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氯丙烯对神经细胞NO、MDA含量和NOS、SOD、GSH-PX活性的影响
引用本文:赵丽,谢克勤,张旻,孙克任. 氯丙烯对神经细胞NO、MDA含量和NOS、SOD、GSH-PX活性的影响[J]. 山东大学学报(医学版), 2001, 39(2): 76-178
作者姓名:赵丽  谢克勤  张旻  孙克任
作者单位:山东大学公共卫生学院毒理学研究室
基金项目:山东省自然科学基金资助课题(Y97C13049)
摘    要:探讨氯丙烯对神经细胞NO生成系统和抗氧化系统的影响。方法用NO、MDA、NOS、SOD、GSH-PH检测试剂盒研究了氯丙烯对鸡胚脑神经细胞NO、MDA含量和NOS、SOD、GSH-PX活性的影响。结果与对照组相比,随着氯丙烯浓度的增加,NO含量细胞内明显增加(P<0.01),细胞外无显著差异;NOS活性细胞内中、高剂量组显著增加(P<0.05,P<0.01),细胞外活性仅高剂量组显著增加(P<0.01);细胞MDA含量明显降低,并呈明显的剂量-效应关系(r=-0.9693,P<0.05);GSH-PX活性细胞内逐渐升高,呈明显的剂量-效应关系(r=0.9872,P<0.05),细胞外仅高剂量组明显升高(P<0.01);细胞内T-SOD和CuZn-SOD活性在3个剂量均明显下降(P<0.01)。结论氯丙烯可影响NO生成系统和细胞内抗氧化系统,这可能是氯丙烯引起细胞内Ca2+稳态失调的原因之一。

关 键 词:氯丙烯;神经细胞;一氧化氮;丙二醛;一氧化氮合酶;超氧化物歧化酶;谷胱甘肽过氧化物酶
文章编号:1000-0496(2001)02-0176-03
修稿时间:2000-03-09

EFFECTS OF ALLYL CHLORIDEON NO, MDA CONTENTS AND NOS, SOD,GSH-PX ACTIVITIES IN NERVE CELLES
ZHAO Li,XIE Ke qin,ZHANG Min,et al. EFFECTS OF ALLYL CHLORIDEON NO, MDA CONTENTS AND NOS, SOD,GSH-PX ACTIVITIES IN NERVE CELLES[J]. Journal of Shandong University:Health Sciences, 2001, 39(2): 76-178
Authors:ZHAO Li  XIE Ke qin  ZHANG Min  et al
Abstract:Objective:To research the poisioning mechanisms of allyl chloride and probe into its effects on NO sythesis system and antioxidation system in chicken embryo nerve cells.Methods:The contents of NO and MDA and the activities of NOS,SOD,GSH PX were done with related kits.Results:With allyl chloride increasing,the content of NO increased signifcantly in cells(P<0.01),but it appeared no different in medium.The activities of NOS increased significantly (P<0.01)both in nerve cells and medium.Cell MDA contents decreased significantly (P< 0.01 ) but GSH PX activity increased significantly both in nerve cells and in medium,(P< 0.01 ).T SOD and CuZn SOD activities decreased markedly (P<0.01).Conclusion:Allyl chloride can disturb NO synthesis and antioxidation in nerve cells.It might be one of the mechanisms of calcium unhomeostasis induced by allyl chloride.
Keywords:Allyl chloride  Neurons  Nitric oxide  Nitric oxide synthase  Superoxide dismutase  Malondialdehyde  Glutathione perxidase
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