摘要
[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 study the effects of calcium on mitoehondrial injury of kidney in offspring rats following maternal fluoride treatment via water drinking. [ Methods ] A total of 100 early weaning SD female rats were randomly divided into control group, fluoride group （100mg/L NaF）, low calcium group （0.063% CaCO3）, low calcium plus fluoride group （100mg/L NaF＋0.063% CaCO3）, and high calcium plus fluoride group （100mg/L NaF＋7% CaCO3）. After three months of feeding, the rats were mated for 1 ： 1 and the 14- and 28-day-old offspring rats were sampled to determine succinate dehydrogenase （SDHase） activity, malondialdehyde （MDA） level, renal cell apoptosis, and expression levels of fission/fusion proteins Fisl, Drpl, and Mfn2 in mitochondria. [ Results ] Compared with the fluoride group, the activity of SDHase was increased in the high calcium plus fluoride group （P 〈 0.05）, and was decreased in the low calcium plus fluoride group （P 〈 0.01）. Compared with the control group, the mitochondria MDA level and the apoptosis cells of the fluoride treated groups were significantly increased. Compared with the fluoride group, the apoptosis cells were increased in the low calcium plus fluoride group and decreased in the high calcium plus fluoride group. Compared with the control group, the expression levels of fission protein Fisl were increased in the 14-day-old male offspring rats of the low calcium plus fluoride group （P 〈 0.05）; the expression levels of fission protein Drpl were increased in the 28-day-old male offspring rats of the low calcium plus fluoride group and the high calcium plus fluoride group （P 〈 0.05）. [ Conclusion ] The results suggest that kidney mitochondrial impairment is caused by fluorosis through regulating the expression of fission/fusion proteins Fisl, Drpl, and Mfn2. High calcium intake can decrease lipid peroxidation in mitochondria, thus reducing fluorosis induced cytotoxicity to offspring rat＇s renal cells, but low calcium intake can exacerbate the toxic effect.
出处
《环境与职业医学》
CAS
CSCD
北大核心
2017年第2期154-159,共6页
Journal of Environmental and Occupational Medicine
基金
国家自然科学基金(编号:81273015
81573101)
