Effects of methyl (+) (3S)-1,2,3,4-tetrahydro-3-hydroxymethyl-beta-carboline-2- carbodithioate(THC), a new hepatoprotective agent, on protein synthesis and chronic liver injury induced by carbon tetrachroride in rats.

Abstract

The effects of oral administration of methyl (+) (3S)-1,2,3,4-tetrahydro-3-hydroxymethyl-beta-carboline-2-carbodithioa te (THC) on protein synthesis in the liver and chronic liver injury induced by carbon tetrachloride (CCl4) in rats were studied. THC increased liver weight and the contents of protein and ribonucleic acid, but not deoxyribonucleic acid, in the liver. THC also accelerated the 14C-leucine incorporation into hepatic microsomal and cytosol proteins in rats when the animals were treated with THC 24 h before sacrifice. In addition, when the animals were treated with THC during the latter half of a 5 weeks CCl4-treatment period, THC had a marked therapeutic effect on CCl4-induced chronic liver injury in rats by an improvement of the decreased body weight gain, suppression of the elevated serum enzyme activities (glutamic pyruvic transaminase, glutamic oxaloacetic transaminase and alkaline phosphatase) and increases in the decreased serum total protein and glucose contents. In the liver, THC also improved the decreased protein content, the increased triglyceride content and histopathological changes. These results suggested that THC stimulates protein synthesis in the liver and has a therapeutic effect on chronic liver injury induced by CCl4.