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为了进一步阐明氟中毒时肾脏损伤是否与脂质过氧化反应增强有关，特用含氟饮水给Wistar大鼠染氟，造成慢性氟中毒后，检查其肾脏超微结构变化，同时测定肾组织中SOD活性及MDA含量，并观察绞股兰皂甙-丹参复方中药抗氧化剂对肾脏损伤有无须防作用。取Wistar大鼠40只，随机分为3组：1组为正常对照组；2组为染氟对照组；3组为复方中药-染氟组。结果显示：与1组相比，2组动物尿氟、肾组织氟含量明显高于正常，血、肾SOD活性显著低于正常，肾MDA含量显著高于正常，电镜检查发现近曲小管上皮细胞变性；复方中药-染氟组，肾氟含量低于染氟对照组，血、肾SOD活性及MDA含量均保持在正常水平，肾小管上皮细胞超微结构无明显变化。结果提示：慢性氟中毒对肾小管上皮细胞有损伤作用，其机制可能与氟使肾组织内SOD活性降低及脂质过氧化过程加强有关；复方中药抗氧化剂能升高体内SOD活性，消除氟中毒时通过自由基对肾小管上皮细胞的脂质过氧化损伤作用。
In order to further clarify whether renal damage caused by fluorosis is related to the enhancement of lipid peroxidation, fluorine-containing drinking water is used to stain the Wistar rats with fluorine, which causes chronic fluorosis. The renal ultrastructural changes were examined. Activity and MDA content, and observed Gynostemma glycosides - Danshen compound Chinese medicine anti-oxidant on kidney injury with or without preventive effect. Forty Wistar rats were randomly divided into three groups: one group as normal control group, two groups as control group and three groups as compound traditional Chinese medicine-fluoride group. The results showed that compared with group 1, the fluorine content in urinary and renal tissues of the two groups was significantly higher than that of normal group. The SOD activity in blood and kidney were significantly lower than that in normal group. The content of MDA in kidney was significantly higher than that in normal group. Electron microscopy revealed that proximal tubular epithelial cells Dextran; compound Chinese medicine - dye fluorine group, the renal fluorine content was lower than the fluoride control group, blood, kidney SOD activity and MDA levels were maintained at normal levels, no significant changes in renal tubular epithelial ultrastructure. The results suggest that chronic fluorosis can damage renal tubular epithelial cells, and its mechanism may be related to the decrease of SOD activity and the increase of lipid peroxidation in renal tissue by fluoride. Antioxidant compound can increase SOD activity in vivo and eliminate the toxic effects of fluorosis When the free radicals on the renal tubular epithelial cells by lipid peroxidation injury.