College of Veterinary Medicine, Northeast Agricultural University, Harbin, 150030, PR China.
College of Veterinary Medicine, Northeast Agricultural University, Harbin, 150030, PR China; Key Laboratory of the Provincial Education Department of Heilongjiang for Common Animal Disease Prevention and Treatment, Northeast Agricultural University, Harbin, 150030, PR China; Heilongjiang Key Laboratory for Laboratory Animals and Comparative Medicine, Northeast Agricultural University, Harbin, 150030, PR China.
Chemosphere. 2022 Dec;308(Pt 1):136275. doi: 10.1016/j.chemosphere.2022.136275. Epub 2022 Sep 1.
As one of the most used phthalates, Di (2-ethylhexyl) phthalate (DEHP) is a widespread environmental contaminant. Extremely persistent plastic can enter the food chain of animals through the aquatic environment, affect metabolic pathways and cause damage to the digestive system. But the molecular mechanism of its toxic effects on the duodenum in birds has not been elucidated. To investigate the toxicity of phthalates in the duodenum, quails were gavaged with 250, 500, and 750 mg/kg doses of DEHP for 45 days, and water and oil control groups were retained. This study revealed that subchronic exposure to DEHP could lead to duodenal barrier defect in quail. The damage to duodenum was reflected in a reduction in V/C and tight junction proteins. Moreover, DEHP also led to a breakdown of antimicrobial defenses through the flora derangement, which acted as a biological barrier. The massive presence of Lipopolysaccharide (LPS) led to the activation of TLR4 receptors. In addition, DEHP activated oxidative stress, which synergized the inflammatory response induced by the TLR4-NFκB pathway, and further promoted duodenum damage. This study provides a base for the further effect of phthalates on the microbiota-barrier-immune interaction.
作为最常用的邻苯二甲酸酯之一，邻苯二甲酸二（2-乙基己基）酯（DEHP）是一种广泛存在的环境污染物。极难降解的塑料可以通过水环境污染进入动物食物链，影响代谢途径，并对消化系统造成损害。但它对禽类十二指肠的毒性作用的分子机制尚未阐明。为了研究邻苯二甲酸酯在十二指肠中的毒性，鹌鹑被灌胃给予 250、500 和 750mg/kg 剂量的 DEHP，持续 45 天，并保留水和油对照组。本研究表明，亚慢性 DEHP 暴露可导致鹌鹑十二指肠屏障缺陷。这种对十二指肠的损伤反映在 V/C 和紧密连接蛋白的减少上。此外，DEHP 还通过菌群失调破坏了抗菌防御系统，而菌群失调充当了生物屏障。大量脂多糖（LPS）的存在导致 TLR4 受体的激活。此外，DEHP 还激活了氧化应激，这与 TLR4-NFκB 通路诱导的炎症反应协同作用，进一步促进了十二指肠损伤。本研究为邻苯二甲酸酯对微生物群-屏障-免疫相互作用的进一步影响提供了依据。
