【摘要】 目的　寻找铅神经毒性的超微病理学基础以及引起这些变化的血铅和脑铅阈值。方法　用电镜硝酸镧示踪 ,钙细胞化学以及原子吸收等方法 ,观察大鼠饮用 10和 3 0mg·L 1含铅水 3个月后 ,血铅与其脑铅浓度以及神经细胞轴突树突质膜通透性、钙分布以及微管、微丝超微结构变化的关系。结果　血铅浓度 0 .3 1mol·L 1时 ,观察指标无明显变化 ;血铅浓度 0 .46mol·L 1时 ,观察指标均已变化。结论　血铅浓度超过一定限度 ,铅透过血脑屏障在脑内蓄积 ,是神经细胞中毒的基础。由此造成轴突内微管解聚 ,出现双股螺旋细丝 ,可能是铅引起作业工人学习与注意力受损的超微病理学基础更多还原

【Abstract】 Objective To explore ultrastructural pathology bases of lead toxic effects on the central nervous system and the blood and the brain lead threshold levels which induce the ultrastructural pathology changes in brain. Methods Using La tracing and calcium cytochemistry techniques of electron microscope as well as atomic absorption, it was observed that the relationship between blood lead and brain lead, permeability of plasma membrane, calcium distribution as well as ultrastructural changes of microtubules and filaments in brain tissues of rats that were fed with water containing 10 and 30mg·L 1 of lead for three months. Results The observed markers were no obvious damaged as blood lead level was 0.31mol·L 1 but were all changed as blood lead level reached 0.46mol·L 1 . Conclusion It is toxic basis of neurocytes that lead seeped into brain tissues through blood brain barrier and accumulated in brain when blood lead level exceed threshold level the microtubule disintegration and paired helical filaments may be ultrastructural pathology basis for the decrease in cognitive function and attention of workers exposed to lead.更多还原