脑前突触神经终端中诱导的兴奋毒性:碳质空气中的颗粒模拟剂的调节作用
Nataliya Krisanova1, Artem Pastukhov1, Mariia Dekaliuk1
1The Department of Neurochemistry, The Palladin Institute of Biochemistry, The National Academy of Sciences of Ukraine, 9 Leontovicha Street, Kiev, 01054, Ukraine.
Environmental science and pollution research international
|December 12, 2023
概括
来自酸/尿素的碳点通过减少大鼠神经末端中的谷氨酸释放来减轻引起的神经毒性. 这一发现突显了特定的碳状颗粒对抗的潜力.
科学领域:
- 环境科学 环境科学
- 神经毒理学 神经毒理学
- 纳米材料科学 科学 纳米材料科学
背景情况:
- (Hg2+) 和碳状空气颗粒是已知的神经毒剂.
- 了解它们的综合健康风险需要多污染物方法.
- 突触前大鼠皮层神经终端为研究神经毒性提供了一个模型.
研究的目的:
- 调查碳酸空气颗粒模拟剂对引起的神经毒性的神经保护潜力.
- 评估碳点和纳米钻石调节细胞外L-[14C]谷氨酸水平的能力,在神经末端暴露于HgCl2.2.
- 探索生物系统中和碳质物质之间的复杂形成.
主要方法:
- 作为一种生物系统,利用了大鼠前突触皮质神经终端.
- 测量了细胞外L-[14C]谷氨酸水平作为神经毒性的标志物.
- 应用 (HgCl2) 来诱导神经毒性.
- 测试了从酸/尿素和β-氨酸衍生的碳点,以及纳米钻石,以测试它们减轻Hg2+诱导的影响的能力.
- 通过度分析证实了复杂的形成.
主要成果:
- HgCl2 (≥5μM) 引起了细胞外L-[14C]谷氨酸酸的急性,度依赖的增加.
- 来自酸/尿素的碳点显著减轻了Hg2+诱导的谷氨酸增加37%.
- 这些碳点和Hg2+之间的复杂形成被光谱学证实.
- 来自β-氨酸的纳米钻石和碳点没有显示出保护作用.
结论:
- 从酸/尿素合成的碳点显示了神经终端对急性毒性的神经保护性质.
- 这凸显了空气中碳质颗粒的多样化影响及其对调节相关健康风险的潜力.
- 开发的方法适用于评估生物系统中各种粒子的Hg2+化能力.
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