood, skeletal muscle and liver with electronic paramagnetic resonance (EPR) method. We also studied the concentration and activity of antioxidant enzymes. Our experiments on adult white male rats of mixed population with sarcoma C-45 and mice with Ehrlich carcinoma have shown that malignant tumor growth leads to enhanced lipid peroxidation (LPO): production of potent LPO promoters - Fe2+, Mn+2+, NO, ubiquinone; depression of antioxidant defence - reduced production of total ceruloplasmin, elevated blood levels of oxidized ceruloplasmin and enhanced catalase activity. It is suggested that malignant tumor growth is associated with marked paraneoplastic shifts in tissue redox-potential. These alterations are involved in mechanisms of paraneoplastic changes of red cells, microhemocirculation and circulation intensity. All these interrelated processes result in generalized paraneoplastic hypoxia of the organs and tissues. Basing on our and literature data, we propose an original scheme of the mechanisms of paraneoplastic disorders of tissue redox-status, microcirculation and erythrocytes.

[Role of peroxidation processes and nitric oxide in mechanisms of paraneoplastic alterations of hemocirculation].

The present work was aimed to study mechanisms of paraneoplastic alterations of tissue redox-status, intensity of local blood flow in liver and their possible interrelations in case of malignant tumor growth. It has been investigated the electronic paramagnetic centres of blood and liver using the electronic paramagnetic resonance (EPR) method and intensity of local hemocirculation with the use of H(+) clearance polarography method. Experiments have been carried out on adult white rats of mixed population with carcinoma Walker and mice -- with carcinoma Ehrlich. It has been shown that malignant tumor growth displays conditions that lead to exaggerated lipid peroxidation (production of POL promoters -- Fe(2+), Mn(2+), NO, ubiquinone) and suppression of antioxidant protection of organism (reduction of total ceruloplasmin concentration in blood and increased concentration of oxidized ceruloplasmin). It has been suggested that in case of malignant tumor growth sharp paraneoplastic alterations of redox-status plays essential role in mechanisms of paraneoplastic disorders of tissues blood supply. All of these interrelated processes result in generalized paraneoplastic hypoxia in organs and tissues.