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A study was made of permeability of the lysosome membranes and subcellular distribution of acid hydrolases in chronic hepatitis caused by CCl4 inhalation and during the restoration of the liver after injury. No normalization of the indices under study occurred during the period of up to 14 days after the last CCl4 inhalation: changes in the stability of the lysosome membran persisted and redistribution of acid hydrolases was noted. This redistribution was associated with both the processes of injury and restoration of the liver.

Physical and chemical properties of the rat liver lysosomes with single Triton WR 1339 overloading were studied during the administration of a detergent to intact rats and those with acute toxic hepatitis. Administration of the latter to intact animals was accompanied by a reduction of the floating density of the particles, solubilization of the lysosome enzymes and by increased fragility of the particles in the hypotonic medium. Lysosomes of the hepatocytes in rats with toxic hepatitis also displayed signs of overloading of the vacuolar apparatus with the preparation administered. The most pronounced solubilization of the lysosomal enzymes beta-galactosidase, acid RNA-ase, cathepsin D--was noted in case of combined action of CCl4 and Triton WR 1339 24, 48, 72 hours and 7 days after the CCl4 poisoning. Possible consequences of overloading of the vacuolar apparatus of the rat hepatocytes are discussed.

It was established in experiments on 47 rats that administration of carbon tetrachloride entails the increased permeability of the hematocellular barrier of the heart, lungs, skeletal muscles, adrenals, liver and kidneys. Administration of ethimisole promotes normalization of the permeability of the test organs.

Hepatic lesions in white rats were produced by administering the hepatotropic alkaloid heliotrin. Four series of experiments in different combinations were conducted (poisoning of female and male rats alone and simultaneously with subsequent crossing). The animals with heliotrin-induced hepatitis showed a tendency to a later coming of conception, to a decreased number of fetuses, and their unequal distribution in uterine horns. The morphologic appearance of the ovaries exposed to heliotrin was examined. The evidence obtained indicates that in toxic hepatitis (apparently in infectious hepatitis as well) the generative function gets destroyed that can be seen from changes in coming, developing, preserving and completion of pregnancy.

Biomicroscopic and morphological studies demonstrated that in experimental heliotrine affection of the liver there occurred very early and marked microcirculatory disturbances which preceded the parenchymal damage. With the further progress of the pathomorphological changes and chronization of the pathological process in the liver one of the leading roles was played by the advance of microcirculatory disturbances and of the tissue-vascular permeability leading to hypoxia of the hepatic tissue and derangement of the metabolic processes in the organ.

Suramin that accumulates in rat liver Kupffer cell lysosomes and inhibits the intralysosomal proteolysis was used to suppress the functional activity of these particles during liver damage (acute CCl4 hepatitis). Polyvinylpyrrolidone that does not disturb protein catabolism in liver lysosomes was employed for reference. According to the characteristic changes in lysosomes induced by suramin (inhibition of acid phosphatase, decrease of the rate of the intralysosomal proteolysis in the liver) and PVP the damaged liver was able to accumulate the lysosomotropic substances under study. Suramin aggravated liver damage and increased the lysosomal labilization, whereas PVP exhibited the protective action. The unfavourable effect of suramin may be linked with the suppression of catabolism of Kupffer cell lysosomes. The data obtained suggest the lack of safety of using the inhibitors of intralysosomal proteolysis in patients with acute hepatitis.

The number of Kupffer cells increased up to necroses and processes of liver regeneration following carbon tetrachloride-induced injury. Mouse Kupffer cells migrated to the necrotic centrolobular zones 48 h after CCl4-induced necroses. During regeneration, Kupffer cells migrated to the sinusoids from the necrotic centrolobular zones. Study of the ultrastructure of Kupffer cells indicates activation of their function during all observation periods.