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A hepatoprotector of phospholipid nature eplir extracted from silt mud was shown to prevent like essentiale in CCl4-hepatitis in rats the development of the liver parenchyma necroses, to promote the maintenance of the normal activity of enzymes in hepatocytes, to stabilize lysosomes, to stimulate the antitoxic and excretory functions of the liver, to reduce hyperfermentemia. The mechanism of action of eplir is determined by the antioxidant properties, a decrease of lysophosphatide formation and the inclusion of phosphatidylcholine in membranes.

Two intragastric administrations of 500 mg/kg of D-galactosamine reduce the RNA and the cytochrome P-45, and b5 content in the hepatic microsomes of rats; inhibit the activity of aminopyrine-N-demethylase, hexobarbital hydroxylase, aniline-p-hydroxylase, and glutathione-S-transferase; reduce the rate of NADP.H and NAD.H oxidation; accelerate inactivation of cytochrome P-450 to cytochrome P-420; reduce the number of points of hexobarbital binding with N-octilamine, though increase the hemoprotein affinity to these substrates. Destruction of the nucleus, endoplasmic reticulum, and mitochondria occurs in the hepatocytes of D-galactosamine poisoned rats.

The hepatoprotective agents silybinin, essentiale and eplir (the complex of phospholipids and caratinoids from the mud) prevent in D-galactosamine-induced intoxication of rats the development of hepatitis, hepatocyte necrosis, a decrease in hepatocytes of the activity of the enzymes of mitochondria and endoplasmic reticulum, labilization of lysosomes. These drugs stimulate D-galactosamine-suppressed antitoxic function of the liver: they increase the contents of RNA, cytochromes P-450, b5, the activity of amidopyrine-D-demethylase, hydroxylases of hexobarbital and aniline, improve the activity of the respiratory chain of microsomes, counteract inactivation of cytochrome P-450 into cytochrome P-420. Essentiale and eplir activate conjugation of xenobiotics with reduced glutathione.

The administration of an antiepileptic drug--benzobamilum-to rats with CCl4-induced hepatitis prevents the development of liver parenchyma necrosis, promotes the retention of normal enzyme activity in hepatocytes, stimulates the excretory and antitoxic liver functions. The drug has antioxidant properties, inhibits the production of lysophosphatidylcholine and the reduction in phosphatidylcholine content in the liver homogenates but fails to intensify CCl4-induced steatosis.