摘要
目的：为探讨金属离子络合及ＶｉｔＢ６代谢障碍在二硫化碳（ＣＳ２）神经毒作用中的作用；方法：测定ＣＳ２染毒大鼠脑组织中微量元素铜的含量，并用ＶｉｔＢ６及谷胱甘肽（ＧＳＨ）进行干预。以ＳＤ雄性大鼠为中毒模型，检测不同浓度（０，３００，６００，１２００，２４００ｍｇ／ｍ３）染毒两个月后脑组织铜的含量；同时在高浓度（２４００ｍｇ／ｍ３）组给予两种干预药物：ＧＳＨ（１００ｍｇ／ｋｇ，腹腔注射，一次／日），ＶｉｔＢ６（灌胃，一次／日，０．４ｍｇ／日），观察对大鼠行为及酶活性的影响。结果：ＣＳ２染毒大鼠脑组织铜含量无明显改变；ＧＳＨ，ＶｉｔＢ６对ＣＳ２致运动协调能力障碍无明显改善，对反映学习记忆能力的指标（步下法）有改善作用；ＧＳＨ对Ｎａ＋－Ｋ＋－ＡＴＰ酶活性有升高作用。结论：ＣＳ２所致中枢神经系统与外周神经系统毒性在机制上可能有所不同。
Two long held hypotheses to explain mechanism of carbon disulfide are metal ion chelation and induction of vitamin B 6 dificiency. This study detect the content of copper in rats exposed to CS 2 at the concentration of 0,300,600,1200,or 2400mg/m 3 for two months and provide glutathione (GSH)(100mg/kg,ip,1 time per day)and vitamin B 6 (0.4mg/day,oral) in 2400mg/m 3 CS 2 exposed group.The result showed that no significant effect was found in the content of copper.Two behavior tests:rotarod test and step down revealed significant decrease in CS 2 exposed rats.Two interfering groups have an improvement in rotarod test,while no improvement in step down test.The activity of Na + K + ATPase was increased in GSH interfering group.
关键词
二硫化碳
谷胱甘肽
维生素B6
Carbon disulfide Behavior Glutathione Vitamin B 6 Na + K + ATPase
