氧化纳米颗粒破坏过氧体-内等离子体网膜接触,并增加非常长链脂肪酸含量
Juncheng Zhong1, Xuebo Liu1, Jiawei Wang1
1College of Marine Sciences, South China Agricultural University, Guangzhou, China; Fisheries Research Institute of South China Agricultural University, Guangzhou, China.
氧化纳米颗粒 (ZnO NPs) 通过损害非常长链脂肪酸 (VLCFA) 代谢来破坏脂质平衡. 这通过SIRT1/FOXO3/ACBD5通路发生,影响过氧体功能和肝脏健康.
科学领域:
- 生物化学 生物化学
- 细胞生物学 细胞生物学
- 环境毒理学环境毒理学
背景情况:
- 非常长链脂肪酸 (VLCFA) 对于生理功能至关重要.
- 氧化纳米颗粒 (ZnO NPs) 被广泛使用,但它们对脂质代谢的影响尚未完全理解.
- 了解ZnO NP对脂质平衡的影响对于健康和安全至关重要.
研究的目的:
- 为了研究 ZnO NPs 对黄色鱼 (Pelteobagrus fulvidraco) 的VLCFA代谢的影响.
- 阐明ZnO NP诱导的脂质平衡的变化背后的分子机制.
- 为了确定参与ZnO NPs.VLCFA代谢中断的关键调节途径.
主要方法:
- 在体内养研究中,黄色鱼暴露于ZnO NPs.
- 在体外研究中使用黄色鱼肝细胞.
- 分析肝脏的VLCFA,甘油三 (TG) 和总胆固醇 (T-CHO) 水平.
- 对过氧体β-氧化和过氧体-ER (Po-ER) 接触的研究.
- 对ACBD5,FOXO3和SIRT1.1的基因表达和蛋白质定位分析.
主要成果:
- ZnO NPs显著增加了肝脏的VLCFA,TG和T-CHO水平.
- ZnO NPs减少了过氧体β氧化和Po-ER接触.
- ZnO NPs通过SIRT1/FOXO3轴降低了ACBD5的表达和定位.
- 破坏SIRT1/FOXO3通路抑制了FOXO3的核进入,并降低了SIRT1水平.
结论:
- ZnO NPs通过SIRT1-FOXO3-ACBD5通路破坏VLCFA代谢,从而破坏脂质平衡.
- 这项研究强调了过氧体功能和Po-ER接触在ZnO NP毒性的作用.
- 结果提供了关于管理由环境因素引起的VLCFA相关代谢障碍的见解.
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