Mechanism of toxic effects of Nano-ZnO on cell cycle of zebrafish (Danio rerio)

被引:40
作者
Hou, Jing [1 ]
Liu, Haiqiang [1 ]
Zhang, Siyi [1 ]
Liu, Xinhui [2 ]
Hayat, Tasawar [3 ]
Alsaedi, Ahmed [3 ]
Wang, Xiangke [1 ]
机构
[1] North China Elect Power Univ, Coll Environm Sci & Engn, MOE Key Lab Resources & Environm Syst Optimizat, Beijing 102206, Peoples R China
[2] Dongguan Univ Technol, Res Ctr Eca Environm Engn, Dongguan 523808, Guangdong, Peoples R China
[3] King Abdulaziz Univ, Fac Sci, NAAM Res Grp, Jeddah 21589, Saudi Arabia
基金
中国国家自然科学基金;
关键词
Nano-ZnO; Toxicity; Cell cycle; DNA replication; Cyclins; ZINC-OXIDE NANOPARTICLES; ESCHERICHIA-COLI; OXIDATIVE STRESS; DNA-REPLICATION; RE-REPLICATION; DAPHNIA-MAGNA; STEM-CELLS; PLURIPOTENCY; EXPOSURE; TIO2;
D O I
10.1016/j.chemosphere.2019.04.217
中图分类号
X [环境科学、安全科学];
学科分类号
08 ; 0830 ;
摘要
The release of nano-zinc oxide (nano-ZnO) into the environment may lead to unpredictable risks, thus it is necessary to study its potential harm to organisms. In this study, zebrafish exposed to nano-ZnO were analyzed through cDNA microarrays to provide insight into the toxic effect of nano-ZnO on aquatic organisms at the molecular level. Results found that nano-ZnO inhibited the normal growth and development of zebrafish and other life activities by affecting the process of cell cycle. The nano-ZnO inhibited the expression of the cyclins (Cycs), cyclin-dependent kinases (CDK) and the minichromosome maintenance (MCM), making the activation of Cyc/CDK complexs (CycD/CDK4, 6; CycE/CDK2; CycA/CDK2) and MCM fail and resulting in DNA replication disorder in different periods (G1, M and G2 phase). Therefore, the normal activities of individual organism such as cell division, differentiation and proliferation and the functions of DNA binding and intracellular transfer were disturbed. These findings contribute to our understanding of the toxicity of ZnO NPs to aquatic organisms, and also provide an evaluation basis for assessing the environmental impact of nano materials. (C) 2019 Elsevier Ltd. All rights reserved.
引用
收藏
页码:206 / 213
页数:8
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