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目的阐明饮水氟含量与肾脏脂质过氧化和细胞凋亡的时间效应和剂量效应关系,初步探讨二者在氟中毒肾损伤发生、发展过程中的作用。方法在饮水中加入不同剂量的氟化钠喂饲大鼠60、90、120 d后,检测肾脏细胞中MDA含量及细胞凋亡水平。结果 90 d高氟组和120 d中、高氟组MDA含量较相同时间对照组显著升高,且氟致肾脏中MDA含量增高呈明显剂量-效应和时间-效应关系;不同染毒时间下,低、中、高剂量氟诱导肾脏细胞凋亡与相同时间对照组比较差异无统计学意义。同一剂量下,不同剂量组间肾脏中MDA含量和细胞凋亡水平未见显著性差异。结论过量氟可导致机体脂质过氧化作用增强,在120 d染氟周期,一定剂量氟不能诱导肾脏发生病理性凋亡,因此,脂质过氧化是氟中毒肾损伤的始动环节,且氟致肾脏损害很可能是继发于氟作用于DNA损伤检查点中的关键分子来达成。
Objective To elucidate the relationship between fluoride content in drinking water and renal lipid peroxidation and apoptosis in time and dose-dependent manner, and to explore their roles in the occurrence and development of renal damage induced by fluoride poisoning. Methods After 60, 90 and 120 days of feeding different doses of sodium fluoride in drinking water, the content of MDA and the level of apoptosis in renal cells were detected. Results Compared with the control group, the content of MDA in 90-day high fluoride group and 120-day medium and high fluoride group increased significantly, and the dose-effect and time-effect relationship of fluoride content in kidney increased significantly. Under different exposure time, Low, medium and high doses of fluorine induced renal cell apoptosis compared with the control group at the same time no significant difference. Under the same dose, there was no significant difference in the content of MDA and the level of apoptosis between different dose groups. Conclusion Excessive fluoride can lead to the enhancement of lipid peroxidation in the body. A dose of fluorine can not induce pathological apoptosis in the kidney in a dose-dependent manner for 120 days. Therefore, lipid peroxidation is the first step of renal injury induced by fluoride poisoning. Kidney damage is likely to be secondary to fluoride acting on DNA damage checkpoints in the key molecules to achieve.