Fc receptors in sinusoidal cells and immune complex uptake were studied histologically in D-galactosamine HCl (GalN)-induced liver injury in rats. Kupffer cells and monocytes were distinguished from sinusoidal endothelial cells and from each other by endogenous peroxidase staining. Fc receptors were found along the sinusoidal endothelium throughout the lobules in normal livers. In acute injury caused by 300 or 750 mg/kg of GalN, Fc receptors were preserved within necrotic foci until the foci were infiltrated by inflammatory cells. The endothelial Fc receptor activity altered, as demonstrated by their capacity to bind immune complexes, after GalN injection. The activity decreased from 24 h after injection in the periportal areas in both dose groups, and increased transiently with dose-dependence in the remaining areas. Kupffer cell numbers also showed a transient dose-dependent increase, except in the periphery of lobules where they generally decreased. In chronic injury with 400 mg/kg, Fc receptors were lost and Kupffer cells decreased in the periportal areas. Circulating immune complexes were ingested by Kupffer cells and endothelial cells in normal and injured livers, showing the the same distribution as that of Fc receptors except that the complexes decreased gradually towards the centrilobular zones.