抄録
To elucidate the mechanism of increase in the serum vitamin B_<12> concentration in acute hepatitis or hepatic necrosis, this experiment was performed. In rabbits, a single subcutaneous injection of 0.5 or 1.0ml of 20 per cent solution of carbon tetrachloride per kg caused liver damages developing in a day or two. The central lobular necrosis was most characteristic of the damages, and the accumulation of fat and the disappearance of glycogen and pyroninophilic substance in central zones and mid-zones were histochemically observed. In the period when the hepatic damages were developing, the serum vitamin B_<12> concentration, especially that of the bound form, increased remarkably and simultaneously the content of the vitamin in the liver decreased. The increase of the vitamin contents in the total serum was almost the same in extent as the decrease of the vitamin in the total liver. The increase of the serum vitamin B_<12> began to decline after about ten days until returned to normal value on the 31st day. The content of the vitamin in damaged liver recovered gradually from deficiency, but the rate of recovery was slower than that of the histological damages. Vitamin B_<12> in normal rabbit liver cells is distributed mainly in mitochondria and in the cells of the damaged liver the vitamin in this fraction decreases. From the facts obtained in these experiments it may be postulated that when the liver cells are damaged to acute necrosis vitamin B_<12> in the cells is rapidly released into blood stream and pathologic high levels of the serum vitamin B_<12> occur.
