论文部分内容阅读
给ＳＤ大鼠饮用含氟、硒、及氟加硒的水溶液８周，观察硒对氟致肾损害的影响。结果表明：氟可使肾脏脂质过氧化物含量明显增加，肾近曲小管上皮细胞变性、坏死，线粒体数目增多，线粒体嵴减少，基底膜局部增厚，并可使肾近曲小管上皮细胞的琥珀酸脱氢酶（ＳＤＨ）和碱性磷酸酶（ＡＬＰ）活性明显降低，乳酸脱氢酶（ＬＤＨ）和酸性磷酸酶（ＡＣＰ）活性明显增高。补硒后则可促进肾脏的氟排泄，降低肾脏脂质过氧化物含量，肾脏的组织病理学和超微结构改变明显减轻，ＳＤＨ活性增加，ＡＣＰ活性降低。结果提示，硒对氟导致的肾损害具有明显的拮抗作用。
To SD rats drinking fluorine, selenium, and fluoride plus selenium aqueous solution for 8 weeks to observe the impact of selenium on renal damage caused by fluoride. The results showed that fluoride could significantly increase the content of renal lipid peroxidation, the renal proximal tubule epithelial cells degeneration, necrosis, increased number of mitochondria, mitochondrial crest, basement membrane local thickening, and renal proximal tubule epithelial cells Superoxide dismutase (SDH) and alkaline phosphatase (ALP) activity were significantly decreased, and lactate dehydrogenase (LDH) and acid phosphatase (ACP) activity was significantly increased. Selenium can promote renal excretion of fluoride, reduce renal lipid peroxidation, renal histopathology and ultrastructural changes significantly reduced, SDH activity increased, ACP activity decreased. The results suggest that selenium has a significant antagonistic effect on renal damage induced by fluoride.