Guan Z Z, Xiao K Q, Zeng X Y, Long Y G, Cheng Y H, Jiang S F, Wang Y N
Department of NEUROTEC, Huddinge Hospital B84, Karolinska Institutet, Sweden.
Arch Toxicol. 2000 Dec;74(10):602-8. doi: 10.1007/s002040000177.
An animal model of chronic fluorosis was produced by subjecting Wistar rats to high doses of fluoride in drinking water for a prolonged period. Phospholipid and neutral lipid contents in rat kidney were then analyzed by high-performance liquid chromatography (HPLC), and fatty acid compositions from individual phospholipids were measured by gas chromatography. Lipid peroxidation was detected by the thiobarbituric-acid-reactive substance assay. Results showed that the total phospholipid content significantly decreased in the kidney of the rats treated with high doses of fluoride and the main species influenced were phosphatidylethanolamine (PE) and phosphatidylcholine (PC). Decreased proportions of polyunsaturated fatty acids were observed in PE and PC in kidney of fluoride-treated animals compared to controls. No changes could be detected in the amounts of cholesterol and dolichol in kidneys between the rats treated with fluoride and controls. A significant decrease of ubiquinone in rat kidney was observed in the groups treated with excessive fluoride. High levels of lipid peroxidation were detected in kidney of the rats with fluorosis. It is plausible that the specific modification of lipid composition results from lipid peroxidation. The oxidative stress and modification of cellular membrane lipids may be involved in the pathogenesis of chronic fluorosis and provide a possible explanation for the gross system damage observed in the body, especially in soft tissues and organs.
通过让Wistar大鼠长期饮用高剂量氟化物来建立慢性氟中毒动物模型。然后用高效液相色谱法（HPLC）分析大鼠肾脏中的磷脂和中性脂质含量，并用气相色谱法测量各个磷脂的脂肪酸组成。通过硫代巴比妥酸反应物质测定法检测脂质过氧化。结果显示，高剂量氟化物处理的大鼠肾脏中总磷脂含量显著降低，受影响的主要磷脂种类是磷脂酰乙醇胺（PE）和磷脂酰胆碱（PC）。与对照组相比，氟化物处理动物肾脏中的PE和PC中多不饱和脂肪酸比例降低。氟化物处理大鼠与对照组之间肾脏中胆固醇和多萜醇的含量未检测到变化。在过量氟化物处理组中观察到大鼠肾脏中泛醌显著减少。在氟中毒大鼠的肾脏中检测到高水平的脂质过氧化。脂质组成的特定改变可能是由脂质过氧化引起的。氧化应激和细胞膜脂质的改变可能参与慢性氟中毒发病机制，并为在体内观察到的总体系统损害，特别是在软组织和器官中的损害提供一种可能的解释。
