目的　探讨铁剂对黑质多巴胺 (DA)能神经元的毒性作用 ,为阐明帕金森病 (PD)发病机制提供资料。　方法　将铁剂定向注射至大鼠一侧黑质 ,6周后通过酪氨酸羟化酶 (TH)免疫组化染色观察黑质DA能神经元的损伤情况 ,高压液相色谱 电化学法 (HPLC ECD)检测DA及其代谢产物含量 ,化学分光比色法检测中脑自由基代谢变化。　结果　大剂量铁剂 (4 0 μg)可诱发大鼠黑质TH阳性细胞显著变性、丢失 ,纹状体DA及其代谢产物含量显著降低 ,中脑脂质过氧化产物丙二醛 (MDA)升高、谷胱甘肽 (GSH)含量降低。小剂量铁剂 (4 μg)无明显致TH阳性细胞丢失作用 ,但也可使中脑MDA升高。　结论　铁剂可造成中脑黑质DA能神经元变性丢失 ,铁介导的自由基生成增加在PD发病过程中起重要作用。 Objective To investigate the toxic effects of iron on dopaminergic neurons in substantia nigra and provide information for elucidating the pathogenesis of Parkinson’s disease (PD). Methods Iron was injected into the substantia nigra of one side of rats. After 6 weeks, the injury of dopaminergic neurons in substantia nigra was observed by tyrosine hydroxylase (TH) immunohistochemical staining. High pressure liquid chromatography HPLC ECD) was used to detect the contents of DA and its metabolites. The changes of free radical metabolism in midbrain were detected by chemiluminescence spectrophotometry. Results Large doses of iron (40 μg) induced markedly degeneration and loss of TH positive cells in the substantia nigra and significantly decreased the content of DA and its metabolites in the striatum. The malondialdehyde (MDA) High, glutathione (GSH) content decreased. Small dose of iron (4 μg) did not significantly reduce TH-positive cells, but also increased midbrain MDA. Conclusion Iron can cause degeneration of DA neurons in midbrain substantia nigra, and the increase of iron-mediated free radical generation plays an important role in the pathogenesis of PD.