Tennekoon G, Aitchison C S, Frangia J, Price D L, Goldberg A M
Ann Neurol. 1979 Jun;5(6):558-64. doi: 10.1002/ana.410050611.
The effects of chronic lead intoxication were studied by examining the optic nerve of mice given lead-containing mother's milk from day 1 to day 21 of life. Biochemical assays for myelin basic protein, 2',3'-cyclic nucleotide phosphodieterase, and cerebroside sulfotransferase showed that the total amount of myelin produced by the lead-exposed animals was decreased. Lead exposure did not alter the number of oligodendroglia or the relationship between axons and myelin sheaths. The hypomyelination was paralleled by a reduction in size of optic axons in the lead-exposed animals. The data suggest that chronic exposure to lead in developing mice results in a primary effect on neurons and that hypomyelination is secondary to reduction in axon size.
通过检查出生第1天到第21天食用含铅母乳的小鼠的视神经,研究了慢性铅中毒的影响。对髓鞘碱性蛋白、2',3'-环核苷酸磷酸二酯酶和脑苷脂硫酸转移酶的生化分析表明,接触铅的动物产生的髓鞘总量减少。铅暴露并未改变少突胶质细胞的数量或轴突与髓鞘之间的关系。在接触铅的动物中,髓鞘形成不足与视神经轴突大小的减小同时出现。数据表明,发育中小鼠长期接触铅会对神经元产生原发性影响,髓鞘形成不足是轴突大小减小的继发结果。