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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。
OBJECTIVE: To investigate the effect of metal ion complexation and VitB6 metabolic disorder on neurotoxicity of carbon disulfide (CS2) in rats. Methods: The contents of trace copper in brain tissue of CS2-treated rats were determined. VitB6 and glutathione ) Intervention. The SD rats were used as poisoning model to detect the content of copper in brain tissue of rats exposed to different concentrations (0, 300, 600, 1200 and 2400 mg / m3) for two months. Two interventions were given in high concentration (2400 mg / m3) Drugs: GSH (100mg / kg, intraperitoneal injection, once a day), VitB6 (intragastric administration, once a day, 0.4mg / day) were used to observe the effect on the behavior and enzyme activity in rats. Results: There was no significant change in the content of copper in brain tissue of CS2-treated rats. GSH and VitB6 had no effect on CS2-induced motor coordination disorder, which could improve the learning and memory ability (GSK) -ATP enzyme activity has increased role. Conclusion: The mechanism of CS2-induced central nervous system and peripheral nervous system toxicity may be different.