CAJ | 학술논문

目的观察慢性氟中毒大鼠肾脏细胞线粒体分裂蛋白Fis1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、50 mg/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Fis1 mRNA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Fis1 mRNA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Fis1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＜0.05)；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Fis1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.
목적 관찰만성불중독대서신장세포선립체분렬단백Fis1표체화선립체초미결구개변,탐토기재만성불중독신장세포선립체손상중적궤제.방법 장60지SD대서안성별화체질량수궤분위3조:대조조、저불조、고불조,매조20지,분별음용가입0、10、50 mg/L불화납적자래수.6개월시,채용실시형광정량PCR화면역조직화학기술검측신장세포Fis1 mRNA화단백표체,채용전경관찰신장세포선립체형태.결과 여대조조대서(28.70±12.41)비교,저、고불조대서신장세포Fis1 mRNA표체(91.48±34.83화582.09±184.69)명현승고(P균＜ 0.05)；저、고불조대서신장Fis1단백표체(16.33±10.26화21.50±5.24)여대조조(10.49±7.66)비교,유증고추세,기중고불조명현고우대조조(P＜0.05)；전경하,저、고불조대서신장세포선립체척모호혹소실,출현선립체분렬절면.결론 만성불중독가치신장세포선립체손상,유도Fis1재전록수평화단백수평표체,치선립체융합분렬장애화선립체초미결구이상,해과정재만성불중독대서신장세포선립체손상적발생궤제중가능기중요작용.
Objective To observe the expression of mitochondrial fission protein locus Fis1 and ultrastructural 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 mg/L,respectively).Six-month later,the expression of Fisl in renal cells was determined by real-time fluorenscence quantitative PCR and immunohistochemistry technology,the mitochondrial morphology of renal cells was observed under transmission electron microscopy (TEM).Results As compared with the control group(28.70 ± 12.41),Fis1 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 Fis1 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 cells of rats with chronic fluorosis.