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Toxins 2017, 9(6), 188; doi:10.3390/toxins9060188

Embryotoxicity Caused by DON-Induced Oxidative Stress Mediated by Nrf2/HO-1 Pathway

1,2,3,†
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1,2,†
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1,2,†
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1,2
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1
Department of Nutrition and Food Hygiene, Hubei Key Laboratory of Food Nutrition and Safety, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, 13 Hangkong Road, Wuhan 430030, China
2
Ministry of Education Key Lab of Environment and Health, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, 13 Hangkong Road, Wuhan 430030, China
3
Wuxi School of Medicine, Jiangnan University, 1800 Lihu Road, Wuxi 214122, China
4
Department of Traumatology, BG Trauma center, Eberhard Karls University of Tübingen, Schnarrenbergstr. 95, 72076 Tübingen, Germany
These authors contributed equally to this work.
*
Author to whom correspondence should be addressed.
Academic Editor: Marc Maresca
Received: 17 April 2017 / Revised: 2 June 2017 / Accepted: 6 June 2017 / Published: 9 June 2017
(This article belongs to the Section Mycotoxins)
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Abstract

Deoxynivalenol (DON) belongs to the type B group of trichothecenes family, which is composed of sesquiterpenoid metabolites produced by Fusarium and other fungi in grain. DON may cause various toxicities, such as cytotoxicity, immunotoxicity, genotoxicity as well as teratogenicity and carcinogenicity. In the present study, we focus on a hypothesis that DON alters the expressions of Nrf2/HO-1 pathway by inducing embryotoxicity in C57BL/6 mouse (5.0, 2.5, 1.0, and 0 mg/kg/day) and BeWo cell lines (0 and 50 nM; 3 h, 12 h and 24 h). Our results indicate that DON treatment in mice during pregnancy leads to ROS accumulation in the placenta, which results in embryotoxicity. At the same time Nrf2/HO-1 pathway is up-regulated by ROS to protect placenta cells from oxidative damage. In DON-treated BeWo cells, the level of ROS has time–effect and dose–effect relationships with HO-1 expression. Moderate increase in HO-1 protects the cell from oxidative damage, while excessive increase in HO-1 aggravates the oxidative damage, which is called in some studies the “threshold effect”. Therefore, oxidative stress may be the critical molecular mechanism for DON-induced embryotoxicity. Besides, Nrf2/HO-1 pathway accompanied by the “threshold effect” also plays an important role against DON-induced oxidative damage in this process. View Full-Text
Keywords: skeleton abnormalities; reactive oxygen species; anti-oxidative system; Nrf2 translocation skeleton abnormalities; reactive oxygen species; anti-oxidative system; Nrf2 translocation
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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MDPI and ACS Style

Yu, M.; Chen, L.; Peng, Z.; Wang, D.; Song, Y.; Wang, H.; Yao, P.; Yan, H.; Nüssler, A.K.; Liu, L.; Yang, W. Embryotoxicity Caused by DON-Induced Oxidative Stress Mediated by Nrf2/HO-1 Pathway. Toxins 2017, 9, 188.

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