Vegetable carbon (E153) and titanium dioxide (E171) are widely used as black and white food colour additives. The aim of this study was to assess gastrointestinal tight junction and systemic genotoxic effects in rats following exposure to E153 and E171 for 10 weeks by oral gavage once a week. The expression of tight junction proteins was assessed in intestinal tissues. Levels of DNA strand breaks, oxidatively damaged DNA and telomere length were assessed in secondary organs. Hydrodynamic suspensions of E153 and E173 indicated mean particles sizes of 230 and 270 nm, respectively, and only E153 gave rise to intracellular production of reactive oxygen species in colon epithelial (Caco-2) cells. Rats exposed to E153 (6.4 mg/kg/week) or E171 (500 mg/kg/week) had decreased gene expression of the tight junction protein TJP1 (P < 0.05). E153 (6.4 mg/kg/week) also decreased OCLN (P < 0.05) in the colon and occludin protein expression in the small intestine (P < 0.05). Furthermore, E153 or E171 exposed rats had shorter telomeres in the lung (P < 0.05). Plasma from particle-exposed rats also produced telomere shortening in cultured lung epithelial cells. There were unaltered levels of oxidatively damaged DNA in the liver and lung and no changes in the DNA repair activity of oxidatively damaged DNA in the lung. Altogether, these results indicate that intragastric exposure to E153 and E171 is associated with reduced tight junction protein expression in the intestinal barrier and telomere length shortening in the lung in rats.

中文翻译：

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胃内暴露于食品级二氧化钛和植物碳颗粒后，大鼠肺的端粒长度和遗传毒性。

植物碳（E153）和二氧化钛（E171）被广泛用作黑白食用色素添加剂。这项研究的目的是通过每周一次的管饲法，对暴露于E153和E171 10周的大鼠评估胃肠道紧密连接和全身遗传毒性作用。评估肠组织中紧密连接蛋白的表达。在次级器官中评估了DNA链断裂，DNA氧化损伤和端粒长度的水平。E153和E173的流体动力学悬浮液分别指示平均粒径为230和270 nm，只有E153引起结肠上皮（Caco-2）细胞中活性氧的胞内产生。暴露于E153（6.4 mg / kg /周）或E171（500 mg / kg /周）的大鼠的紧密连接蛋白TJP1的基因表达降低（P <0.05）。E153（6。4 mg / kg /周）还降低了结肠中的OCLN（P <0.05），并降低了小肠中的occludin蛋白表达（P <0.05）。此外，暴露于E153或E171的大鼠的肺端粒较短（P <0.05）。暴露于颗粒的大鼠的血浆在培养的肺上皮细胞中也会产生端粒缩短。肝和肺中氧化损伤的DNA的水平没有改变，肺中氧化损伤的DNA的DNA修复活性没有变化。总而言之，这些结果表明胃内暴露于E153和E171与大鼠肠屏障中紧密连​​接蛋白表达降低和肺中端粒长度缩短有关。暴露于E153或E171的大鼠的肺端粒较短（P <0.05）。暴露于颗粒的大鼠的血浆在培养的肺上皮细胞中也会产生端粒缩短。肝和肺中氧化损伤的DNA的水平没有改变，肺中氧化损伤的DNA的DNA修复活性没有变化。总而言之，这些结果表明胃内暴露于E153和E171与大鼠肠屏障中紧密连​​接蛋白表达降低和肺中端粒长度缩短有关。暴露于E153或E171的大鼠的肺端粒较短（P <0.05）。暴露于颗粒的大鼠的血浆在培养的肺上皮细胞中也会产生端粒缩短。肝和肺中氧化损伤的DNA的水平没有改变，肺中氧化损伤的DNA的DNA修复活性没有变化。总而言之，这些结果表明胃内暴露于E153和E171与大鼠肠屏障中紧密连​​接蛋白表达降低和肺中端粒长度缩短有关。肝和肺中氧化损伤的DNA的水平没有改变，肺中氧化损伤的DNA的DNA修复活性没有变化。总而言之，这些结果表明胃内暴露于E153和E171与大鼠肠屏障中紧密连​​接蛋白表达降低和肺中端粒长度缩短有关。肝和肺中氧化损伤的DNA的水平没有改变，肺中氧化损伤的DNA的DNA修复活性没有变化。总而言之，这些结果表明，胃内暴露于E153和E171与大鼠肠屏障中紧密连​​接蛋白表达的降低以及肺中端粒长度的缩短有关。