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氨基功能化碳点破坏脂质代谢,损害斑马鱼的胚胎生成
Long Chuan Zhang1, Li Qiang Chen2, Lei Zhan1
1Key Laboratory of Biomedical Analytics (Southwest University), Chongqing Science and Technology Bureau, College of Pharmaceutical Sciences, Southwest University, Chongqing 400715, PR China.
Journal of hazardous materials
|August 12, 2025
概括
氨基功能化碳点 (PCD) 通过诱导氧化应激和破坏细胞膜,导致斑马鱼胚胎的发育缺陷. 这项研究揭示了用于更安全的纳米材料应用的毒性机制.
科学领域:
- 纳米材料科学 科学 纳米材料科学
- 毒理学 毒理学 毒理学
- 生物医学工程 生物医学工程
背景情况:
- 碳点 (CD) 是生物医学用途的有希望的纳米材料.
- 对于CDs的体内毒性机制尚不清楚.
- 表面功能化可以改变CD的特性和潜在的毒性.
研究的目的:
- 使用简单的热水方法合成氨基功能化碳点 (PCD).
- 研究斑马鱼胚胎中PCDs的体内毒性机制.
- 建立一个分子框架来评估功能化CD的生物安全性.
主要方法:
- 氨基功能化碳点 (PCD) 的一步热水合成.
- 斑马鱼胚胎暴露于不同度的PCDs.
- 评估发育缺陷,氧化应激标志物 (氨酸,SOD,GST,CAT) 和综合代谢/脂质分析.
主要成果:
- 在斑马鱼胚胎中,PCD暴露导致了剂量依赖的发育缺陷,包括胀和脊柱曲.
- 观察到显著的氧化应激,高水平的甲和改变的抗氧化酶活动.
- 代谢和脂质组分析显示了脂质代谢的破坏,特别是糖脂和酸路径,表明脂质过氧化.
结论:
- PCD的表面化学会引发氧化应激和脂质过氧化,从而导致胚胎毒性.
- 活性氧物种是PCD诱导毒性的关键媒介.
- 这些发现为评估和减轻功能化CD在生物医学和环境环境中的风险提供了机制的理解.
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