甲基甲酸和二甲基甲酸破坏了HepG2细胞中的Sirtuins表达
Ana K Gutiérrez-García1,2, Daniel A Torres-García1, Antonio De Leon-Rodriguez1
1División de Biología Molecular, Instituto Potosino de Investigación Científica y Tecnológica, A.C., Camino a la Presa San José 2055, Col. Lomas 4a Sección, San Luis Potosí, SLP, 78216, México.
Toxicology research
|July 15, 2024
概括
低度的二甲基甲酸 (DEP) 和二甲基甲酸 (DBP) 破坏了HepG2细胞中的Sirtuin基因表达. 这些内分泌干扰剂还增加了活性氧物种 (ROS),并在较高剂量时降低了细胞活力.
科学领域:
- 毒理学 毒理学 毒理学
- 细胞生物学 细胞生物学
- 内分泌学 在内分泌学.
背景情况:
- 酸盐,包括乙 (DEP) 和乙 (DBP),是内分泌干扰剂.
- 甲酸盐暴露与代谢障碍有关.
研究的目的:
- 研究DEP和DBP对HepG2细胞活性的影响.
- 评估DEP和DBP对活性氧物种 (ROS) 生产的影响.
- 确定HepG2细胞中DEP和DBP对Sirtuins的调节.
主要方法:
- 在48-72小时内,HepG2细胞被暴露在DEP和DBP (0.1100μg/mL) 中.
- 使用qRT-PCR量化Sirtuins的基因表达.
- 通过Western-Blot.com分析了Sirtuins的蛋白质水平.
主要成果:
- 低度 (0.1微克/毫升) 的DEP和DBP改变了sirtuin基因表达 (Sirt3,Sirt4,Sirt5).
- DEP (≥1μg/mL) 降低了Sirt1蛋白,而DBP (100μg/mL) 降低了Sirt3蛋白.
- 细胞活力在100微克/毫升下降,而ROS产量在10和100微克/毫升上升,对于两个酸盐.
结论:
- 低剂量的DEP和DBP暴露会对Sirtuin表达产生负面影响.
- 酸盐可以诱导氧化应激并降低HepG2细胞中的细胞活力.
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