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铅对大鼠脑突触体钙调素的抑制作用
引用本文:丁训诚,郑晔.铅对大鼠脑突触体钙调素的抑制作用[J].卫生毒理学杂志,1993,7(4):209-211.
作者姓名:丁训诚  郑晔
作者单位:中国生育调节药物毒理检测中心,中国生育调节药物毒理检测中心,中国生育调节药物毒理检测中心,中国生育调节药物毒理检测中心 上海 200032,上海 200032,上海 200032,上海 200032
摘    要:用体外法,将大鼠脑突触体膜,在不同浓度的Pb~(2+)作用下分别测定CaM依赖的Ca~(2+)-ATP酶和CaM活性的IC_(50)值。结果表明,Pb~(2+)对Ca~(2+)-ATP酶活性IC_(50)为 1.62mM;对CaM活性IC_(50)为3.85mM。当向不含CaM的脑突触体加入3.0~10.0μg的外源性CaM后,被Pb~(2+)抑制的Ca~(2+)-ATP酶活性均有显著的逆转而恢复或接近正常水平。推测Pb~(2+)主要直接作用在脑突触体膜的CaM,通过CaM分子构象改变,抑制Ca~(2+)-ATP酶,这可能是铅神经毒性的分子基础。

关 键 词:  调钙蛋白  毒理学  无机毒物

Inhibition of lead on calmoduin of rat brain synaptosomes
Ding Xuncheng et al National Evaluation Centre for the Toxicology of Fertility Regulating Druges shanghai.Inhibition of lead on calmoduin of rat brain synaptosomes[J].Journal of Health Toxicology,1993,7(4):209-211.
Authors:Ding Xuncheng  National Evaluation Centre for the Toxicology of Fertility Regulating Druges shanghai
Institution:Ding Xuncheng et al National Evaluation Centre for the Toxicology of Fertility Regulating Druges shanghai 200032
Abstract:In vitro effects of lead on Ca~(2+)-ATPase of rat brain synaptosomes in the absence andpresence of calmoduin (CaM) were studied. The rat synaptic membrances were prepared andCaM was depleted by washing with 1mM EGTA. Pb~(2+). inhibited the basal as well as CaM-stimulated Ca~(2+)-ATPase in a concentration-dependent manner, suggesting the Pb~(2+) interactionwith calcium pump. Further, the inhibition of CaM-stimulated Ca~(2+)-ATPase activity by Pb~(2+)could be reversed by excessive addition of CaM. Exogenous CaM restored the Pb~(2+) inhibitedCa~(2+)-ATPase activity approximate the original level. These results suggest that Pb~(2+) mayalter calmodulin-regalated synaptic processes in the brain and could constitute a possiblemolecular mechanism for the lead nurotoxicity.
Keywords:Lead  Calmodulin  Ca~(2+)-ATPase
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