摘要
目的动态观察亚慢性氟中毒大鼠骨组织的超微结构变化，分析亚慢性氟中毒大鼠骨组织病变特征。方法将雄性Wistar大鼠按体质量随机分成2个组，氟化钠组每日饮用含氟150mg／L的氟化钠水溶液，正常对照组饮用自来水，共饲养6个月，每月处死1批大鼠，光镜观察长骨干骺端的病变特点，常规透射电镜观察骨组织中各细胞成分的超微结构病变特点。结果成功地复制出了大鼠氟中毒的模型：随着染氟时间的延长，氟化钠组大鼠的骨小梁密度同对照组相比明显增加。电镜观察中可见氟中毒组大鼠骨细胞变性坏死明显，成骨细胞和破骨细胞都异常活跃，其细胞器结构都有不同程度的损伤：破骨细胞表现为溶酶体数量减少并伴有溶酶体酶的合成减少。结论高剂量氟可以直接对大鼠骨组织中的各种细胞成分造成破坏，并不同程度地促进成骨细胞和破骨细胞的活跃，最终表现为骨转换增强。
Objective To observe and analyze the pathologic change of bone ultrastructure in the progression of subchronic fluorosis. Methods Male Wistar rats were randomly divided into two groups according to body weight, i.e. sodium fluoride group and normal control group. Sodium fluoride group was given drinking water with 150 mg/L sodium fluoride, and normai control group was given only distilled water. The animals were bred for six months. Every month some rats were sacrificed for pathologic study of metaphysis of long bone by light microscope and for the observation of the change of bone ultrastructur by routine transmission electron microscope. Results The rat fluorosis model was established. With time of exposure of fluorine, the density of bone trabecula in the sodium fluoride group was markedly higher than that in the normal control group. Under electron microscope, more cell degeneration and necrosis of bone cell were observed, and abnormal proliferation of osteoblast and osteoelast were found. Structure of organell was damaged to different extent, and the number of lysosome and synthesis of lysosoma enzyme in osteoclast were decreased. Conclusion Fluoride at high level could continuously destroy cell organell of bone, promote activity of osteoblast and osteoclast to different extent and finally reinforce bone turnover.
出处
《中国地方病学杂志》
CAS
CSCD
北大核心
2007年第1期18-21,共4页
Chinese Jouranl of Endemiology
基金
国家自然科学基金资助项目（30371251）
