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机构地区:[1]北京医科大学神经科学研究中心,北京医科大学生理教研室,大连医学院生化教研室
出 处:《中华劳动卫生职业病杂志》1994年第5期269-271,共3页Chinese Journal of Industrial Hygiene and Occupational Diseases
摘 要:观察了四氯化碳(CCl4)中毒时大鼠肝脏鞘糖脂总量及其组成的变化。结果表明:CCI4染毒后,神经节苷脂和中性鞘糖脂总量均有所增加;神经节苷脂GD3和GM1组分分别在染毒12h和24h后明显增加;染毒24h后还出现了正常鼠肝中未检测出的GM2组分。中性鞘糖脂在染毒24h和48hCTH组分明显增加,并于48h出现了CXH未知新组分。这提示CCI4中毒后,鼠肝的鞘糖脂组成与含量均有变化,但其意义尚待阐明。Rats were treated by gastrogavage of CCI4 and sacrified after l2,24,48 hours,respectively. Using solvent ex-traction and column chromatography,the total gangliosides( GLS))and totaI neutral glycosphingolipid(NGSL) were separated and purified,and the amount were expressed by LBSA and sphingosine contents,respectively.TheresuIts showed that CCI4 could induce the increase of the content of glycosphingolipids(including GLs and NGSL)inrat liver.After 12 to 24 h of intoxication,GD3 significantly increased, and after 24 to 48 h of intoxication, GM1 and CTH increased, and GM2 and CXH( an unidentified NGSL component) which were not seen in normal rat liver,appeared in the intoxicated liver.These results suggested that CCI4 intoxication might cause the increase of totalGSL and also the increase of GM2,GD,GM1,CTH,CXH.
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