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Acute in vitro and in vivo toxicity of a commercial grade boron nitride nanotube mixture

机译：急性体外和商业级氮化硼纳米管混合物的体内毒性

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Boron nitride nanotubes (BNNTs) are an emerging engineered nanomaterial attracting significant attention due to superior electrical, chemical and thermal properties. Currently, the toxicity profile of this material is largely unknown. Commercial grade BNNTs are composed of a mixture (BNNT-M) of similar to 50-60% BNNTs, and similar to 40-50% impurities of boron and hexagonal boron nitride. We performed acute in vitro and in vivo studies with commercial grade BNNT-M, dispersed by sonication in vehicle, in comparison to the extensively studied multiwalled carbon nanotube-7 (MWCNT-7). THP-1 wild-type and NLRP3-deficient human monocytic cells were exposed to 0-100 mu g/ml and C57BL/6J male mice were treated with 40 mu g of BNNT-M for in vitro and in vivo studies, respectively. In vitro, BNNT-M induced a dose-dependent increase in cytotoxicity and oxidative stress. This was confirmed in vivo following acute exposure increase in bronchoalveolar lavage levels of lactate dehydrogenase, pulmonary polymorphonuclear cell influx, loss in mitochondrial membrane potential and augmented levels of 4-hydroxynonenal. Uptake of this material caused lysosomal destabilization, pyroptosis and inflammasome activation, corroborated by an increase in cathepsin B, caspase 1, increased protein levels of IL-1 beta and IL-18 both in vitro and in vivo. Attenuation of these effects in NLRP3-deficient THP-1 cells confirmed NLRP3-dependent inflammasome activation by BNNT-M. BNNT-M induced a similar profile of inflammatory pulmonary protein production when compared to MWCNT-7. Functionally, pretreatment with BNNT-M caused suppression in bacterial uptake by THP-1 cells, an effect that was mirrored in challenged alveolar macrophages collected from exposed mice and attenuated with NLRP3 deficiency. Analysis of cytokines secreted by LPS-challenged alveolar macrophages collected after in vivo exposure to dispersions of BNNT-M showed a differential macrophage response. The observed results demonstrated acu
机译：氮化硼纳米管（BNNT）是一种由于优异的电气，化学和热性能而引起的显着关注的新兴的工程化纳米材料。目前，这种材料的毒性概况在很大程度上是未知的。商业级BNNTS由类似于50-60％BNNT的混合物（BNNT-M）组成，并且类似于硼和六边形氮化硼的40-50％的杂质。与广泛研究的多壁碳纳米管-7（MWCNT-7）相比，我们在车辆中的超声处理和商业级BNNT-M进行了体外和体内研究的急性研究。将THP-1野生型和NLRP3缺陷的人单核细胞暴露于0-100μmg/ ml，分别用40μg的BNNT-M处理C57BL / 6J雄性小鼠，分别用于体外和体内研究。体外，BNNT-M诱导细胞毒性和氧化应激的剂量依赖性增加。在乳酸脱氢酶的支气管肺泡灌洗水平，肺多态核细胞流入，线粒体膜损失和4-羟基的增强水平的情况下，在急性暴露血液血液灌洗水平术后确认。吸收这种物质引起溶酶体稳定化，糊酶和炎症组活化，通过在体外和体内增加了Caspsin B，Caspase 1，IL-1β和IL-18的蛋白质水平增加。 NLRP3缺陷型THP-1细胞中这些效果的衰减证实了BNNT-M的NLRP3依赖性炎症组活化。与MWCNT-7相比，BNNT-M在与MWCNT-7相比时诱导炎性肺蛋白质产生相似的型材。在功能上，通过THP-1细胞对BNNT-M的预处理导致细菌摄取的抑制，其在从暴露小鼠收集并衰减NLRP3缺乏的攻击肺泡巨噬细胞中镜像的效果。在体内暴露于BNNT-M的分散体内收集的LPS攻击的肺泡巨噬细胞分泌的细胞因子显示差异巨噬细胞反应。观察结果证明了ACU

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