Stephens M C, Gerber G B
Toxicol Lett. 1981 Feb;7(4-5):373-8. doi: 10.1016/0378-4274(81)90063-1.
Lead (0.01% or 0.1% in the diet) was given to rats from conception to an age of 14, 21 or 32 days, and the development of brain cerebrosides, sulfatides and gangliosides was followed. Animals which had received 0.1% lead displayed a marked retardation in the onset and a reduction in the final level (at 32 days) of the lipids characteristic for the myelination process (cerebrosides and sulfatides). A slight decrease was also seen in the level of gangliosides at 32 days. It is suggested that certain aspects of lead encephalopathy might be explained by the toxic effects of lead on the glia population and the consequent interference with normal formation of myelin.
从受孕开始至14、21或32日龄,给大鼠喂食含0.01%或0.1%铅的食物,然后追踪其脑内脑苷脂、硫脂和神经节苷脂的发育情况。摄入0.1%铅的动物在髓鞘形成过程中具有特征性的脂质(脑苷脂和硫脂)的起始出现明显延迟,且最终水平(32日龄时)降低。32日龄时神经节苷脂水平也略有下降。有人提出,铅中毒性脑病的某些方面可能是由于铅对神经胶质细胞群的毒性作用以及随之而来的对正常髓鞘形成的干扰所致。