揭示大气细颗粒物对红血细胞有害影响的潜在因果成分

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Yuzhu Zhang^1,2, Laijin Zhong³, Jing Zhan⁴

¹State Key Laboratory of Environmental Chemistry and Ecotoxicology, Research Center for Eco-Environmental Sciences, Chinese Academy of Sciences, Beijing 100085, China.

Environmental science & technology

|November 27, 2024

概括

细颗粒物 (PM2.5) 暴露会损害红细胞 (RBC),减少ATP和增加脂暴露. 溶解的有机物和烟尘颗粒被确定为PM2.5的主要贡献者.

科学领域:

环境健康环境健康
血液学血液学血液学
毒理学毒理学毒理学

背景情况:

大气中的细颗粒物 (PM2.5) 是已知的心血管风险因素.
红细胞 (RBC) 在血液健康和疾病 (包括血栓形成) 中发挥着关键作用.
了解PM2.5对红细胞的影响对于阐明心血管影响至关重要.

研究的目的:

为了研究PM2.5对小鼠红细胞的毒性影响.
为了确定PM2.5中负责RBC损伤的特定组件.
探索将PM2.5暴露与心血管风险联系在一起的机制.

主要方法:

在四个季节中从北京的城市地点收集PM2.5样本.
对小鼠红细胞的PM2.5毒性的评估,测量腺三酸盐 (ATP) 水平和酸 (PS) 外化.
化学分析PM2.5成分,包括溶解有机物 (DOM) 和碳质材料.
在PM2.5特性和红细胞损伤标志物之间的相关性分析.
使用碳黑 (CB) 和氧化CB (OCB) 纳米材料进行模拟试验.

主要成果:

暴露在PM2.5下降了红细胞ATP水平,增加了PS的外部化,导致了形态变化.
在PM2.5中DOM的芳香度与红细胞PS暴露呈正相关,涉及素类化合物.
在PM2.5泽塔潜力和RBCPS暴露之间存在负相关性,表明颗粒生物活性.
碳黑和氧化碳黑证实了颗粒碳的作用,氧化烟尘被确定为贡献者.
这项研究是首次证明红细胞中PM2.5诱导的PS暴露.

结论:

暴露于PM2.5会对红细胞造成重大损害,包括减少ATP和增加PS外部化.
具有高芳香度的溶解有机物 (DOM) 和氧化烟尘颗粒被确定为PM2.5诱导的红细胞毒性的关键致病成分.
这些发现为PM2.5对心血管疾病,特别是血栓形成的贡献背后的机制提供了新的见解.

关键词:

溶解的有机物质是一种有机物质.微细颗粒物质的细颗粒物质的细颗粒物质的细颗粒物质的细颗粒物质.暴露于脂胺的情况.红细胞是血液中的红细胞.苏苏苏苏

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