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在替那唑酸和棒曲霉素共同暴露于 Caco-2 细胞中协同毒性作用的代谢组学及其机制分析。

Metabolome and Its Mechanism Profiling in the Synergistic Toxic Effects Induced by Co-Exposure of Tenuazonic Acid and Patulin in Caco-2 Cells.

机构信息

College of Food Science, Southwest University, Chongqing 400715, China.

Chongqing Key Laboratory of Speciality Food Co-Built by Sichuan and Chongqing, Chongqing 400715, China.

出版信息

Toxins (Basel). 2024 Jul 15;16(7):319. doi: 10.3390/toxins16070319.

Abstract

Tenuazonic acid (TeA), usually found in cereals, fruits, vegetables, oil crops, and their products, was classified as one of the highest public health problems by EFSA as early as 2011, but it has still not been regulated by legislation due to the limited toxicological profile. Moreover, it has been reported that the coexistence of TeA and patulin (PAT) has been found in certain agricultural products; however, there are no available data about the combined toxicity. Considering that the gastrointestinal tract is the physiological barrier of the body, it would be the first target site at which exogenous substances interact with the body. Thus, we assessed the combined toxicity (cell viability, ROS, CAT, and ATP) in Caco-2 cells using mathematical modeling (Chou-Talalay) and explored mechanisms using non-targeted metabolomics and molecular biology methods. It revealed that the co-exposure of TeA + PAT (12.5 μg/mL + 0.5 μg/mL) can induce enhanced toxic effects and more severe oxidative stress. Mechanistically, the lipid and amino acid metabolisms and PI3K/AKT/FOXO signaling pathways were mainly involved in the TeA + PAT-induced synergistic toxic effects. Our study not only enriches the scientific basis for the development of regulatory policies but also provides potential targets and treatment options for alleviating toxicities.

摘要

涕灭威酸(TeA)通常存在于谷物、水果、蔬菜、油料作物及其产品中,早在 2011 年就被 EFSA 列为最严重的公共卫生问题之一,但由于毒理学特征有限,尚未被立法所监管。此外,据报道,涕灭威酸(TeA)和棒曲霉素(PAT)在某些农产品中同时存在,但尚无关于联合毒性的可用数据。鉴于胃肠道是人体的生理屏障,它将是外源物质与身体相互作用的第一个靶位。因此,我们使用数学建模(Chou-Talalay)方法评估了 Caco-2 细胞中的联合毒性(细胞活力、ROS、CAT 和 ATP),并使用非靶向代谢组学和分子生物学方法探索了机制。结果表明,TeA+PAT(12.5μg/mL+0.5μg/mL)共暴露可诱导增强的毒性作用和更严重的氧化应激。从机制上讲,脂质和氨基酸代谢以及 PI3K/AKT/FOXO 信号通路主要参与了 TeA+PAT 诱导的协同毒性作用。我们的研究不仅丰富了制定监管政策的科学依据,还为减轻毒性提供了潜在的靶标和治疗选择。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/12ab/11281550/fccb4f729f50/toxins-16-00319-g001.jpg

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