Workers, who had worked in a power plant for cleaning up the inside of a fuel oil burner, wore affected by a vanadium compound contained in the scale which adhered to the wall, manifesting several characteristic symptoms. Among them, the symptom in the upper respiratory organs due to local irritation has been predominant but the hepatic disorder during the course of poisoning, chiefly fatty metamorphosis, has attracted our attention. It has been reported by Lewis that the disturbances of lipid metabolism, mainly hypocholesterolemia, were observed among vanadium workers with chronic poisoning. The objective of the present study is therefore to confirm the fact that the liver injuries observed among workers are the result of acute vanadium poisoning. The dose response of rats due to vonadium (5mg-30mg V/kg) injection and its course during 4-72 hrs. after injection were observed, the injection being performed subcutaneously with 0.3% NH4 VO3 aqueous solution. In subacute poisoning, 0.03% NH4 VO3 aqueous solution was administered subcutaneously in a dose of 1mg V/kg daily for 30 days. In acute oral poisoning, 0.3% NH4 VO3 aqueous solution was administered by a gastric tube in a dose of 20mg V/kg. The number of rats used (Donryu-Strain) was 125 of about 200g body weight. All rats, including the control group (10 rats) were sacrificed by decapitation, and lipid contents in both the serum and the liver and enzyme activity in the serum were assayed. Histological examinations of the liver were carried out by haematoxylin-eosin staining, and in some cause also by Sudan 3 staining. The following results were obtained: The liver and serum triglycerides increased prominently depending on the dose of V. The highest level of the liver triglyceride level was reached also 48 hrs. after the injection and the high level was maintained for 4 to 48 hrs. after the injection, the level decreasing gradually after that. S-total cholesterol level decreased gradually to the lowest level after 24 hrs. and then gradually recovered to the level of the control. In other doses except thet of 10mgV/kg, the correlation between the amount of cholesterol and the dose of vanadium administered was not recognized. S-free fatty acid level decreased gradually after 4 to 72 hrs., but the fluctuation of the level was not correlated to the dose of vanadium. The ratio of S-ester cholesterol to S-total cholesterol showed almost the same pattern with that of S-total cholesterol level in both the dose response and the course after injection. S-GOT activity increased according to the dose of V and high activity was maintained after 4 to 48 hrs., and then decreased to the level of the control. S-GPT changed to almost the same extent as S-GOT in both the dose response and the course after injection. No remarkable changes were observed on the S-LAP activity. Histological changes found in the liver were congestion of blood vessels and accumulation of fat droplets. In some cases necrosis of hepatic cells was observed. After 48 hrs. after the injection, at the time of the highest level of the liver triglyceride, fatty degeneration was observed in many cases. However, the histological changes was not always the same with respect to the dose or time factor. Biochemically, no remarkable change except S-total cholesterol, S-cholesterol ester ratio and S-triglyceride, was observed in acute oral administration. In subacute administration, S-total cholesterol and S-cholesterol ester ratio showed more clear changes than those observed in the oral administration. It has been speculated, howener, that if the remarkable fatty accumulation were biochemically observed, this would eventually invite histological changes in the course of poisoning. Consequently, in omnivorous rats, hepatic injuries (chiefly fatty degeneration and hepatic cell necrosis with circulatory changes) might have surely been induced by vanadium compound.