摘要
目的:探究壬基酚对NCTC1469细胞的损伤作用及细胞内活性氧类、还原型谷胱甘肽含量的影响。方法:通过体外细胞实验,用不同质量浓度壬基酚作用NCTC1469细胞24 h;CCK-8法检测细胞存活率;测定药物作用后培养液上清中乳酸脱氢酶(lactate dehydrogenase,LDH)、谷丙转氨酶(alanine aminotransferase,ALT)和谷草转氨酶(aspartate transaminase,AST)活性及细胞内还原型谷胱甘肽含量;流式细胞仪检测细胞内活性氧类水平。结果:壬基酚可显著抑制NCTC1469细胞增殖及促进活性氧类生成(P<0.05),呈一定剂量依赖性;培养液上清液中LDH、ALT活性在壬基酚浓度大于0.1μmol/L处理组中,与自然释放对照组相比显著升高(P<0.05);且壬基酚在高剂量(1、10、100μmol/L)能明显增加培养液上清中AST活性(P<0.01);壬基酚呈剂量依赖性降低细胞内还原型谷胱甘肽含量,与空白对照组比较有显著差异(P<0.05)。结论:推测壬基酚可能通过上调细胞内活性氧类水平,下调胞内还原型谷胱甘肽含量,引起氧化应激反应,从而对NCTC1469细胞产生损伤作用。
Objective：To explore the effect of nonylphenol（NP） on inducing injury and changing ROS and GSH contents in NCTC1469 cells. Methods： Cultured cells were treated with NP（0, 0. 01, 0.1, 1, 10 μmol/L and 100 μmol/L） for 24 h. Then, cell viability was assessed with a cell counting kit; the NP-induced injury was evaluated by detecting lactate dehydrogenase（LDH）, alanine aminotransamine（ALT） and aspartate aminotransaminase（AST） activities in cell culture supernatant and the contents of intracellular glutathione（GSH） and reactive oxygen species（ROS） were assayed by flow cytometric method. Results： NP could inhibit NCTC1469 cell proliferation and promote ROS generation significantly in a dose-dependent manner. Compared with the control group, the LDH and ALT activities in cell culture supernatant from 0.1–100 μmol/L NP groups had a significant increase, while the AST activity increased dramatically only in 1–100 μmol/L NP groups. NP could decrease intracellular GSH content in a dose-dependent manner, and there was a significant difference when compared with the control group. Conclusion： NP can induce NCTC1469 cells injury by up-regulating the level of ROS and downregulating the content of GSH.
出处
《食品科学》
EI
CAS
CSCD
北大核心
2014年第3期198-202,共5页
Food Science
基金
国家"973"计划项目(2012CB720805)
科技部国际合作项目(2010DFA31780)
国家基金委中德科学基金中心合作项目(GZ731)
