Hepatic Necrosis Due to Bromobenzene and its Dependence upon Available Sulfur Amino Acids. ∗

Abstract

Summary

Intraperitoneal administration of bromobenzene produces acute centrolobular hepatic necrosis, its severity depending on the preceding protein depletion. Methionine and cysteine given prior to bromobenzene administration prevent the lesion. The lesion is an example of interlocked toxicity and deficiency effect; since bromobenzene drains sulfur amino acid from the body.