甲基醇对肠道细胞的影响:对表观遗传调节酶的洞察
Camilla Morresi1, Giulia Feliziani2,3, Luisa Bellachioma1
1Department of Life and Environmental Sciences, Polytechnic University of Marche, Ancona, Italy.
IUBMB life
|December 8, 2025
概括
甲基醇 (MGO) 是加工食品中发现的一种反应性化合物,通过增加氧化应激和DNA损伤来损害肠道细胞. 它还破坏了表观遗传调节剂,如基因素脱乙酶 (HDAC) 和十-十一转位 (TET) 酶.
科学领域:
- 细胞生物学 细胞生物学
- 分子生物学分子生物学
- 毒理学 毒理学 毒理学
背景情况:
- 甲基醇 (MGO) 是一种内源性和外源性反应性化合物,涉及到细胞损伤.
- 消化系统会从代谢副产品和饮食中遇到MGO,特别是超加工食品.
- 转基因对肠道细胞的影响及其潜在的分子机制,包括表观遗传改变,仍然不太清楚.
研究的目的:
- 为了研究MGO对肠道细胞的影响.
- 阐明涉及MGO诱导的肠道细胞损伤的分子机制.
- 检查MGO对表观遗传调节酶 (HDAC,TET,DNMT) 的影响.
主要方法:
- 差异化Caco-2细胞单层暴露于MGO.
- 对肠道屏障功能的评估.
- 测量反应性氧物种 (ROS),亡和DNA损伤标记物 (γH2AX).
- 对NFκB通路激活,促炎分子 (TNF-α) 和抗氧化酶 (SOD1,触酶) 的分析.
- 对表观遗传酶表达 (HDAC1/2,TET1/2) 和基因素乙化水平的评估.
主要成果:
- 在Caco-2细胞中,MGO暴露损害了肠道屏障功能.
- MGO诱导了亡和细胞质和线粒体ROS的增加.
- 由MGO触发的氧化应激激活了NFκB通路,增加了TNF-α和抗氧化酶.
- 有证据表明DNA损伤 (γH2AX) 和表观遗传平衡的破坏,包括减少HDAC1/2和TET蛋白表达,以及增加基因素H4乙化.
- 暴露于MGO导致促进炎症分子和抗氧化酶水平的增加.
结论:
- MGO在肠道细胞中引起显著的细胞损伤,其特征是屏障功能障碍,亡和氧化应激.
- 暴露于MGO会破坏DNA完整性和表观遗传机制,影响HDAC和TET等关键酶.
- 这些发现强调MGO是通过破坏细胞平衡和表观遗传调节来导致肠道病理的潜在贡献者.
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