Uninterrupted protein synthesis is essential for survival in the early stages of carbon tetrachloride-induced hepatocellular necrosis in the mouse.
The fatal syndrome produced by cycloheximide given 6 h after a hepatonecrogenic dose of CCl4 is due neither to direct toxic synergism between CCl4 and cycloheximide nor to transient sinusoidal thrombosis. It is suggested that survival in the presence of unknown factors released from dying liver cells requires uninterrupted protein synthesis. The life-saving effect of sterilization of the intestine by antibiotics indicates that the gut flora or its products play a vital role in pathogenesis.
D000818:Animals; D000900:Anti-Bacterial Agents / Q000494:pharmacology; D002252:Carbon Tetrachloride Poisoning / Q000401:mortality* / Q000473:pathology; D003513:Cycloheximide / Q000494:pharmacology; D004357:Drug Synergism; D006493:Heparin / Q000494:pharmacology; D007422:Intestines / Q000382:microbiology; D008099:Liver / Q000187:drug effects / Q000473:pathology*; D051379:Mice; D009336:Necrosis; D014176:Protein Biosynthesis; D013997:Time Factors
D000900:Anti-Bacterial Agents; D006493:Heparin; D003513:Cycloheximide