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.
References
Parry, E. W., J. comp. Path., in press (1984).
Parry, E. W., J. comp. Path.94 (1984) 101.
Trakatellis, A. C., Montjar, M., and Axelrod, A. E., Biochemistry4 (1965) 2065.
van der Waaij, D., and Sturm, C. A., Lab. Anim. Care18 (1968) 1.
Gans, H., Surgery77 (1975) 602.
Author information
Authors and Affiliations
Additional information
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.
Rights and permissions
About this article
Cite this article
Parry, E.W. Uninterrupted protein synthesis is essential for survival in the early stages of carbontetrachloride-induced hepatocellular necrosis in the mouse. Experientia 41, 1319–1320 (1985). https://doi.org/10.1007/BF01952074
Issue Date:
DOI: https://doi.org/10.1007/BF01952074