王菲迪^1,2,
张海军^1,,,
耿柠波¹,
任晓倩^1,3,
张保琴¹,
宫玉峰¹,
陈吉平^1,,
1. 中国科学院大连化学物理研究所, 大连 116023;
2. 省部共建国家重点实验室培育基地-浙江省植物有害生物防控重点实验室 浙江省农业科学院农产品质量标准研究所, 杭州 310021;
3. 中国科学院大学, 北京 100049

作者简介: 王菲迪(1991-),女,博士研究生,研究方向为环境毒理学,E-mail:wangfd@zaas.ac.cn.

通讯作者: 张海军,hjzhang@dicp.ac.cn ; 陈吉平,chenjp@dicp.ac.cn

基金项目: 国家“973”项目(2015CB453100)；国家自然科学基金(91543201，21337002，21277141)


中图分类号: X171.5

Combined Effects of SCCPs and PAHs on the Antioxidant System in HepG2 Cells

Wang Feidi^1,2,
Zhang Haijun^1,,,
Geng Ningbo¹,
Ren Xiaoqian^1,3,
Zhang Baoqin¹,
Gong Yufeng¹,
Chen Jiping^1,,
1. Dalian Institute of Chemical Physics, Chinese Academy of Sciences, Dalian 116023, China;
2. State Key Laboratory Breeding Base for Zhejiang Sustainable Pest and Disease Control, Institute of Quality and Standard for Agro-Products, Zhejiang Academy of Agricultural Sciences, Hangzhou 310021, China;
3. University of Chinese Academy of Sciences, Beijing 100049, China

Corresponding authors: Zhang Haijun,hjzhang@dicp.ac.cn ; Chen Jiping,chenjp@dicp.ac.cn

CLC number: X171.5

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摘要:环境污染物的低剂量、联合毒性效应已经成为毒理学研究中的热点问题。短链氯化石蜡(SCCPs)和多环芳烃(PAHs)都是典型的有机污染物且在人母乳和血液中都以较高的浓度水平存在。为探究PAHs和SCCPs的联合暴露毒性效应,选择了HepG2细胞作为受试模型,测定了PAHs、SCCPs和它们的混合物暴露后细胞增殖活性及抗氧化系统指标。结果表明,PAHs和SCCPs暴露都能引发ROS的产生,两者混合时更加剧了ROS的产生,表现为协同效应。另外,PAHs和SCCPs暴露都能引起过氧化物歧化酶(SOD)活性的降低,因此两者混合时共同抑制SOD酶活性,表现为协同效应。而PAHs引起过氧化氢酶(CAT)活性升高,SCCPs则显著抑制CAT酶活性,两者联合暴露时CAT酶活性仍降低,但表现为拮抗效应。另外,PAHs和SCCPs暴露都引起谷胱甘肽(GSH)含量的轻微下降,只有SCCPs暴露引起丙二醛(MDA)含量显著升高,而两者联合暴露对GSH含量和MDA含量的影响表现为拮抗效应。表明不管是PAHs和SCCPs单独暴露还是联合暴露都能够干扰HepG2细胞内部的抗氧化系统,破坏抗氧化系统和自由基之间的平衡,使细胞氧化性损伤,甚至造成细胞凋亡。
关键词: SCCPs/
PAHs/
HepG2细胞/
抗氧化系统/
联合暴露

Abstract:The combined effects of different chemical contaminants at low doses has become a hot issue in toxicology research. Previous studies have indicated that two typical organic mixtures, polycyclic aromatic hydrocarbons (PAHs) and short-chain chlorinated paraffins (SCCPs), were both accumulated in human milk and blood at relative high levels. To investigate the combined effect of PAHs and SCCPs, HepG2 cells were utilized for testing the cell viability and antioxidant index. The results showed that PAHs and SCCPs both induced the production of ROS in HepG2 cells, and thus their mixture induced a synergistic up-regulation of ROS production. PAHs and SCCPs both inhibited the activities of superoxide dismutase (SOD) in HepG2 cells, and thus their mixture induced a synergistic down-regulation of SOD activities. PAHs enhanced the activities of catalase (CAT), while SCCPs and their mixture inhibited the activities of CAT, and their mixture induced an antagonistic effect on the activities of CAT. PAHs and SCCPs both induced a slight down-regulation of the glutathione (GSH) levels, and the levels of malondialdehyde (MDA) was significantly up-regulated by SCCPs. The mixture of PAHs and SCCPs induced an antagonistic effect on the changes of GSH and MDA levels. These results indicated that PAHs, SCCPs and their mixture all disrupted the antioxidant system in HepG2 cells, even lead to apoptosis of cells.
Key words:SCCPs/
PAHs/
HepG2 cells/
antioxidant system/
combined exposure.