At present the disorders of lipid metabolism and connected diseases are studied insufficiently. Some disorders with the basis of lipid metabolism disorders are combined into the lipid distress-syndrome. The clinical study of 60 patients with expressed dislipoproteidemia (48 female and 12 male) in the age 46-79 years were made by the clinical observation, estimation of biochemical indexes, lipid blood spectrum, viral hepatitis markers, ultrasonic and liver biopsy. Obtained results showed that the patients with dislipoproteidemia had the expressed liver disorders which were typical for the clinical-morphological characteristics of non-alcoholic steatohepatitis. In patients with cardio-vascular pathology, atherosclerosis and dislipoproteidemia in 90% of cases the detected liver dystrophy can be considered as pre-stage of NASH.

There was a study of lipid peroxidation activity, ceruloplasmin level, bile acids content, and the liver detoxifying function state in 37 patients with chronic hepatitis types B and C of viral etiology. Changes of the indices under study were most apparent in patients with HCV. It was revealed that the degree of impairment of detoxifying and bile-producing functions of the liver are closely interrelated to the activity of the inflammatory reaction and lipid peroxidation processes. The increasing ceruloplasmin level in this category of patients hampers the reduction of the activity of lipid peroxidation processes, which is apparently related not only to the direct cytotoxic viral effect but also to the negative effect of superoxide ions on the cell membrane. Along with this, in cases of viral lesions of hepatocytes there are changes in the synthesis and conjugation of bile acids leading to the derangement of their correlation, their increased aggregate content and accumulation in tissues, which can also enhance the intensity of destruction of liver tissues and is an extra factor contributing to the intensification of lipid peroxidation processes.

The nonenzymatic conjugation of metabolites is decreased in chronic diseases of the liver, which is caused by decreased concentration of glutathione. The activities of glutathione enzymes are increased, this indicating the development of compensatory processes of mobilization of the second phase of detoxication, that is, increased conjugation under conditions of suppression of the cytochrome P-450 system. Measurement of liver glutathione transferase is a highly informative test for assessing the activity of the pathological process, particularly important in patients with chronic active hepatitis and cirrhosis of the liver.

It is shown that chronic hepatobiliary pathology is associated with a fall in spontaneous metabolite conjugation related to reduced concentration of hepatic glutathione. There was also enhanced activity of glutathione-dependent enzymes. This indicates progress of compensatory processes associated with mobilization of detoxication phase 2, i.e. stimulation of conjugation processes under depression of cytochrome P-450 system. The authors ascertain high informative value of hepatic glutathione transferase in assessment of disease activity in patients with chronic active hepatitis and hepatic cirrhosis.

Repression of cytochrom P-450-dependent hydroxylation and demethylation in liver was demonstrated in bioptats of patients with chronic liver diseases. The inhibition of cytochrome P450 system was provoked by oxidative modification of proteins-enzymes in patients with chronic liver changes as was proposed at the same time. The activation of glutathione-dependent enzymes was revealed. So the intensification of conjugation and development processes was revealed as the compensation mechanisms of detoxication with chronic liver diseases.

Patients with chronic hepatic disease have higher superoxide dismutase (SOD) activity and lower erythrocytic glutathione levels. There was a decrease in plasma SOD activity in cirrhosis, a feedback between the dismutase and oxidase activities of ceruloplasmin in cholestatic damages to the liver. Drug therapy resulted in positive dynamics in the levels of SOD, glutathione peroxidase, glutathione, ceruloplasmin, which is likely to be associated with the control of the enzymatic mechanisms of antioxidative protection. It is suggested that the enhanced erythrocytic SOD activity in hepatic diseases might trigger free radical oxidation.

Chronic diseases of the liver were found to be associated with microsomal hydroxylation reactions inhibition, this inhibition depending on the disease activity and stage. Chronic cholestatic hepatitis and primary biliary cirrhosis are associated with a more marked suppression of these reactions, the degree of inhibition being in proportion with the cholestatic syndrome severity. Demethylation process was found inhibited in active liver cirrhosis and primary biliary cirrhosis. The authors believe that assessment of the rate of microsomal oxidation in a liver biopsy specimen will help objectively assess the first phase of cytochrome P-450 effected biotransformation (hydroxylation) in patients with chronic disease.

Biopsy of the liver of 73 patients with chronic affection of the hepatobiliary system was conducted to study the enzymatic system of inactivation of the active forms of hepatic oxygen according to the stage of the chronic process. Reduced activity of superoxide dismutase and catalase and disruption of their relationship in chronic active hepatitis were revealed. Significantly diminished rate of inactivation of superoxide radicals was encountered in fibrosis and primary biliary cirrhosis. The informative importance of the catalase/NADP H-peroxidase index in appraising chronic affection of the hepatic tissue is shown. It is concluded that the interrelation of the antioxidative enzymes as a system of antioxidant protection of hepatocytes is impaired in chronic diseases of the liver.

A decrease in activity of main enzymes responsible for inactivation of reactive intermediates of oxygen was found in patients with chronic impairments of liver tissue. In chronic active hepatitis superoxide dismutase and catalase activities were decreased, while more pronounced alterations in the enzymatic activity were observed in primary biliary cirrhosis. Alterations in the rate of antioxidation enzymes activity correlated with severity of pathological process: less distinct alterations in superoxide dismutase and catalase activities were detected in adipose degeneration of liver tissue as compared with those in active chronic hepatitis, and, especially, in primary biliary cirrhosis. The data obtained by means of correlation analysis suggest that interrelationship of the antioxidation system components was deteriorated. The decrease in activity of these enzymes appears to be related to destructive alterations developed in chronic impairments of liver tissue.

The method of man hepatobioptate study based on the change of cell adhesion is suggested to diagnose cholestatic syndrome. The quantitative assessment of cell adhesion in the liver was carried out with disconnected coefficient estimated as ratio of the quantity of single cells. Eight groups of patients suffering from chronic hepatic pathologies were studied. The disconnected coefficients of hepatobioptates for patients suffering from cholestatic syndrome were 3-8 times higher than that for patients in other groups.

Hepatotropic drugs were shown to decrease blood lipid peroxidation activity (LPO) in patients with chronic diffuse liver diseases. A positive time course of LPO indices was noted in the treatment of chronic active hepatitis and liver cirrhosis of moderate activity. Comparison of antioxidant features of the drugs were suggestive of a noticeable effect of trophopar and essential in patients with chronic active hepatitis, trophopar in patients with liver lipodystrophy, and drugs of a silimarina series in patients with liver cirrhosis. Under clinical conditions the effect of the drugs on LPO processes was less noticeable than in experiments in vitro. It is assumed that the pharmacological effect of the hepatotropic drugs is associated with their antioxidant activity.

Material of puncture biopsy of the human liver left after morphological study was used to explore enzymatic and non-enzymatic lipid peroxidation, NADH-ferricyanide reductase activity, the content of triglycerides, cholesterol and protein. It was shown that the degree of lipid peroxidation varies considerably in different liver diseases. The highest degree of lipid peroxidation was discovered in patients with fibrosis accompanied by the symptoms of fatty dystrophy. It was established that the rate of peroxidation does not directly correlate with the level of liver lipid infiltration. It is concluded that NADH-ferricyanide reductase activity mirrors adequately the nature of a liver disease and can be used as a highly sensitive and very specific enzymatic test.