Carbon nanotubes: Structural defects as stressors inducing lung cell toxicity

IF 4.7 2区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY
Rossella Daniela Bengalli , Giuseppe Zerbi , Andrea Lucotti , Tiziano Catelani , Paride Mantecca
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Abstract

Lung toxicity of carbon nanotubes (CNTs) is matter of concern since very long time. However, their mechanism of toxicity is still not yet well defined. In this work, the role of structural defects as organic stressors of CNTs able to trigger their potential toxicity is investigated. Four commercial CNTs, with different carbon purity grade, are morphologically characterized by transmission electron microscopy (TEM) and the relative amount of structural defects are estimated through Raman spectroscopy, by measuring the intensity ratio D/G (ID/IG). The oxidative potential of CNTs is evaluated with cytochrome-C assay and reactive oxygen species (ROS) detection. Data show that CNTs with larger amounts of structural defects (higher ID/IG ratio) induce an increased ROS generation and consequent cytotoxicity and cellular damage, shown by TEM images of CNTs-cells interaction. Raman analyses of cells exposed to CNTs point out that the spectra of the CNTs inside the cells show no differences with respect of the signal recorded for cell-free CNTs, evidencing their biopersistence in lung cells. Raman spectra cannot provide direct indication of the existence of metals as impurity. It follows that the intensity ratio ID/IG can be taken as a predictive marker of the toxicity of a given CNT.

Abstract Image

碳纳米管:结构缺陷作为应激源诱导肺细胞毒性
长期以来,碳纳米管的肺毒性一直是人们关注的问题。然而,它们的毒性机制尚未明确。在这项工作中,研究了结构缺陷作为碳纳米管的有机应力源的作用,从而触发其潜在的毒性。采用透射电子显微镜(TEM)对4种不同碳纯度等级的商品CNTs进行形貌表征,并通过拉曼光谱测量强度比D/G (ID/IG)来估计结构缺陷的相对数量。通过细胞色素- c测定和活性氧(ROS)检测评估CNTs的氧化电位。数据显示,碳纳米管-细胞相互作用的TEM图像显示,具有较大结构缺陷(更高的ID/IG比)的碳纳米管诱导ROS生成增加,从而导致细胞毒性和细胞损伤。对暴露于碳纳米管的细胞进行的拉曼分析指出,细胞内碳纳米管的光谱与细胞外碳纳米管记录的信号没有差异,这证明了它们在肺细胞中的生物持久性。拉曼光谱不能直接指示金属作为杂质的存在。因此,强度比ID/IG可以作为给定碳纳米管毒性的预测标记。
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来源期刊
CiteScore
7.70
自引率
3.90%
发文量
410
审稿时长
36 days
期刊介绍: Chemico-Biological Interactions publishes research reports and review articles that examine the molecular, cellular, and/or biochemical basis of toxicologically relevant outcomes. Special emphasis is placed on toxicological mechanisms associated with interactions between chemicals and biological systems. Outcomes may include all traditional endpoints caused by synthetic or naturally occurring chemicals, both in vivo and in vitro. Endpoints of interest include, but are not limited to carcinogenesis, mutagenesis, respiratory toxicology, neurotoxicology, reproductive and developmental toxicology, and immunotoxicology.
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