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

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文献类型：外文期刊

作者： Wu, Kejia ¹ ; Liu, Xin ¹ ; Fang, Min ¹ ; Wu, Yongning ³ ; Gong, Zhiyong ¹ ;

作者机构： 1.WuHan Polytech Univ, Inst Food Sci & Engn, Wuhan 430023, Peoples R China

2.Hubei Collaborat Innovat Ctr Proc Agr Prod, Yichang, Hubei, South Korea

3.China Natl Ctr Food Safety Risk Assessment, Beijing 100050, Peoples R China

关键词： Zearalenone;Keap1;Nrf2;HO-1;Antioxidant enzyme

期刊名称：MOLECULAR & CELLULAR TOXICOLOGY （影响因子：1.08；五年影响因子：1.184 ）

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收录情况： SCI

摘要： 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 itivestigated 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 Keapl, 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 Keapl up-regulation, Nrf2 and HO-1 down-regulation.

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