锰接触所引起全血中PARK2基因表达变化

目的通过比较染锰大鼠和锰接触职业工人全血中PARK2基因表达的变化,探索锰所致神经系统危害的早期生物标志和可能的作用机制。方法雄性SD大鼠24只随机分为对照组（n=8）,低剂量组（n=8）和高剂量组（n=8）。通过腹腔注射锰溶液（0、1、5mg/kg）每周5次,共4周。石墨炉原子吸收光谱法测全血中锰的含量;实时荧光定量聚合酶链反应（RT-PCR）法测PARK2基因的表达。结果大鼠高剂量、低剂量与对照组比较,高剂量组PARK2基因表达明显下降;锰接触职业工人比非锰接触职业工人PARK2基因表达下降。结论大鼠和职业工人的全血中PARK2基因的表达变化一致,全血中PARK2基因的表达变化可作为锰中毒的早期生物标志;PARK2基因异常导致UPP途径紊乱可能是锰引起神经中毒的一个作用机制。

PARK2 expression alteration in the blood of manganese exposed animal and human beings

Objective To Explore the mechanism ofmanganism by comparing the PARK2 expression in the blood of man- ganese exposed to rats and occupational manganese exposure subjects, and to know whether PARK2 can work as an early biomarker ofmanganism injury in the central nervous system. Methods Twenty four rats were randomly divided into three groups： low dosage group （LD group, n=8）, high dosage group （HD group, n=8） and control group （n=8）, respectively. Rats received MnCL2 （0, 1, 5 mg/kg, i.p.） 5 time per week for 4 weeks. The manganese level and PARK2 expression both in the blood of the rat and in the blood of manganese exposure workers were measured by atomic absorption spectroscopy （AAS） and RT-PCR respectively. Results The PARK2 expression decreased both in the manganese exposed rats and in the occupational exposure workers. Conclusion The PARK2 expression alteration in the blood could work as the early manga- nese toxicity biomarker. Abnormal PARK2 expression might be a mechanism of manganism in the brain by disturbing the