Biochemical effects of CCl4 on rat intestinal mucosa

Davis H. Alpers, Kurt J. Isselbacher

Research output: Contribution to journalArticle

13 Scopus citations

Abstract

1. 1. The effects of CCl4 on the intestine were studied and compared with the effects of this agent on liver. CCl4 caused inhibition of protein synthesis and polyribosome breakdown in rat intestine when given in vivo. In addition, dietary lipid accumulated in the intestine after CCl4 administration. Experiments with intestinal slices demonstrated that CCl4 inhibited protein synthesis when added in vitro. These effects were similar to those previously demonstrated in liver after CCl4 administration both in vivo and in vitro. 2. 2. Contrary to the effects observed in the liver following the oral administration of CCl4, the intestinal inhibition of protein synthesis produced by CCl4 was found to be a transient phenomenon, lasting only 30-60 min. Moreover, CCl4 led to necrosis in the liver but not in the intestine. It is suggested that these differences may be explained by the fact that CCl4 is concentrated and retained by the liver cells, whereas this toxin may be only transiently present in the intestinal mucosa. 3. 3. 14CCl4 was metabolized to 14CO2 to a much greater extent by liver slices than by intestinal slices. Furthermore, while CCl4 enhanced lipid peroxidation in hepatic subcellular fractions, no lipid peroxidation could be detected in intestinal cell fractions either in the presence of absence of CCl4. It is suggested that, if metabolism of CCl4 and lipid peroxidation are important for the toxic actions of CCl4 on liver, other mechanisms must account for its effects on the intestinal mucosa. 4. 4. Pretreatment with cycloheximide partially reversed the effects of CCl4 on protein synthesis in both liver and intestine. This effect is consistent with the hypothesis that CCl4 produces a decreased synthesis or increased breakdown of messenger RNA.

Original languageEnglish
Pages (from-to)414-424
Number of pages11
JournalBBA - General Subjects
Volume158
Issue number3
DOIs
StatePublished - Jun 24 1968
Externally publishedYes

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