Using the human gastric cell line GES-1, AFG1 upregulated CYP2E1 through NF-κB, causing oxidative DNA damage in vitro. TNF-α-mediated inflammation plays an important role in AFG1-induced gastric cell damage. Treatment with the soluble TNF-α receptor sTNFR:Fc inhibited AFG1-induced gastric inflammation, and reversed CYP2E1 upregulation and DNA damage in mouse GECs. Oral administration of AFG1 induced gastric inflammation and DNA damage in mouse GECs associated with P450 2E1 (CYP2E1) upregulation. In this study, we explored whether and how AFG1-induced gastric inflammation regulates cytochrome P450 to contribute to DNA damage in GECs. However, the toxicity of AFG1 to gastric epithelial cells (GECs) remains unclear. Epithelial cells in the gastrointestinal tract are the first line of defense against ingested mycotoxins. Aflatoxin G1 (AFG1), a member of the aflatoxin family with cytotoxic and carcinogenic properties, is one of the most common mycotoxins occurring in various agricultural products, animal feed, and human foods and drinks worldwide.
0 Comments
Leave a Reply. |