论文部分内容阅读
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 To investigate the effect of oxidative stress on renal injury in chronic fluorosis rats. Methods Rats were exposed to fluoride for 3 months. The levels of uric acid (UA) and malondialdehyde (MDA) in serum were measured by biochemical techniques and the activities of antioxidant enzymes such as superoxide dismutase (SOD), glutathione The activity of GSH-Px was extracted. The total RNA of renal tissues was extracted and the mRNA expression of GSH-Px, SOD and Trx in tissues was detected by RT-PCR. Results The levels of GSH-Px, SOD and MDA in serum of rats fed with Freund’s Hypoglycemic rats increased to some extent, and the increase of GSH-Px was statistically significant (P <0.05), while the serum MDA Compared with the control group, the content of uric acid in serum was significantly lower than that of the control group in the 100 mg F- / L group and 100 mg F- / L group. The contents of GSH-Px, SOD and Trx in the kidney of the normal diet group increased at different levels and the SOD gene expression was significantly increased (P <0.05), and the expression of SOD gene in the kidney tissue of the partial eclipse control group Significantly increased. Conclusions The expression of antioxidant enzymes in renal tissue at a certain concentration of fluoride is consistent with the increase of serum antioxidant enzyme activity. Low-calcium synergizes with fluoride to further aggravate the oxidative stress in the kidney, Oxidative stress has a role.