The present study was undertaken to determine whether the transfer of cerebroside from the site of synthesis (microsome) to the site of myelin assembly was impaired in rats fed on a nicotinic acid-deficient diet. We measured the radioactivity in cerebroside in subcellular fractions (microsome and myelin) after intracerebral injection of [U-^<14>C]-L-serine in the brain of 22 day old rats which received nicotinic acid or saline and they were fed on the nicotinic acid-deficient diet for 10 days from 12th days after birth. In both the groups which received nicotinic acid or saline, the specific activity of cerebroside in microsome increased sharply 4 h after injection of ^<14>C-serine and then declined during the next 24 h. On the other hand, the specific activity of cerebroside in myelin increased during these periods. This observation indicated that cerebroside synthesized in microsome fraction was transferred to myelin in both the nicotinic acid-deficient rats which received nicotinic acid or saline.
To study the effect of vitamin B_<12> deprivation on the levels of heme proteins in the liver, hepatic catalase and tryptophan pyrrolase activities were examined in the rats fed on a vitamin B_<12> deprived diet for 140 days or 210 days. Then, microsomal cytochrbme P-450 and cytochrome b_5 concentrations in the liver were also examined after 140 days of vitamin B_<12> deprivation. Vitamin B_<12> deprivation elevated progressively urinary MMA content to high value in 120 days leading to plateau level in 210 days. Vitamin B_<12> concentrations in the liver and plasma decreased markedly when rat were fed on a vitamin B_<12> deprived diet for 140 days and 210 days. Hepatic catalase and tryptophan pyrrolase activities were depressed in 140-day and 210-day when rats were kept on the same diet. However, no differences in the activities due to the experimental period was observed. Moreover, it was recognized that microsomal cytochrome P-450 and cytochrome b_5 concentrations in the liver of vitamin B_<12> deprived rats decreased compared with those of the vitamin B_<12> Supplemented group. These results suggest that vitamin B_<12> deprivation affects the level of heme proteins in rat liver.