Protein deficiency in carbon tetrachloride-induced hepatic lesions.
The influence of protein deficiency on the hepatotoxicity of carbon tetrachloride (CCl4) was investigated in a group of rhesus monkeys.  Animals fed a protein-rich diet served as controls.  The results indicate that protein-deficiency protects the liver against acute hepatotoxicity of this drug.  The protective effect is abolished if the animals are administered phenobarbital prior to the administration of CCl4.  The protective action is due to a reduction, in protein deficiency, of the endoplasmic reticulum associated enzymes involved in hepatotoxicity of CCl4.  Repeated administration of CCl4, which induces hepatic regeneration, resulted in disappearance of fat from periportal cells in protein-deficient animals.  The regenerating cells (because of their better enzyme system) acquire "nutritional autonomy" and are thus able to synthesize adequate amounts of lipoproteins for mobilization of liver triglycerides.
D000818:Animals; D002252:Carbon Tetrachloride Poisoning / Q000201:enzymology / Q000473:pathology*; D056486:Chemical and Drug Induced Liver Injury / Q000201:enzymology / Q000473:pathology* / Q000517:prevention & control; D005234:Fatty Liver / Q000473:pathology; D005952:Glucose-6-Phosphatase / Q000378:metabolism; D006651:Histocytochemistry; D008099:Liver / Q000201:enzymology / Q000473:pathology*; D008253:Macaca mulatta; D008297:Male; D009336:Necrosis; D010634:Phenobarbital / Q000494:pharmacology; D011488:Protein Deficiency / Q000150:complications*
D005952:Glucose-6-Phosphatase; D010634:Phenobarbital