抄録
The effect of NiA on myelination was studied during brain development. 1) NiA-deficient rats and rats receiving 3-acetylpyridine (3-AP) showed lower values in yield of myelin, content of cerebrosides and specific activity of 2', 3'-cyclic nucleotide-3-phosphohydrolase (CNP), when compared with those of pair-fed and ad libitum controls. 2) Despite the changing yield of myelin, the ratio of protein to total lipids, and the percentage composition of lipids were not different between the groups fed on the NiA-deficient and the NiA-supplemented diet. 3) The ratio of long chain nonhydroxy fatty acid (C_<20-24>/C_<14-18>) and synthesis of cerebrosides with nonhydroxy fatty acid were markedly decreased in NiA-deficient rats. 4) The transfer of cerebrosides from the site of synthesis (microsome) to the site of myelin assembly was not impaired in NiA-deficient rats. 5) Biosynthetic activity of lipids in brain slices, and the activities of the microsomal fatty acid elongating system in the brain were decreased in the NiA-deficient rats and rats receiving 3-AP. 6) The rats receiving 3-AP and pair-fed control showed lower values of DNA and RNA in the brain and the concentration of thyroid hormon in the serum when compared with ad libitum control. These results indicated that undernourishment from restricted food intake imposed during the brain development caught up to some extent. Our observations suggest that NiA can influence myelination through the metabolism of cerebrosides which contain long-chain fatty acids.
