目的探讨锰超氧化物歧化酶(MnSOD)基因表达水平与锰神经毒性的关系。方法筛选31例职业性慢性锰中毒病例及31例同等暴露条件的对照组,提取全血RNA,采用反转录一聚合酶链反应(RT.PCR)法检测MnSOD基因mRNA表达水平,分析病例组与对照组间的差异;以PCI2细胞为模型,给予0、100、200、400、600、800、1000p,mol/L浓度的MnCl2分别作用1、2、3、4d,噻唑蓝(MTr)法检测细胞抑制率,RT-PCR方法检测MnSODmRNA表达水平。结果病例组与对照组MnSOD基因表达水平分别为0.390±0.080和0.582±0.219,病例组较对照组降低,差异有统计学意义(P〈0.05);MnCl2对PCI2细胞具有毒性作用,浓度越高,毒性作用越强,MnSODmRNA的表达越少。结论MnSOD基因可能参与了锰致神经细胞损伤的过程,推测其高表达可能对锰的神经毒性起到抑制作用。
Objective To investigate the relationship between mRNA expression of manganese superoxide dismutase (MnSOD) and manganese neurotoxieity. Methods Thirty-one patients with occupational chronic manganese poisoning (case group), as well as 31 controls exposed to the same condition (control group), were included in the study. Whole blood RNA was extracted, and the mRNA expression of MnSOD was measured by RT-PCR; the two groups were compared in terms of the mRNA expression of MnSOD. PC12 cells were treated with 0, 100, 200, 400, 600, 800, and 1000 p.mol/L MnC12 for l, 2, 3, and 4 d; the cell viability was determined by MTY assay, and the mRNA expression of MnSOD was measured by RT-PCR. Results The case group had significantly lower mRNA expression of MnSOD than the control group (0.390±0.080 vs 0.582±0.219, P〈0.05). MnC12 had a toxic effect on PC12 cells; the concentration of MnC12 was positively correlated with the toxic effect but negatively correlated with the mRNA expression of MnSOD. Conclusion MnSOD mRNA may be involved in the manganese-induced damage of nerve cells. It is hypothesized that high mRNA expression of MnSOD may play an inhibitory effect on manganese neurotoxicity.