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目的 探讨发育期铅暴露所致神经毒性机制。方法 母鼠从怀孕始至仔鼠出生后 7d染铅致新生大鼠染铅模型 ,测定新生大鼠血、脑铅含量 ;同时测定脑组织脂质过氧化物 (LPO)水平、谷胱甘肽 (GSH)含量及超氧化物歧化酶(SOD)活性 ;另外应用原位末端标记TUNEL法测定脑组织海马区及其附近皮质细胞凋亡数量。结果 染铅使出生后 7d幼鼠脑LPO水平升高 ,GSH含量下降 ,SOD活性降低 ,且海马区附近皮质细胞凋亡数量增加 (高剂量染铅组每计数 10 0个细胞中凋亡细胞数为 2 2 6 7± 4 0 3,而对照组为 17 44± 3 32 ,P <0 0 5。)结论 铅所致发育神经毒性可能与活性氧自由基 (ROS)增加和细胞凋亡数量升高有关
Objective To explore the mechanism of neurotoxicity induced by lead exposure during developmental period. Methods The lead-induced neonatal rat model of lead exposure was established on the 7th day after birth and the offspring of neonatal rats were sacrificed. The contents of blood and brain lead in neonatal rats were measured. The levels of lipid peroxide (LPO), glutathione (GSH) and superoxide dismutase (SOD) activity in brain tissue were detected by flow cytometry. In addition, TUNEL method was used to detect the apoptosis of hippocampus and its vicinity. Results Lead exposure increased LPO level, GSH level, and SOD activity in neonatal rats 7d after birth, and increased the number of apoptotic cortical cells in hippocampus (apoptotic cells per 100 cells in high-dose lead group) (22 44 ± 32 32, P 0 05) .Conclusion The lead-induced neurotoxicity may be associated with increased reactive oxygen species (ROS) and increased number of apoptotic cells High related