摘要
目的 观察超氧化物歧化酶模型配合物（MSOD）对过量摄氟大鼠的保护作用。方法Wister雄性大鼠40只,随机分为4组:对照组（A组）、氟中毒组（B组）、MSOD保护组（C组）和治疗对照组（D组）。饲养5个月后处死,取肾脏标本,在光镜和电镜下进行形态学观察。结果 光镜:A组肾小球结构完整清晰,肾小管上皮细胞无坏死及炎性细胞浸润。B组肾近曲小管上皮细胞浆中可见粉染颗粒,肾近曲小管上皮细胞胞浆疏松,可见大小不等空泡。C组同A组肾小管上皮细胞无空泡及坏死,亦无炎性细胞浸润,肾间质无血管扩张;电镜:A组肾近曲小管上皮细胞排列整齐,微细胞器呈正常态。B组肾近曲小管上皮细胞排列紊乱,胞质的线粒体增多呈圆泡状,嵴膜不清,细胞坏死。C组肾小球结构清晰,肾近曲小管上皮细胞发育良好,线粒体嵴膜清楚与对照组基本相同。D组肾近曲小管上皮细胞排列整齐,腔面微绒毛疏松,基底褶平展,线粒体以小圆形为多,粗面内质网轻度扩张,部分脱颗粒,胞质基质密度降低。结论 从形态学角度证明了长期过量摄氟后,大鼠肾脏均发生细胞和亚细胞水平损害,而MSOD保护组的显微和亚显微结构基本正常,证明MSOD可以阻断氟中毒的发生,进一步说明了氟中毒的发病与自由基密切相关。
Objective To explore the protective effects of Model SOD (SOD-model coordination compound, MSOD) on Kidney damage in rats caused by overdose fluoride.Methods Forty male Wister rats were divided randomly into four groups. These rats were sacrificed 5 months later, then the microstructure and substructure of kidney were observed by microscope and electron microscope. Results Group A: the configuration of glomerulus's was integral and clear, the necrosis and inflammatory cellular infiltrition of epithelial cells of urinif-erous tubules weren't found. Group B: the epithelial cells of convoluted renal tubules were severely damaged, the array of epithelial cells of uriniferous tubules was out of order, which were necrotic. In cells, chondriosomes looked like vacuole, the crests of which were blur. Group C: the configuration was similar to Group A. Group D: better then Group B, but no significant protective effects in this group. Conclusions This study morphologically proved that the overdose fluoride intake for a long term could cause the damage of kidney in the microstructure and ultrastructure and protected by MSOD. Thus suggestively come on the fluorosis and free radical is closely related.
出处
《中国地方病学杂志》
CAS
CSCD
北大核心
2002年第2期103-105,共3页
Chinese Jouranl of Endemiology
基金
国家自然科学基金资助项目(39470632)
