摘要
目的探讨硒对氟中毒致大鼠肝脏损伤的干预作用。方法以不同方式(先分别喂饲0.375、0.75和1.5mg/L亚硒酸钠溶液6个月,再喂饲50mg/L氟化钠溶液6个月或先饲喂50mg/L氟化钠溶液6个月,再分别饲喂0.375、0.75和1.5mg/L亚硒酸钠溶液6个月)喂饲大鼠,对大鼠肝脏进行组织病理学观察,并测定肝组织谷胱甘肽过氧化物酶(GSH-Px)及超氧化物歧化酶(SOD)活力、丙二醛(MDA)含量及核转录因子κB(NF-κB)表达水平。结果 (1)预防组系列:与先水后氟(水—氟)对照组比,先低硒后氟组(低硒—氟)GSH-Px、SOD活力显著升高(P<0.05);先中硒后氟组(中硒—氟)GSH-Px活力显著升高(P<0.05);各先硒后氟组MDA含量均显著降低(P<0.05)。(2)治疗组系列:与先氟后水(氟—水)对照组比,先氟后低硒组(氟—低硒)和先氟后高硒组(氟—高硒)GSH-Px活力显著升高(P<0.05);先氟后中硒组(氟—中硒)SOD活力显著升高(P<0.05);各先氟后硒组MDA含量均显著降低(P<0.05)。结论硒对氟中毒致大鼠肝脏损伤有一定的干预作用,预防效果好于治疗效果,其中0.375mg/L是本实验条件下硒对慢性氟中毒致大鼠肝脏损伤的最佳预防作用浓度。
Objective To further explore the intervention of selenium on liver impairment induced by chronic fluorosis in rats. Methods Animals were divided into 8 groups and treated by different programs （In the 4 prevention groups, 0, 0. 375, 0.75 and 1.5mg/L sodium selenite solution were given for 6 months and then 50mg/L fluoride solution for another 6 months. In the 4 treatment groups, 50mg/L fluoride solution was given for 6 months and then 0, 0. 375, 0.75 and 1.5mg/L sodium selenite solution for another 6 months）. The pathological change of liver was observed. The activities of GSH- Px, SOD, the level of MDA and the expression of NF-KB in liver were also determined. Results In the prevention groups, the activity of GSH-Px in the LSe--F and MSe--F groups was higher than the noSe--F control group （P 〈 0.05）. The activity of SOD in the LSe--F group was higher than the noSe--F control group （P 〈 0.05）. The MDA levels in LSe--F, MSe--F and HSe--F groups were lower than the noSe--F control group （P 〈 O. 05）. In the treatment groups, the activity of GSH-Px in the F--LSe and F--HSe groups was higher than the F--noSe control group （P 〈 O. 05 ）. The activity of SOD in the F--MSe group was higher than the F--noSe control group （P 〈 O. 05 ）. The MDA levels in the F--LSe, F--MSe and F--HSe groups were lower than the F--noSe control group （P 〈 O. 05）. Conclusion There were a certain effects of selenium intervention on liver impairment induced by chronic fluorosis in rats. The preventive effect of selenium was better than the therapeutic effect, and the level of O. 375mg/L Na2SeO3 was considered as the optimal concentration for the prevention of liver impairment induced by chronic fluorosis under this experimental condition.
出处
《卫生研究》
CAS
CSCD
北大核心
2012年第4期627-631,共5页
Journal of Hygiene Research
基金
国家自然科学基金(No.30872195)
浙江省自然科学基金(No.Y2100431)
关键词
硒
氟中毒
肝脏
脂质过氧化作用
核转录因子ΚB
selenium, chronic fluorosis, liver, lipid peroxidation, nuclear factor kappa B
