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同时接触波尔多液和 TiO₂(E171)或 SiO₂(E551)下调小肠上皮细胞模型中细胞连接基因的表达,并增加农药的转移。

Co-exposure to boscalid and TiO (E171) or SiO (E551) downregulates cell junction gene expression in small intestinal epithelium cellular model and increases pesticide translocation.

机构信息

Center for Nanotechnology and Nanotoxicology, Department of Environmental Health, Harvard T. H. Chan School of Public Health, Boston, MA 02115, USA.

National Center for Toxicological Research, Division of Microbiology, U.S. Food & Drug Administration, Jefferson, AR 72079, USA.

出版信息

NanoImpact. 2021 Apr;22:100306. doi: 10.1016/j.impact.2021.100306. Epub 2021 Mar 10.

DOI:10.1016/j.impact.2021.100306
PMID:35559963
Abstract

A recent published study showed that TiO (E171) and SiO (E551), two widely used nano-enabled food additives, increased the translocation of the commonly used pesticide boscalid by 20% and 30% respectively. Such increased absorption of pesticides due to the presence of engineered nanomaterials (ENMs) in food raises health concerns for these food additives. In this companion study, mRNA expression of genes related to cell junctions in a small intestinal epithelial cellular model after exposure to simulated digestas of fasting food model (phosphate buffer) containing boscalid (150 ppm) with or without either TiO or SiO (1% w/w) were analyzed. Specific changes in cell barrier function underlying or contributing to the increased translocation of boscalid observed in the previous study were assessed. Results showed that exposure to boscalid alone has no significant effect on cell junction genes, however, co-exposure to boscalid and TiO significantly regulated expression of cell-matrix junction focal adhesion-related genes, e.g., downregulating Cav1 (-1.39-fold, p < 0.05), upregulating Cav3 (+ 3.30-fold, p < 0.01) and Itga4 (+ 3.30-fold, p < 0.05). Similarly, co-exposure to boscalid and SiO significantly downregulated multiple cell-cell junction genes, including tight junction genes (Cldn1, Cldn11, Cldn16, Cldn18, and Jam3), adherens junction genes (Notch1, Notch3, Pvrl1) and gap junction genes (Gja3 and Gjb2), as well as cell-matrix junction focal adhesion genes (Itga4, Itga6, Itga7). Together, these findings suggest that co-ingestion of boscalid with TiO (E171) or SiO (E551) could cause weakening of cell junctions and intercellular adhesion, which could result in dysregulation of paracellular transport, and presumably contributed to the previously observed increased translocation of boscalid at the presence of these ENMs. This novel finding raises health safety concerns for such popular food additives.

摘要

最近发表的一项研究表明,两种广泛使用的纳米级食品添加剂 TiO(E171)和 SiO(E551),分别使常用农药啶酰菌胺的透肠吸收率增加了 20%和 30%。由于食品中存在工程纳米材料(ENMs),导致这些食品添加剂吸收更多的农药,这引起了人们对这些食品添加剂的健康担忧。在这项伴随研究中,分析了暴露于含有啶酰菌胺(150ppm)的禁食食品模型(磷酸盐缓冲液)模拟消化液后,小肠上皮细胞模型中与细胞连接相关的基因的 mRNA 表达,这些消化液中存在 TiO 或 SiO(1%w/w)。评估了先前研究中观察到的啶酰菌胺透肠吸收率增加的潜在或促成的特定细胞屏障功能变化。结果表明,单独暴露于啶酰菌胺对细胞连接基因没有显著影响,然而,啶酰菌胺与 TiO 的共同暴露显著调节了细胞-基质连接焦点黏附相关基因的表达,例如,下调 Cav1(-1.39 倍,p<0.05),上调 Cav3(+3.30 倍,p<0.01)和 Itga4(+3.30 倍,p<0.05)。同样,啶酰菌胺与 SiO 的共同暴露也显著下调了多个细胞-细胞连接基因,包括紧密连接基因(Cldn1、Cldn11、Cldn16、Cldn18 和 Jam3)、黏着连接基因(Notch1、Notch3、Pvrl1)和缝隙连接基因(Gja3 和 Gjb2),以及细胞-基质连接焦点黏附基因(Itga4、Itga6、Itga7)。总的来说,这些发现表明,啶酰菌胺与 TiO(E171)或 SiO(E551)共同摄入可能导致细胞连接和细胞间黏附减弱,这可能导致细胞旁转运失调,并且可能促成了先前观察到的这些 ENMs 存在下啶酰菌胺透肠吸收率增加。这一新发现引起了人们对这些流行食品添加剂的健康安全担忧。

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