2026-10-14T13:12:56Z https://api.figshare.com/v2/oai

oai:figshare.com:article/34025356 2026-09-29T17:17:25Z category_4 category_12 category_13 category_14 category_16 category_19 category_272 category_873 category_39 category_69 category_132 category_135 portal_63 item_type_6 month_year_09_2026

Intestinal Organoid-Based Toxicity Study on Co-exposure to Food Contaminants Deoxynivalenol and Tenuazonic Acid Huikang Lin (13548221) Bingxuan Jia (23642661) Binhe Chang (23642664) Yingzhu Tan (23642667) Ye Tian (220278) Na Liu (102929) Aibo Wu (1430200) Biochemistry Cell Biology Genetics Molecular Biology Physiology Pharmacology Environmental Sciences not elsewhere classified Chemical Sciences not elsewhere classified Ecology Inorganic Chemistry Infectious Diseases Computational Biology requiring targeted measures reducing canonical enterocytes main toxic target inducing ribotoxic stress emerging tenuazonic acid cell transcriptome revealed cell cycle arrest disrupting organoid development intestinal barrier function intestinal organoid model primary exposure site food contaminants deoxynivalenol based toxicity study intestinal organoid intestinal risk lipid toxicity high toxicity ta cells synergistic effects ppar pathway oxidation genes exposure risks core targets animal health Environmental mycotoxins threaten human and animal health. Deoxynivalenol (DON) and emerging tenuazonic acid (TeA) severely contaminate food crops. The intestine is DON’s main toxic target and TeA’s primary exposure site, but TeA’s intestinal risk and their combined toxicity remain understudied. In this study, using an intestinal organoid model, we found that DON and TeA significantly suppressed cell viability (toxicity ratio ∼ 1:20) with synergistic effects under high toxicity, disrupting organoid development and intestinal barrier function (cell cycle arrest, reduced tight junction proteins, increased goblet cells), linked to their ribotoxicity and inducing lipid metabolism disorders (downregulated fatty acid β-oxidation genes) via the PPAR pathway. Single-cell transcriptome revealed that they impaired intestinal cell proliferation/differentiation, inducing ribotoxic stress in stem/TA cells and reducing canonical enterocytes (ECs), and ECs were core targets of their lipid toxicity. In conclusion, DON and TeA share intestinal toxicological characteristics, and their combined exposure potentiates toxicity, requiring targeted measures to mitigate co-exposure risks. 2026-09-29T00:00:00Z Text Journal contribution 10.1021/acs.jafc.6c07522.s001 https://figshare.com/articles/journal_contribution/Intestinal_Organoid-Based_Toxicity_Study_on_Co-exposure_to_Food_Contaminants_Deoxynivalenol_and_Tenuazonic_Acid/34025356 CC BY-NC 4.0