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Ｗｉｓｔａｒ大鼠饮１．５８、２．６３ｍｍｏｌ／Ｌ高氟水１４个月造成慢性氟中毒，另２组大鼠在饮高氟水同时加饲２．０ｍｇ／ｋｇ硒饲料。在氟中毒不同时期分３批测其血清、尿液氟（Ｆ）、硒（Ｓｅ）含量；全血、血清、肝、肾脏谷胱甘肽过氧化物酶（ＧＳＨ－Ｐｘ）、超氧化物歧化酶（ＳＯＤ）活性；还原、氧化型谷胱甘肽（ＧＳＨ、ＧＳＳＧ）和脂质过氧化物（ＬＰＯ）含量。结果：氟中毒大鼠尿、血Ｆ升高；血清、组织ＬＰＯ在氟中毒早、中、晚期持续升高；ＧＳＨ－Ｐｘ、ＳＯＤ和ＧＳＨ早期上升，中、晚期明显下降。提示氟中毒大鼠存在明显脂质过氧化损伤，抗氧化酶类和抗氧化剂表现为从代偿到失代偿，最终造成自由基代谢紊乱。补Ｓｅ后氟中毒大鼠尿Ｆ排泄，血Ｆ下降；ＧＳＨ－Ｐｘ、ＳＯＤ和ＧＳＨ恢复，ＬＰＯ下降。此与Ｓｅ拮抗高Ｆ及对抗氧化酶类、抗氧化剂和脂质过氧化物产生直接或间接作用有关。
Wistar rats drinking 1.58,2.63mmol / L of high-fluoride water for 14 months caused by chronic fluorosis, and the other two groups in drinking high-fluoride water while feeding 2.0mg / kg selenium feed. The contents of fluorine (F) and selenium (Se) in serum and urine were measured in 3 batches during the period of fluorosis. The content of glutathione peroxidase (GSH-Px), superoxide Dismutase (SOD) activity; Reduced, oxidized glutathione (GSH, GSSG) and lipid peroxidation (LPO) content. Results: Urine and blood F increased in fluorosis rats. Serum and tissue LPO levels continued to increase in the early, middle and late stages of fluorosis. GSH-Px, SOD and GSH increased in the early, middle and late stages. It is suggested that there is obvious lipid peroxidation injury in rats with fluorosis, and the antioxidant enzymes and antioxidants manifest from compensatory to decompensated, eventually resulting in the disorder of free radical metabolism. After Se supplementation, urinary F excretion and F decreased in Fluorosis rats. GSH-Px, SOD and GSH recovered and LPO decreased. This is related to Se’s antagonism of high F and its direct or indirect effects on antioxidant enzymes, antioxidants and lipid peroxides.