Abstract
In rats a single dose of allyl alcohol (100 microliter per kg body weight) was given to produce periportal liver damage. Prothrombin index was reduced to a minimum after 12 hours and reestablished after 24 hours. The galactose elimination capacity was not changed. Hepatic glutathione content was unchanged for the first 24 hours but was then elevated twofold. Microsomal p-nitro-anisole demethylation showed a slight initial increase and a subsequent reduction. The pattern of these changes is similar to that seen after centrilobular liver damage from acetaminophen overdose (Poulsen et al. 1981 a; Poulsen et al., unpublished results), with the exception that the latter causes glutathione depletion. This indicates that in chemical liver damage ribosomal function, e.g. protein synthesis and drug hydroxylation, is more vulnerable than cytosolic phosphorylation of carbohydrate.
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