[The anticytolytic activity of ubiquinone-10 in a liver lesion from chlorinated hydrocarbons].

Antioxidative activity of ubiquinone-10, exceeding the level of that of vitamin E more than five times and anticytolytic activity of vitamin E and particularly of ubiquinone-10 manifested in decreasing activities of blood serum alanine aminotransferase and histidineammoniumlyase, which might be determined only during toxic liver damage, have been demonstrated. The activity of histidineammoniumlyase was considerably decreased under the effect of vitamin E and particularly in the presence of ubiquinone-10. Decreasing of activity of blood serum enzyme markers of cytolysis of hepatocytes is connected with the hepatocytes biomembrane stabilizing effect of antioxidants which was confirmed by the electron microscope investigation method.

[Experimental antioxidant therapy in toxic liver damage from CCl4 and chloxyl].

The authors studied the pharmacotherapeutic efficacy of antioxidants vitamin E, sodium selenite, and their combination in damage to rat liver by CCl4 and the anthelmintic agent chloxyl. Changes of the intensity of peroxidation of biological membrane lipids, the activity of enzymes-markers of hepatocyte cytolysis--alanine aminotransferase and aspartate aminotransferase--in blood serum, and changes in the structure of the liver were studied. Antioxidants and their combination blocked lipid peroxidation, reduced the activity of alanine aminotransferase and aspartate aminotransferase in blood serum considerably, and caused a protective effect on the structure of rat liver in its damage by CCl4 and chloxyl.

[Pathogenetic mechanisms of liver damage by the anthelmintic preparation chloxyl].

The pathogenetic mechanisms of hepatotoxicity of an anthelminthic drug chloxyl as compared with the mechanisms of CCl4 hepatotoxicity were studied on the basis of the change of the liver content of the primary (conjugated dienes) and secondary (malondialdehyde) products of lipid peroxidation. the activity of alanine aminotransferase and aspartate aminotransferase in the blood serum of rats and on the basis of the change of the liver structure. The pathogenetic mechanisms of chloxyl hepatotoxicity are close to those of CCl4 and consist in the activation of membrane lipid peroxidation, that is, an increase of the liver contents of the primary and secondary products of lipid peroxidation, an impairment of permeability of membranes of hepatocytes and their destruction with the release in the blood of cytoplasmic enzymes of alanine aminotransferase and aspartate aminotransferase.

[Antioxidant activity of ubiquinone-9 and its combinations with vitamin E and sodium selenite in toxic lesions of the liver].

It was established that ubiquinone-9 (30 mg/kg per course) decreases in rats the content of primary products of lipid peroxidation--diene conjugates--in the liver by 12 times greater than vitamin E (a course dose of 30 mg/kg). Ubiquinone-9, vitamin E and sodium selenite (a course dose of 90 mg/kg) equally reduced the content of a secondary product of lipid peroxidation--malon dialdehyde. In this case the activity of sodium selenite was 300 times higher than the activity of ubiquinone-9 and vitamin E.