Deducing in vivo toxicity of combustion-derived nanoparticles from a cell-free oxidative potency assay and metabolic activation of organic compounds.
Deducing in vivo toxicity of combustion-derived nanoparticles from a cell-free oxidative potency assay and metabolic activation of organic compounds.
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DOI：
10.1289/ehp.11370
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发表时间：
2009-01
影响因子：
10.4
通讯作者：
Schmid, Otmar
中科院分区：
文献类型：
--
作者：
Stoeger, Tobias;Takenaka, Shinji;Frankenberger, Birgit;Ritter, Baerbel;Karg, Erwin;Maier, Konrad;Schulz, Holger;Schmid, Otmar
关键词：
吸入燃烧衍生的纳米颗粒（CDNP）被认为会引起氧化应激反应，这反过来可能导致肺部甚至全身炎症。在这项研究中，我们评估了小鼠对CDNPs的体内炎症反应-通常称为颗粒毒性-是否可以通过无细胞抗坏血酸盐试验在体外预测颗粒的表面反应性或更准确地说，氧化效能（OxPot）。对于具有广泛变化的粒径（10-50 nm）、有机物含量（OC; 1-20%）和比Brunauer、Emmett和Teller（BET）表面积（43-800 m2/g）的六种类型的CDNP，OxPot与体内炎症反应（肺内颗粒滴注后24小时的肺多形中性粒细胞流入）强烈相关。然而，对于具有高有机含量的CDNP，OxPot不能解释观察到的炎症反应，可能是由于有机涂层屏蔽了CDNP的碳核的OxPot。另一方面，特定途径的基因表达筛选表明，对于富含多环芳烃（PAH）的颗粒，细胞色素P450 1A 1（CYP 1A 1）酶介导的生物可利用有机物的生物转化可能会产生氧化应激，从而增强体内炎症反应。这两种效应的补偿性质（碳核的屏蔽和多环芳烃的生物转化）导致所有CDNP的炎症反应和BET表面积之间的良好相关性。因此，体内炎症反应可以通过BET表面积或通过基于体外OxPot和Cyp 1a 1诱导的简单定量模型来预测。
The inhalation of combustion-derived nanoparticles (CDNPs) is believed to cause an oxidative stress response, which in turn may lead to pulmonary or even systemic inflammation. In this study we assessed whether the in vivo inflammatory response—which is generally referred to as particle toxicity—of mice to CDNPs can be predicted in vitro by a cell-free ascorbate test for the surface reactivity or, more precisely, oxidative potency (OxPot) of particles. For six types of CDNPs with widely varying particle diameter (10–50 nm), organic content (OC; 1–20%), and specific Brunauer, Emmett, and Teller (BET) surface area (43–800 m2/g), OxPot correlated strongly with the in vivo inflammatory response (pulmonary polymorphonuclear neutrophil influx 24 hr after intratracheal particle instillation). However, for CDNPs with high organic content, OxPot could not explain the observed inflammatory response, possibly due to shielding of the OxPot of the carbon core of CDNPs by an organic coating. On the other hand, a pathway-specific gene expression screen indicated that, for particles rich in polycyclic aromatic hydrocarbon (PAHs), cytochrome P450 1A1 (CYP1A1) enzyme-mediated biotransformation of bio-available organics may generate oxidative stress and thus enhance the in vivo inflammatory response. The compensatory nature of both effects (shielding of carbon core and biotransformation of PAHs) results in a good correlation between inflammatory response and BET surface area for all CDNPs. Hence, the in vivo inflammatory response can either be predicted by BET surface area or by a simple quantitative model, based on in vitro OxPot and Cyp1a1 induction.
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影响因子：
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作者：
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DOI：
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发表时间：
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