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当前位置: 首页 > 文章 > 黄曲霉毒素的细胞毒性及机制 乳业科学与技术 2018 (3)
Position: Home > Articles > 黄曲霉毒素的细胞毒性及机制 Journal of Dairy Science and Technology 2018 (3)

黄曲霉毒素的细胞毒性及机制

作  者：
徐明芳;耿梦梦
关键词：
黄曲霉毒素B1;液态乳;风险评估;人胚胎肝细胞(L-02细胞);氧化应激
摘  要：
以正常人肝细胞(L-02细胞)为研究对象,根据细胞增殖率、活性氧(reactive oxygen species,ROS)含量、丙二醛(malondialdehyde,MDA)含量等指标的变化研究黄曲霉毒素B1(aflatoxin B1,AFB1)的毒性作用及氧化应激损伤,选用VC作为AFB1损伤肝细胞的保护剂,通过比色法测定细胞的相对存活率,从细胞周期的变化和细胞凋亡率研究AFB1引起L-02细胞凋亡的程度及机制.结果表明:根据AFB1的半数细胞抑制率(inhibition of cell,IC)(IC50)值,选择AFB1组的暴露质量浓度为40?μg/m L,VC的质量浓度选择在细胞活性最高区域的0.0250.250 mg/m L;当VC质量浓度≥0.5 mg/m L时,细胞活性与AFB1损伤组相近;对于L-02细胞,VC处理组及VC+AFB1处理组细胞的ROS水平较空白对照组高,但较AFB1处理组低,表明添加VC能够帮助L-02细胞降低胞内MDA水平、减小拮抗氧化损伤;通过细胞凋亡及细胞周期检测,发现AFB1造成L-02细胞中晚期凋亡的细胞所占比例较大,添加VC能有效抑制细胞凋亡的发生;在细胞周期的检测中发现,AFB1能够造成L-02细胞发生G0/G1期阻滞;添加VC后,各细胞周期指标与空白对照组接近.
作  者：
XU Mingfang;GENG Mengmeng;College of Life Science and Technology, Jinan University;
单  位：
XU Mingfang%GENG Mengmeng%College of Life Science and Technology, Jinan University
关键词：
aflatoxin B1(AFB1);;milk;;risk assessment;;normal human liver cell line L-02;;oxidative stress
摘  要：
This study investigated the cytotoxicity of aflatoxin B_1(AFB_1) on normal human liver cell line L-02 and evaluated oxidative damage caused by AFB_1 based on changes in cell proliferation rate, reactive oxygen species(ROS) and malondialdehyde(MDA) contents. The relative survival rate of the cells was determined by colorimetry using VC as a cytoprotectant. The extent of AFB_1-induced apoptosis in L-02 cells as well as the underlying mechanism was assessed by changes in the cell cycle and cell apoptosis rate. The results showed that the AFB_1 exposure concentration was determined as 40 μg/m L based on its half maximum inhibitory concentration(IC_(50)) and VC concentrations for maximum cell viability ranged from 0.025 to 0.250 mg/m L. AFB_1-induced cell damage was not attenuated at VC concentrations ≥ 0.5 mg/m L. ROS levels in the VC and VC + AFB_1 groups were higher than in the control group but lower than in the AFB_1 group, implying that VC can help reduce the MDA level in the cells and attenuate oxidative damage. Cell apoptosis and cycle analysis showed that AFB_1 increased the percentage of apoptotic cells at the mid-late stage of apoptosis and that addition of VC inhibited the occurrence of apoptosis. Moreover, AFB_1 induced cell cycle arrest in the G_0/G1 phase and cell cycle parameters returned to almost normal after addition of VC.

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