自由基与氧化应激在氟中毒骨病变发生中的作用

The role of free radical and oxidative stress in the development of bone lesion in fluorosis

本实验用常规兔饲料饲养家兔，经饮水投氟复制家兔氟中毒模型，检测了自由基代谢指标，表明红细胞超氧化物歧化酶（Ｃｕ－Ｚｎ－ＳＯＤ）、全血谷胱甘肽过氧化物酶（ＧＳＨ－Ｐｘ）等抗氧化酶类测定结果，投氟组与对照组间无显著差异。血清脂质过氧化物（ＬＰＯ）水平高剂量投氟组与对照组未见明显差异，中剂量投氟组较对照组反而降低。用ＥＳＲ测骨组织的自由基信号，高、中剂量投氟组均显著高于对照组。表明氟中毒时可发生自由基增多。自由基和氧化应激改变与过量氟所致骨相或非骨相损害之间缺乏明确的相关性，目前尚得不出氧化应激参与氟中毒骨病变发生机理的结论。

In fluoride-feeding experiment, the free radical metabolism indices were observed. The anti oxidant enzymes such as Cu, Zn, SOD and GSH-Px activities of experimental animals has no obvious difference from those of control animals, serum LPO level ill high-level fluoride group has no obvious difference from that of control animals. But serum LPO level in moderate dosage fluoride group become lowered. Bone free-radical signals were measured using electronic spin resonance(ESR) Method The free-radical signals of both moderate dosage and high dosage fluoride group were both much higher than those of control group. Pathogenesis of fluorosis is related with free radical metabolism. It has been shown the shortage of definite relationship between free radical indices and bone pathological change from the experiment results. We still do not get the conclusions that free radical participates in the mechanism of pathological change due to skeletal fluoride-poisoning.