Abstract
The early biochemical and ultrastructural effects on the liver of CS 2 administration in vivo to fasted rats were compared in animals treated and not treated with phenobarbital, to ascertain whether these effects differed quantitatively and/or qualitatively. Ultrastructural examination showed that in phenobarbital-treated rats, the main lesion induced by CS 2 was an increase in the number and size of the lysosomes containing cell debris from other cell organelles such as mitochondria. The endoplasmic reticulum was unchanged compared to that of rats treated only with phenobarbital. In particular, there was no decrease in the rough endoplasmic reticulum. By contrast, in rats not treated with phenobarbital, the main effect of CS 2 was a decrease in the number of ribosomes bound to the rough endoplasmic reticulum, with little or no change in other cell organelles. Cytochrome P-450 decreased more in phenobarbital-treated than in untreated rats, and cytochrome b5 decreased in phenobarbital-treated rats only. CS 2 lowered aniline hydroxylase activity, expressed per nanomole of cytochrome P-450 in untreated rats, but increased this activity in phenobarbital-treated rats. The opposite was observed for microsomal peroxidase and cytosolic glutathione reductase activities. Liver catalase diminished more in phenobarbital-treated than in untreated rats. The effects of CS 2 on liver endoplasmic reticulum as well as on the respective activities of aniline hydroxylase, microsomal peroxidase, and glutathione peroxidase show that untreated and phenobarbital-treated rats respond to CS 2 administration in qualitatively different ways. It is suggested that in untreated rats, the effects observed are mainly due to CS 2 itself, whereas in phenobarbital-treated animals, the effects are mainly caused by reactive CS 2 metabolites formed by the mixed function oxidase microsomal system.
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