甲基三在人类肝细胞L02细胞中诱导的代谢干扰和转录组变化
Jing An1, Yuting Yi1, Jingjing Jiang1
1Institute of Environmental Pollution and Health, School of Environmental and Chemical Engineering, Shanghai University, Nanchen Road 333, Shanghai 200444, PR China.
Toxicology research
|November 2, 2023
概括
甲基三三 (MTCS) 是三三 (TCS) 的一种副产品,通过引起氧化应激和破坏新陈代谢来损害人类肝细胞. 需要进一步的研究来了解其毒性作用,并确定分子标记物.
科学领域:
- 环境毒理学环境毒理学
- 细胞生物学 细胞生物学
- 生物化学 生物化学
背景情况:
- 三 (TCS) 被广泛使用,导致人们对其副产品如甲基三 (MTCS) 感到担忧.
- 越来越多的证据表明,MTCS可能会给健康带来风险,需要进行详细的毒理学调查.
研究的目的:
- 评估甲基三桑 (MTCS) 在人类肝细胞中的细胞毒性 (L02).
- 阐明MTCS诱导的毒性的潜在分子机制.
主要方法:
- 在实验室中,L02细胞暴露于MTCS的不同度.
- 评估细胞活力,谷氨氧化还原状态和线粒体膜潜力.
- 使用RNA测序和生物信息学分析细胞代谢途径.
主要成果:
- 根据剂量,MTCS降低了细胞活力,破坏了谷氨平衡 (GSH/GSSG),并降低了线粒体膜潜力 (MMP).
- 暴露于MTCS改变了葡萄糖和脂质代谢,增加了葡萄糖转化为乳酸,并提高了甘油三 (TG) 和总胆固醇 (TC) 水平.
- 通过RNA测序确定了与MTCS诱导的代谢失衡相关的潜在分子标记物 (SHMT2,MTHFD2,ASNS,PHGDH).
结论:
- 氧化应激和代谢失调是L02细胞中MTCS细胞毒性的关键机制.
- 已识别的分子标记可以作为MTCS诱导的代谢干扰的指标.
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