Zearalenone induces oxidative damage involving Keap1/Nrf2/HO-1 pathway in hepatic L02 cells

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• 作者：Kejia Wu (1) (2)
  Xin Liu (1) (2)
  Min Fang (1) (2)
  Yongning Wu (3)
  Zhiyong Gong (1) (2)
  
  1. Institute of Food Science and Engineering ; WuHan Polytechnic University ; Xuefu Road 68 ; 430023 ; Wuhan ; P R China
  2. Hu bei Collaborative Innovation Center for Processing of Agricultural Products ; Hubei ; China
  3. China National Center For Food Safety Risk Assessment ; Panjiayuan South Lane 7 ; Chaoyang District ; 100050 ; Beijing ; P R China
  
• 关键词：Zearalenone ; Keap1 ; Nrf2 ; HO ; 1 ; Antioxidant enzyme
• 刊名：Molecular & Cellular Toxicology
• 出版年：2014
• 出版时间：December 2014
• 年：2014
• 卷：10
• 期：4
• 页码：451-457
• 全文大小：338 KB
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• 刊物主题：Cell Biology; Pharmacology/Toxicology;
• 出版者：Springer Netherlands
• ISSN：2092-8467

文摘

Zearalenone (ZEA), a mycotoxin produced by Fusarium fungi, is found in cereal crops. Although the toxic effects of ZEA have been well characterized, the mechanism is not clear, especially with respect to the oxidative damage. In this study, we determined superoxide dismutase (SOD) and malondialdehyde (MDA) levels as indexes of oxidative damage caused by ZEA and investigated whether the damage involved Keap1/Nrf2/HO-1 pathway in hepatic L02 cells. The results indicated that ZEA induced cytotoxicity in L02 cells by reducing cell viability, inhibiting SOD activity and increasing MDA levels. ZEA also altered mRNA and protein expressions of antioxidant genes including Keap1, Nrf2 and its downstream gene HO-1. Furthermore, simultaneous treatment with ZEA and tertiary butylhydroquinone (t-BHQ, and inducer of Nrf2) could restore HO-1 expression level compared with exposed to ZEA alone. In summary, ZEA probably induces oxidative damage through a pathway which involves Keap1 up-regulation, Nrf2 and HO-1 down-regulation.