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[目的]研究饲料钙对母鼠饮水型氟染毒后子代大鼠肾细胞线粒体损伤的影响。[方法]选用健康初断乳SD雌性大鼠100只,随机分为对照组、染氟组(100 mg/L Na F)、低钙组(0.063%CaCO_3)、低钙染氟组(100 mg/L Na F+0.063%CaCO_3)和高钙染氟组(100 mg/L Na F+7%CaCO_3);饲养3个月后,雌雄鼠合笼交配。取日龄14 d及28 d仔鼠雌雄各10只,以其肾脏细胞线粒体标志酶琥珀酸脱氢酶(SDHase)活性及脂质过氧化指标丙二醛(MDA)水平,肾脏细胞凋亡状况,线粒体分裂/融合蛋白Fis1、Drp1和Mfn2表达水平为观察指标。[结果]与染氟组相比,高钙染氟组SDHase活性升高(P<0.05),低钙染氟组SDHase活性降低(P<0.05)。与对照组相比,雌鼠各组肾脏线粒体MDA含量均升高(P<0.05)。与对照组相比,染氟各组仔鼠凋亡细胞增多;与染氟组相比,低钙染氟组凋亡细胞增多,而高钙染氟组凋亡细胞减少。与对照组相比,低钙染氟组14 d雄鼠的分裂蛋白Fis1表达升高(P<0.05);低钙染氟组和高钙染氟组28 d雄鼠的分裂蛋白Drp1升高(P<0.05)。[结论]氟中毒能够造成大鼠肾脏细胞线粒体内分裂/融合蛋白Fis1、Drp1和Mfn2表达异常,引起肾脏细胞线粒体损伤。高钙饲料摄入能降低线粒体内脂质过氧化反应,减轻高氟对子代肾脏细胞的毒性作用,而低钙饲料摄入会加剧高氟的毒性作用。
[Objective] To investigate the effects of dietary calcium on the mitochondrial damage of kidney cells in offsprings of offspring rats exposed to fluoride in drinking water. [Methods] A total of 100 female SD SD rats were randomly divided into control group (100 mg / L Na F), low calcium group (0.063% CaCO 3) and low calcium fluoride group / L Na F + 0.063% CaCO 3) and high calcium-fluoride group (100 mg / L NaF + 7% CaCO 3). After feeding for 3 months, male and female mice were caged. Ten male and 10 female offspring were selected on day 14 and day 28. The activities of SDHase, the lipid peroxidation index (MDA) and the apoptosis of renal cells , Mitochondrial fission / fusion protein Fis1, Drp1 and Mfn2 expression levels as indicators. [Result] The SDHase activity of high calcium fluoride group was higher than that of fluoride group (P <0.05), while the activity of SDHase of low fluoride group was lower (P <0.05). Compared with the control group, the content of MDA in kidney mitochondria increased in all groups (P <0.05). Compared with the control group, apoptotic cells were increased in the fluoride-exposed groups; compared with the fluoride-treated group, the apoptotic cells in the low-calcium-fluoride group increased, while the apoptotic cells in the high-calcium-fluoride group decreased. Compared with the control group, the expression of Fis1 was significantly increased in the F group (P <0.05), while the Fp protein expression in the F group was significantly higher in the F group (P <0.05) P <0.05). [Conclusion] Fluorosis can cause abnormal expression of mitochondrial Fis1, Drp1 and Mfn2 mitochondria in rat kidney cells and cause mitochondrial damage in renal cells. High calcium intake can reduce the mitochondrial lipid peroxidation and reduce the toxic effects of high fluoride on behalf of the kidney cells, and low calcium intake will exacerbate the toxic effects of high fluoride.