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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
Objective To find out the ultrastructural basis of lead neurotoxicity and the blood lead and brain lead thresholds that cause these changes. Methods Electron microscope lanthanum nitrate tracing, calcium cytochemistry and atomic absorption and other methods were used to observe the levels of blood lead and lead concentrations and the dendrites of neurons in neurons after drinking 10 and 30 mg · L -1 lead-containing water for 3 months. Membrane permeability, calcium distribution and ultrastructure of microtubules and microfilaments. Results Blood lead concentration 0. 3 1mol·L 1, no significant changes in the observed indicators; blood lead concentration 0.46mol · L 1, the observed indicators have changed. Conclusion The concentration of lead in blood exceeds a certain limit. Lead accumulates in the brain through the blood-brain barrier, which is the basis of nerve cell poisoning. As a result, microtubules within the axon are depolymerized and double-helical filaments appear, which may be the basis of lead-induced ultrastructural pathology of learning and attention impairment in workers