摘要
目的研究过量摄入氟对大鼠神经系统损伤过程脑细胞氧化应激相关指标和脑细胞周期变化与细胞凋亡率的关系。方法应用饮水加入氟化钠进行大鼠染毒实验,测定大鼠脑细胞谷胱甘肽过氧化物酶(GSH-Px)活性、超氧化物歧化酶(SOD)活性和脂质过氧化终产物丙二醛(MDA)产生水平以及脑细胞周期变化及细胞凋亡率。结果过量氟可使脑细胞氧化应激能力发生改变,SOD活力水平投氟实验组与对照组相比差异不明显(P>0.05),在投氟实验组MDA生成与对照组相比差异不明显(P>0.05),慢性氟中毒大鼠GSH-Px活力增高,在低钙投氟组高于低钙对照组差异显著(P<0.05);低钙饲养组脑细胞增殖能力普遍降低,S期细胞比例降低,脑细胞凋亡率高钙投氟组与高钙对照组相比差异不明显(P>0.05),低钙投氟组明显高于低钙对照组差异显著(P<0.001);低钙投氟组大鼠GSH-Px活力增高与脑细胞凋亡率呈正比。结论过量氟所致的大鼠脑细胞增殖能力下降和脑细胞凋亡率增高,与氟神经毒性作用机制有关,低钙营养可加重氟的神经毒性作用;过量氟可引起脑细胞抗氧化酶类发生不同程度的变化,其中抗氧化酶类活性增强可能是脑神经细胞对氧化侵袭的自身保护性生理调节作用的表现;氧化侵袭对神经系统损伤的确切机制尚需进一步研究。
Objective To study the effect of intake of excessive fluoride on oxidative stress relating indicators and cell cycle and apoptosis rate in process of nerve system injury of rat brain. Methods fluorosis rat were made by drinking diet water with sodium fluoride. GSH-Px activity and the level of SOD and MDA, and also cell cycle and apoptosis rate were tested in rat brain. Results Excessive fluoride may changes oxidative stress status of brain cell, both SOD and MDA level in the fluoride exposed group were not obviously altered than that in the control group （P 〈 0.05）. GSH-Px activity was significantly increased in fluorosis rat, it is higher in the group of low calcium ＋ fluoride than in low calcium control group （P 〈 0.05）. In low calcium group, the proliferative ability of brain cell was commonly decreased, and propotional rate of cell in S phase was low. Apoptotic rate of brain cells in the group of high calcium ＋ fluoride had no difference compared with high calcium control group （P 〉 0.05）, but it was obviously higher in the group of low calcium ＋ fluoride than that in The activity of SOD was lower in the group of low calcium ＋ fluoride than that in low calcium control group （P 〈 0.001）. The increase of GSH-Px activity in the group of low calcium ＋ fluoride was positively proportional to the apoptotic rate of brain cells in rats. Conclusions The decrease of proliferative power and the increase of apoptotic rate in brain cells of rat caused by intake of excessive fluoride was correlated with the mechanism of fluoride neurotoxicity, low calcium may aggregate the role of fluorideneurotoxicity; Excessive fluoride could lead to the changes of anti - oxidases in various degree, among them, the increase of anti - oxsidase activity may be the physiologic-protective regulatory action against oxidative stress of brain nerve cells; The definite mechanism of nerve system injury caused by oxidative stress need further studied.
出处
《中国地方病防治》
CAS
北大核心
2006年第1期7-9,共3页
Chinese Journal of Control of Endemic Diseases
基金
国家自然科学基金重点项目(39730390)
关键词
氟中毒
脑细胞
氧化侵袭
细胞凋亡
Fluorosis
Brain cells
Oxidative stress
Apoptosis
