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作 者:黄琼[1] 许月初[1] 朱惠莲[1] 蒋卓勤[1]
机构地区:[1]中山大学公共卫生学院医学营养系,广东广州510089
出 处:《卫生毒理学杂志》2002年第4期209-212,共4页Journal of Health Toxicology
摘 要:目的 主要探讨饲料钙、锌干预对脑发育期低水平铅暴露致大鼠仔鼠学习记忆障碍保护作用的可能机制。方法 大鼠孕 14d至仔鼠出生 40d饮 10 0mg L含铅水 ,进食加钙 (1 2 5 % )和加锌 (10 0mg kg)配方饲料组 ,观察仔鼠生长发育情况 ,仔鼠 40d取股动脉血分析全血铅含量 ;取右半侧大脑分析脑铅含量 ;取左侧海马和小脑分析NO含量 ,右侧海马分析蛋白激酶C(PKC)活性。结果 两干预组仔鼠脑铅平均值分别为 3 0 5和 0 62 μg g ,明显低于进食普通配方饲料组 ,而加钙组血铅平均值为 0 2 9μmol L,明显低于加锌和普通配方组 ;两干预组海马和小脑一氧化氮 (NO)平均值分别为 2 7 68和 13 82 μmol g组织蛋白 ,均高于普通配方组 ,而海马细胞胞浆蛋白激酶C活性平均值分别为 0 3 3和 0 3 8pmol (min .μg组织蛋白 ) ,均低于普通配方组。结论 饲料中钙、锌干预对低水平铅暴露致大鼠学习记忆障碍的保护作用可能与降低其体内血、脑中铅蓄积水平 。Objective The possible mechanisms of protective effects of calcium and zinc on learning and memory disorders from low level lead exposure were investigated. Methods The pups were given drinking water containting 100 mg/L lead from day 12 of gestation to 40 after birth, and separately given normal AIN\|76 TM diet, +Ca AIN\|76 TM diet (1 25%) and +Zn AIN\|76 TM diet (100 mg/kg). Results Blood and brain lead concentrations of pups fed +Ca diet (0 29 μmol/L,0 62 μg/g) and blood lead concentrations of pups fed +Zn diet (3 05 μg/g) were all significantly lower than those of pups fed normal diet. Nictric oxide (NO) mean contents of both pups fed +Ca (27 68 μmol/g protein) and+Zn diet (13 82 μmol/g protein) were significantly higher than those of pups fed normal diet ( P <0 05) Protein kinase C (PKC) activities of both pups fed+Ca\[0 33 pmol/(min·μg protein)\] and +Zn diet \[0 38 pmol/(min·μg protein)\] were significantly lower than that of pups fed normal diet ( P <0 05).Conclusion These results indicate that the possible mechanisms of protective effects of calcium and zinc on learning and memory disorders from low level lead exposure are decrease on lead accumulation, hippocampus PKC and increase in hippocampus and cerebellum NO content.
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