氯化镧短期重复剂量染毒对ICR小鼠遗传毒性和氧化损伤的影响

目的：研究氯化镧短期重复染毒对ICR小鼠产生的遗传毒性和氧化损伤；方法：ICR小鼠随机分为对照组、低剂量组和高剂量组，分别给予0 mg/kg、20 mg/kg、200 mg/kg氯化镧，连续灌胃7 d，测定外周血淋巴细胞微核，取脏器分别测定丙二醛（ malondiadehyde，MDA）、谷胱甘肽（ glutathione，GSH）、超氧化物歧化酶（ SuperoXide dismutase，SOD）的含量。结果：高剂量组微核率显著高于对照组（ P〈0.05）；镧元素在心脏、肝脏、脾脏和肾脏的蓄积量，高剂量组与低剂量组和对照组相比差异均有统计学意义（ P〈0.05）；高剂量组小鼠脾脏、肾脏组织中MDA含量高于对照组（ P〈0.05）；高剂量组小鼠脾脏、肾脏中 GSH、T -SOD 含量低于低剂量组和对照组（ P〈0.05）。结论：氯化镧经口染毒剂量在200 mg/kg时可在各脏器中蓄积，且可引起小鼠脏器发生氧化损伤和骨髓微核率的增加，提示200 mg/kg氯化镧对小鼠有一定的遗传毒性，氧化损伤可能是其引起遗传毒性的机制之一。

Effects of Short-term repeated EXposure to Lanthanum ChIoride on Genetic ToXicity and OXidatiVe Damage in ICR Mice

ObjectiVe：To inVestigate the genetic toXicity and oXidatiVe damage caused by short-term-repeated eXposure to lanthanum chloride in ICR mice. Methods：ICR mice were randomly diVided into the control group,the low-dose lanthanum chloride group and the high dose- lanthanum chloride group. The mice in the three groups were then giVen by gaVage 0 mg/kg, 20 mg/kg,and 200 mg/kg of lanthanum chloride,respectiVely,for 7 days consecutiVely. Micronucleus frequency in the periph-eral lymphocytes,as well as MDA,GSH and SOD in the tissues was determined. ResuIts：Micronucleus frequency in the high-dose group was significantly higher than that in the control group（ P 〈0. 05）. There was statistically significant difference in the stock Volume of lanthanum in the heart,liVer,spleen and kidney among high-dose,low-dose group and the control group （P 〈 0＆#183; 05）. MDA content in the spleen and kidney of the mice in the high-dose group was also significantly higher than that in the control group（ P 〈0. 05）,while GSH and T-SOD contents in the spleen and kidney of the mice in the high- dose of lanthanum chloride were lower,compared with the low-dose group and the control group（ P 〈0. 05）. ConcIusion：Lanthanum chloride may deposit in eVery organ when it reaches the amount of 200 mg/kg per os,resulting in oXidatiVe damage to mice organs and increases in micronucleus rate. There is a hint that 200 mg / kg of lanthanum chloride could bring about genetic toXicity to certain degree on mice,and oXidatiVe damage may be one of the mechanisms causing genetic toXicity.