Uninterrupted protein synthesis is essential for survival in the early stages of carbontetrachloride-induced hepatocellular necrosis in the mouse

Summary 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.Acknowledgments. I wish to thank Mr C. R. West for carrying out the statistical analysis, Mrs Brenda Brooks for histological processing, and Berk Pharmaceuticals Ltd for information on Ancrod defibrination in mice.