Each experimental mouse of the selenite and the selenite plus carbon tetrachloride groups was given a single dose of 4 ug. of sodium selenite per kilogram of body weight and that of the control and the carbon tetrachloride groups was given 0.1 ml. of distilled water alone.

Six hours after the first administration of distilled water or sodium selenite, the experimental mice of the carbon tetrachloride and the selenite plus carbon tetrachloride groups were given a single dose of l.0 ml. of carbon tetrachloride per kilogram of body weight and those of the selenite groups were given 0.l ml. of paraffin oil alone.

Following the 1ast administration of carbon tetrachloride or paraffin oil, the mice were sacrificed by bleeding (cutting the common carotid artery) at the intervals of 2,3,4,6,8, and 12 hours respectively. Histochemical preparations were stained by the methyl-green and pyronin method and oil red 0 method.

The hepatotoxicity due to the administration of carbon tetrachoride was evident in the hepatic cells; the pyroninophilic granlues were partly reduced in volume in the hepatic cells of the centrilobular and the intermediate zones as early as the 3 hour-period, and markedly reduced or disappeared in the centrilobular and some part of the intermediate zones associated with hydropic degeneration as well as in the 6 hour-period. Thereafter marked reduction or dissolution of the pyroninophilic granules was found and extended as the periportal zone at the 12 hour-period.

However, the pyroninophilic granules in the hepatic cells of selenite plus carbon tetrachbride group showed no significant changes in the hepatic cells of these zones, compared to the histochemical feature of the granules in the hepatic cells of the control and the selenite groups.

Consequently it is suggested that the lipid peroxidative decomposition of the microsomal membranes, which is induced with carbon tetrachloride, would be prevented by a previous administration of sodium selenite.