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目的:探讨急性氟中毒引起肝脏发生脂质过氧化程度与肝损害之间的关系。方法：以NaF0、30、60和120mg／kg灌胃，检测大鼠6、12、24和48小时急性中毒时肝还原型谷胱甘肽（GSH）、丙二醛（MDA）和甘油三酯（TG）含量及血清谷丙转氨酶（SGPT）、肝琥珀酸脱氢酶（SDHase）和葡萄糖-6-磷酸酶（G-6－Pase）活性。结果：急性氟中毒引起大鼠肝GSH含量显著降低。肝MDA和TG含量显著升高，血清SG-PT活性显著增强，肝线粒体和微粒体标志酶SDHase和G-6-Pase活性显著降低，而且在中毒48小时，肝TG含量升高和肝G-6-Pase活性降低均存在显著的剂量效应关系。结论：急性氟中毒引起肝脏损害，其损害的重要机理之一是脂质过氧化，损害的亚细胞部位可能在线粒体和微粒体。
Objective: To investigate the relationship between liver cirrhosis and lipid peroxidation induced by acute fluorosis. Methods: The levels of hepatic reduced glutathione (GSH), malondialdehyde (MDA) and triglyceride (TG) in acute poisoning rats at 6, 12, 24 and 48 h were measured by intragastric administration of NaF0, 30, 60 and 120 mg / (TG), serum alanine aminotransferase (SGPT), hepatic succinate dehydrogenase (SDHase) and glucose-6-phosphatase (G-6-Pase) activity. Results: Acute fluorosis caused a significant decrease of hepatic GSH in rats. Liver MDA and TG levels were significantly increased, serum SG-PT activity was significantly increased, liver mitochondrial and microsomal markers SDHase and G-6-Pase activity was significantly reduced, and 48 hours after poisoning, liver TG content and liver G- 6-Pase activity decreased there is a significant dose-response relationship. CONCLUSION: Acute fluorosis can cause liver damage. One of the important mechanisms of the damage is lipid peroxidation. The damaged subcellular sites may be in mitochondria and microsome.