摘要
目的观察慢性氟中毒大鼠肾脏细胞线粒体分裂蛋白Fisl表达和线粒体超微结构改变，探讨其在慢性氟中毒肾脏细胞线粒体损伤中的机制。方法将60只SD大鼠按性别和体质量随机分为3组：对照组、低氟组、高氟组，每组20只，分别饮用加入0、10、50mg／L氟化钠的自来水。6个月时，采用实时荧光定量PCR和免疫组织化学技术检测肾脏细胞FislmRNA和蛋白表达，采用电镜观察肾脏细胞线粒体形态。结果与对照组大鼠（28．70±12．41）比较，低、高氟组大鼠肾脏细胞FislmRNA表达（91．48±34．83和582．09±184．69）明显升高（P均〈0．05）；低、高氟组大鼠肾脏Fisl蛋白表达（16．33±10．26和21．50±5．24）与对照组（10．49±7．66）比较，有增高趋势，其中高氟组明显高于对照组（P〈o105）；电镜下，低、高氟组大鼠肾脏细胞线粒体嵴模糊或消失，出现线粒体分裂截面。结论慢性氟中毒可致肾脏细胞线粒体损伤，诱导Fisl在转录水平和蛋白水平表达，致线粒体融合分裂障碍和线粒体超微结构异常，该过程在慢性氟中毒大鼠肾脏细胞线粒体损伤的发生机制中可能起重要作用。
Objective To observe the expression of mitochondrial fission protein locus Fisl and ultrastruetural changes in the renal cells of rats with chronic fluorosis, and to reveal the mechanism in mitochondrial damage of the renal cells. Methods Sixty SD rats were randomly divided into 3 groups according to sex and body mass （20 in each group） ： control group, lower fluoride group and higher fluoride group. All the rats were fed with different doses of sodium fluoride in drinking water（0, 10 and 50 rag/L, respectively）. Six-month later, the expression of Fisl in renal cells was determined by real-time fluorenscence quantitative PCR and immunohistoehemistry technology, the mitoehondrial morphology of renal cells was observed under transmission electron microscopy （TEM）. Results As compared with the control group（28.70 ± 12.41）, Fisl mRNA levels（91.48 ±34.83 and 582.09 ± 184.69） in renal cells of the lower fluoride and the higher fluoride groups were increased（all P 〈 0.05）. As compared with the control group（10.49 ± 7.66）, Fisl protein levels（16.33 ± 10.26 and 21.50 ± 5.24） in renal cells of the lower fluoride and the higher fluoride groups showed a trend of increasing, the higher fluoride group was higher than that of the control group（P 〈 0.05）. By TEM, mitochondrial crest in renal cells of the lower fluoride and the higher fluoride groups was vague or disappeared, mitochondrial division section appeared. Conclusions Fluoride is a kind of toxicant that can cause damage to mitochondrion of renal cells, induce the expression of Fisl in transcriptional and protein level, and lead to the obstacles of mitochondrial fusion-fission and ultrastructural abnormality of mitochondrion, which may play an important role in mechanism of mitochondrial damage in the renal ceils of rats with chronic fluorosis.
出处
《中华地方病学杂志》
CAS
CSCD
北大核心
2013年第2期125-128,共4页
Chinese Journal of Endemiology
基金
国家自然科学基金（81160335）
国际科技合作（2010DFB30530）
科技部支撑计划课题（2011BAZ03220）
贵州省科技厅项目（黔科合外G字[2011]7014号）
关键词
氟中毒
大鼠
线粒体分裂蛋白Fis1
线粒体超微结构
Fluomsis
Rats
Mitochondrial fission protein locus Fis 1
Ultrastructure of mitochondrion
