中文摘要：

目的探讨脂质过氧化损伤及内质网应激在铝致神经细胞凋亡中的作用。方法体外培养新生0～3d的大鼠神经元细胞用不同浓度氯化铝染毒。在荧光显微镜和电子显微镜下观察神经元的凋亡和内质网的形态学改变，并检测内质网的超氧化物歧化酶（SOD）活力和丙二醛（MDA）含量及ATP酶活力。结果光学显微镜和电子显微镜形态学观察发现了凋亡的典型形态学改变，电子显微镜下可观察到内质网的变形肿胀及脱颗粒现象。低剂量染毒组SOD和ATP酶的活力明显升高，与对照组比较，差异有统计学意义（P〈0．01），随染毒剂量的加大，酶活力逐渐下降；MDA含量则在低剂量染毒组[（16．42±1．50）nmol／ml]明显下降，与对照组比较，差异有统计学意义（P〈0．01），随染毒剂量的加大，MDA含量逐渐上升。结论铝能诱导神经元凋亡，内质网的脂质过氧化作用在凋亡过程中发挥了重要的调控作用。

英文摘要：

Objective To study the role of lipid peroxidation injury and endoplasmic reficulum stress in Al-induced apoptosis. Methods Neurons from 0-3 day rats were cultured and treated with different concentrations of AlCl3·6H2O. Morphologic changes of neurons and endoplasmic reticulum were Observed under fluorescent and transmission electron microscope; Activities of superoxide dismutase （SOD）, malondialdehyde （MDA） and ATP enzymes were detected. Results Typical morphologic changes in neurons apoptosis and endoplasmic reticulum were found under fluorescent and transmission electron microscope;SOD enzyme viability and ATP enzyme viability were significantly increased in the low-dosage group, but reduced in mid and highdosage group（ P〈0.01 ）, whereas MDA levels decreased in the low-dosage group, but increased in mid and high-dosage group（P〈0.01 ）. Conclusion Aluminum may induce neurons apeptosis, and lipid peroxidation injury in endoplasmic reticulum plays an important role in the apeptosis progression.