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目的 :探讨铅致发育期中枢神经系统脂质过氧化作用。方法 :通过大鼠孕期及哺乳期不同剂量染铅及用维生素E(VitaminE ,VE)干预所致幼鼠模型 ,测定出生后第 7,2 1d幼鼠脑的脂质过氧化产物 (lipidperoxidativeproduct ,LPO)水平 ,谷胱甘肽 (glutathione ,GSH)含量及超氧化物歧化酶 (superoxidedismutase ,SOD)、谷胱甘肽过氧化物酶 (glutathioneperoxidase ,GSH PX)、过氧化氢酶 (catalase ,CAT)活力。 结果 :无论出生后 7d还是 2 1d ,中、高剂量染铅组幼鼠脑组织LPO水平升高、SOD活力下降 (P <0 .0 5 ,P <0 .0 1) ;出生后 7d幼鼠高剂量染铅组GSH含量下降 (P <0 .0 5 ) ;出生后 2 1d中剂量染铅组CAT活力下降 (P <0 .0 5 ) ;且VE拮抗了这种脂质过氧化作用 (P <0 .0 5 )。结论 :铅可能通过增强脑组织脂质过氧化过程而致发育期神经系统的损伤。
Objective: To investigate the lipid peroxidation of the central nervous system during lead development. Methods: The lipid peroxidation products (LPO) in brain of 7th and 21st day after birth were measured by different doses of lead exposure and vitamin E (VE) intervention during pregnancy and lactation in rats. ), Glutathione (GSH) and superoxide dismutase (SOD), glutathioneperoxidase (GSH PX), catalase (CAT) . RESULTS: LPO levels in brain tissue of middle and high dose lead-exposed rats increased and SOD activity decreased at either 7d or 21d after birth (P <0.05, P <0.01); on the 7th day after birth GSH levels in high-dose lead-exposed group decreased (P <0.05); CAT activity in middle-dose lead exposed group decreased significantly (P <0.05) at 21 days after birth; and VE antagonized this lipid peroxidation P <0. 05). Conclusion: Lead may damage the nervous system during development by enhancing lipid peroxidation of brain tissue.