食品传播OTA暴露与胚胎发育之间的关联和毒性机制
Teng Yao1, Xingyun Zhu1, Jiaolong Ma1,2,3,4
1Department of Preventive Medicine, School of Medicine, Shihezi University, Shihezi, Xinjiang, China.
Journal of applied toxicology : JAT
|February 12, 2026
概括
通过破坏PI3K/Akt/Nrf2/HO-1通路,引起胚胎发育毒性,导致氧化应激. 这项研究整合了生物信息学和体内实验,以阐明OTA的毒性机制.
科学领域:
- 毒理学 毒理学 毒理学
- 发展生物学 发展生物学
- 生物信息学是一种生物信息学.
背景情况:
- 通过食物传播的甲毒素A (OTA) 是一种流行的真菌毒素,已知有毒性.
- 了解OTA胚胎发育毒性的特定机制对于公共卫生至关重要.
- 现有的研究需要进一步调查OTA的分子通路和体内效应.
研究的目的:
- 为了研究甲毒素A (OTA) 的胚胎发育毒性.
- 通过生物信息学和体内模型阐明OTA诱导毒性背后的特定分子机制.
- 识别潜在的治疗点和针对食品传播污染物的预防策略.
主要方法:
- 生物信息分析包括基因本体学 (GO),基因和基因组丰富的京都百科全书 (KEGG) 和蛋白质-蛋白质相互作用 (PPI) 网络被用来识别关键基因.
- 在体内实验中,在怀孕的C57BL/6小鼠中建立了OTA暴露模型,以评估胚胎发育和胎盘氧化应激.
- 在分子和蛋白质表达水平上分析了包括PI3K/Akt/Nrf2/HO-1在内的关键途径.
主要成果:
- 生物信息分析揭示了PI3K/Akt通路中差异表达基因的丰富,确定了关键的枢纽基因.
- 在小鼠中,OTA暴露导致母亲体重增加受损,活胎率降低,胎儿形.
- 对OTA的暴露降低了胎盘抗氧化能力 (谷氨) 和升高了氧化应激标志物 (氨),同时抑制了PI3K/Akt和Nrf2/HO-1通路的激活.
结论:
- 奥克拉托辛A抑制PI3K/Akt酸化,影响Nrf2/HO-1信号通路.
- 这种干扰会抑制身体的抗氧化能力,诱导氧化应激并导致胚胎发育毒性.
- 这些发现提供了OTA致病效应的证据,并突出了PI3K/Akt/Nrf2/HO-1通路作为关键目标.
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