摘要
目的探讨氧化应激在慢性氟中毒大鼠肾脏损伤机制的作用。方法给大鼠饮水投氟3个月,通过生化技术测定血清中尿酸(UA)与脂质过氧化产物丙二醛(MDA)的含量及抗氧化酶超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)的活力;抽提肾组织的总RNA并利用RT-PCR方法检测组织中GSH-Px、SOD、硫氧还蛋白(Trx)的mRNA表达水平。结果常食投氟组大鼠血清中GSH-Px、SOD及MDA含量均有不同程度升高,其中GSH-Px的升高有统计学意义(P<0.05),而低钙加氟组的血清MDA含量较之对照组明显升高;血清的尿酸含量在常食100 mg F-/L组和低钙100 mg F-/L组较之相应的对照组明显降低。常食投氟组肾组织的GSH-Px、SOD,Trx在mRNA水平上含量已有不同程度升高,SOD基因表达显著升高(P<0.05),偏食对照组大鼠肾组织SOD基因表达水平亦显著升高。结论一定浓度的氟刺激肾组织抗氧化酶基因的表达,与血清内抗氧化酶活性升高相一致;低钙协同氟的毒性作用,进一步加剧机体的氧化应激态,尿酸在拮抗氟引起的氧化应激中具有一定作用。
Objective The role of oxidative stress in mech - anism of kidney damage of chronic fluorosis rats was ob- served. Methods Rats were exposed to the water with fluoride for 3 months. The content of the uric acid （UA） and malondial- dehyde （MDA） and the vitality of the antioxidant enzyme superoxide dismutase （SOD） and glutathione peroxidase （GSH - Px） in the serum were determined by the methods of biochemical assay. Total RNA was extracted from kidney tissue and the expres- sion of mRNA of GSH - Px, SOD, thioredoxin （Trx） was determined in the kidney tissue by the methods of RT - PCR. Results The content of the GSH - Px, SOD and MDA were increased in serum when the rats were exposed to fluoride with normal diet and the rising of GSH - Px was statistical significance （ P 〈 0.05 ）. As compared with control group, the content of MDA in ser- um in group of low calcium and fluoride treated was significantly increased. As compared with the corresponding control group, the content of uric acid in serum in the normal diet 100 mg F-/L and low calcium 100 mg F-/L group was decreased. The con-tent of GSH - Px, SOD and Trx at the level of mRNA were increased significantly and the gene expression of SOD was significant （ P 〈0.05 ） in the kidney tissue treated with fluoride. The level of gene expression of SOD was increased significantly in the kidney tissue in the low calcium control group either. Conclusions A certain concentration of fluoride stimulated the antioxidant enzyme gene expression in kidney. It was coincident that antioxidant enzyme activity increased in the serum. The oxidative stress should exacerbate when fluoride toxicity combined with low calcium. Uric acid might relieve oxidative stress caused by fluoride.
出处
《中国地方病防治》
CAS
2009年第2期88-90,共3页
Chinese Journal of Control of Endemic Diseases
基金
国家自然科学基金项目(30700688)
吉林省科技发展计划项目(20060419-3)
