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作 者:唐玲芳[1] 陈砚朦[1] 张珍玲[1] 宋玲[1] 杨永年[1] 冯致英[1]
机构地区:[1]南京医科大学卫生毒理学教研室,南京210029
出 处:《癌变.畸变.突变》1999年第6期337-339,共3页Carcinogenesis,Teratogenesis & Mutagenesis
基 金:卫生部科学研究基金;江苏省卫生厅资助
摘 要:采用体外高速梯度离心分离提取的小鼠脑突触小体,观察钙调素拮抗剂对镉接触脑突触小体中3 H- 亮氨酸掺入蛋白质合成的影响。结果表明镉( Cd) 抑制3 H- 亮氨酸掺入突触小体蛋白质合成,3 H- 亮氨酸掺入量与镉浓度呈负相关。这一作用可被钙调素拮抗剂氯丙嗪一定程度上拮抗。提示钙调素参与镉的毒性作用机制。The isolated mice brain synaptosome was measured in vitro. The experiment explored protein biosynthesis by \+3 H-Leu incorporation technique, meanwhile, the influence of Calmodulin(CaM) inhibitor Chlorpromazine(CPZ) on this toxicity was investigated as well. The result indicated that Cd prevented \+3 H-Leu from incorporating into synaptosome, in which the concentration of Cd and the amount incorporated showed negative correlation and this toxic effect may be antagonized by CaM inibitor CPZ to some extend. It is concluded that CaM may be involved in the mechanism of Cd toxicity in brain synaptosome.
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