天津医药

天津医药 ›› 2015, Vol. 43 ›› Issue (10): 1110-1121.doi: 10.11958/j.issn.0253-9896.2015.10.009

• 实验研究 • 上一篇    下一篇

饮水铅暴露对大鼠脑组织过氧化氢、羟自由基和脂质过氧化的影响

  

  1. 南昌大学公共卫生学院 （邮编 330006）
  • 收稿日期:2015-04-16 修回日期:2015-05-18 出版日期:2015-10-15 发布日期:2015-10-22

Effects of lead exposure in drinking water on hydrogen peroxide, hydroxyl free radicals and#br# lipid peroxidation levels in brain tissues of rats

  1. School of Public Health, Nanchang University, Nanchang 330006, China
  • Received:2015-04-16 Revised:2015-05-18 Published:2015-10-15 Online:2015-10-22

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摘要：

摘要： 目的 探讨乙酸铅对大鼠大脑皮质、 小脑、 海马组织自由基和脂质过氧化的影响。方法 48 只刚断乳雄
性 SD 大鼠， 按体质量采用随机区组法分为 4 组 （对照组和低、 中、 高剂量组）， 对照组大鼠饮用去离子水， 低、 中、 高剂
量组分别饮用 200、 400、 800 mg/L 的乙酸铅溶液。连续染毒 60 d 后， 取血进行血铅测定， 取各组脑组织（大脑皮质、
小脑和海马）进行羟自由基抑制活力、 过氧化氢（H2O2）水平及丙二醛（MDA）含量的测定。结果 与对照组相比， 各
染铅组大鼠血铅含量显著升高， 大脑皮质、 小脑和海马组织羟自由基抑制活力明显下降， 且随染铅剂量的升高呈逐
渐下降趋势 （P < 0.05）； 大脑皮质、 小脑和海马组织 H2O2水平及 MDA 含量高于对照组， 并随着染铅剂量的升高呈逐
渐升高趋势（P < 0.05）； 大脑皮质、 小脑和海马组织的羟自由基抑制活力与血铅含量呈负相关（r 分别为-0.505、
-0.414、 -0.448， P < 0.05）， H2O2 和 MDA 含量均与血铅含量呈正相关（r 分别为 0.301、 0.411、 0.378 和 0.404、 0.324、
0.510， P < 0.05）。结论 铅可通过诱发自由基产生， 导致大鼠脑组织发生脂质过氧化反应。

关键词: 铅, 过氧化氢, 丙二醛, 羟自由基, 脂质过氧化作用, 脑组织, 大鼠, Sprague-Dawley

Abstract:

Abstract: Objective To explore the effects of lead acetate on free radicals and lipid peroxidation in the cerebral cor⁃
tex, cerebellum, and hippocampus in rat brains. Methods SD rats (n=48), who were just weaned, were randomly divided in⁃
to 4 groups base on their weight. Then the rats were fed with lead acetate in drinking water at the final concentrations of 0 mg/L
(deionized water), 200 mg/L, 400 mg/L, 800 mg/L respectively. Blood lead level as well as the hydroxyl free radical inhibiting
activity, the levels of hydrogen peroxide (H2O2) and malondialdehyde (MDA) in cerebral cortex, cerebellum, and hippocam⁃
pus were measured 60 days after lead contamination in water. Results Upon lead exposure, blood lead levels increased sig⁃
nificantly as compared with the control. The hydroxyl free radical inhibiting activity in cerebral cortex, cerebellum, and hip⁃
pocampus decreased significantly in a dose dependent manner of lead(P < 0.05). And they all correlated negatively with
blood lead level (r=-0.505,-0.414,-0.448, P < 0.05). By contrast, blood lead level was positively correlated with H2O2 and
MDA in these brain tissues (r=0.301, 0.411, 0.378, and 0.404, 0.324, 0.510， P < 0.05). Conclusion Lead exposure can
lead to lipid peroxidation of rat brain tissues through inducing free radicals.

Key words: lead, hydrogen peroxide, malondialdehyde, hydroxyl radical, lipid peroxidation, brain tissue, rats, SpragueDawley