reamberin and Chemical-and-Drug-Induced-Liver-Injury--Chronic

The level of endogenous S-adenosyl-L-methionine (SAM) production during pharmacological correction of acute toxic (tetrachloromethane) and chronic drug-induced liver injury treated by remaxol, exogenous ademethionine, and reamberin has been studied on 118 outbred male rats. It is established that, upon a single introduction of tetrachlormethane (acute toxic injury model), remaxol and exogenous SAM produced a gain in the endogenous SAM level in hepatocytes. At the same time, in the case of chronic drug-induced injury (antituberculosis drugs), only remaxol caused authentic growth of the endogenous SAM level that was comparable with a compensatory growth of SAM at nontreated animals. Considering the improvement of laboratory indicators and the histological pattern of liver in animals treated by remaxol, it is possible to conclude on the important role of succinic acid along with the induction of SAM, in the hepatoprotective effect of drugs. This is confirmed by the effect of reamberin, which contains only succinic acid without methionine and does not cause induction of endogenous SAM.

Topics: Acute Disease; Animals; Animals, Outbred Strains; Antitubercular Agents; Carbon Tetrachloride; Chemical and Drug Induced Liver Injury, Chronic; Hepatocytes; Liver; Male; Meglumine; Methionine; Protective Agents; Rats; S-Adenosylmethionine; Succinates; Succinic Acid