Zearalenone Induced Hepatocyte Oxidative Damage:Involvement Of Nrf2—keap1/ARE Pathway

Zearalenone (ZEA) is a class of non-steroidal estrogen produced mainly byFusariuman, commonly found in many foods and shown to be carcinogenic,genotoxic and immunotoxic. Although, many studies have demonstrated cytotoxiceffects of zearalenone， the mechanism of ZEA cytotoxicity is not completelyestablished, especially the oxidative stress pathway. This paper adopted L02cellsfor researching ZEA liver toxic effects in vitro toxicity and investigated therelationship with ZEA and the oxidative damage pathway: Nrf2-Keap1/AREpathway. Our results showed that ZEA reduced cell viability，the activity of SODand increased MDA (malondialdehyde) after exposed to ZEA24h. ZEAsignificantly promoted the expression of Keap1. Meanwhile low and high doses ofZEA inhibited the expression of cellular Nrf2gene and its gene transcriptionactivity, and decreasing the expression of the target gene, HO-1(heme oxygenase-1). These results indicated that ZEA promotes cytotoxicity and oxidative damageby the way of modulating Nrf2-Keap1/ARE pathway.