Abstract
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.
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