氯丙烯引起神经细胞钙稳态失衡及细胞骨架损伤  

Unbalanced calcium homeostasis and cytoskeleton injury in nerve cells induced by allyl chloride

作　　者：谢克勤[1] 孙克任[1] 杨东昌[1] 高树君[1] 厉保秋[1] 张磊[1] 

机构地区：[1]山东医科大学毒理研究室

出　　处：《中国药理学与毒理学杂志》1995年第4期292-295,共4页Chinese Journal of Pharmacology and Toxicology

基　　金：国家自然科学基金

摘　　要：用鸡胚脑和兔脑神经细胞研究了氟丙烯（ＡＣ）作用下的细胞内游离钙浓度（［ｃａ２＋］ｉ），细胞骨架形态，细胞骨架蛋白的合成及单位面积离体管蛋白聚合数量的改变。结果显示，在ＡＣ的作用下，［Ｃａ２＋］ｉ随着毒物浓度增高而明显增加；光镜下细胞骨架形态也随ＡＣ增加而由网状分布到断裂，破碎，最后仅剩下细胞核；细胞骨架蛋白的合成随毒物浓度的增高而明显抑制；Ｃａ２＋直接抑制离体管蛋白聚合；随着ＡＣ的浓度增高，单位面积内管蛋白聚合的数量也下降。研究提示ＡＣ引起的周围神经病可能与细胞内Ｃａ２＋稳态失衡及细胞骨架受损有关．Using nerve cells from chicken em-bryo and rabbit brain, the changes of intracellular freecalcium([ Ca2+]i),cytoskeleton morphology,cytoske-leton protein synthesis and tubulin polymerization in-duced by allyl chloride were studied,The results hadshown that after the addition of allyl chloride,[Ca2+]i was significantly increased,cytoskeleton mor-phology was obviously changed from normal to disor-der and breakage,cytoskeleton protein synthesis wasmarkedly inhibited.Ca2+ directly inhibited tubulinpolymerization in vitro and the amount of tubulinpolymerization into microtubules fell down. The studyrevealed that allyl chloride could induce unbalancedintracellular calcium homeostasis,cytoskeleton injury,and toxic peripheral neuropathy as well.

关 键 词：氯丙烯 钙 微管蛋白 细胞骨架 神经毒理学 

分 类 号：R992[医药卫生—毒理学]