Galactosamine injury of rat liver brings about induction of microsomal oxidation enzymes after 24 hours. Such a conclusion may be arrived at on the basis of an analysis of variation in the activity of cytochrome P-450, cytochrome b5, and NADH ferricyanide reductase while comparing normal and galactosamine-treated rats. In vitro galactosamine leads to activation of enzymatic lipid peroxidation. This circumstance may underlie hepatotoxicity of the compound in question. The monitoring coagulation method has revealed a marked hemorrhagic syndrome after galactosamine administration. Upset synthesis of export liver protein is assumed.
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