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The chronic effect of amorphous silica nanoparticles and benzo[a]pyrene co-exposure at low dose in human bronchial epithelial BEAS-2B cells.
Toxicology Research ( IF 2.1 ) Pub Date : 2019-08-12 00:00:00 , DOI: 10.1039/c9tx00112c
Jing Wu 1 , Jie Zhang 1 , Jihua Nie 1 , Junchao Duan 2 , Yanfeng Shi 2 , Lin Feng 2 , Xiaozhe Yang 2 , Yan An 1 , Zhiwei Sun 2
Affiliation  

As the main components of fine particulate matter (PM2.5), silica nanoparticles (SiNPs) and benzo[a]pyrene (B[a]P) have attracted increasing attention recently. However, co-exposure to SiNPs and B[a]P causes pulmonary injury by aggravating toxicity via an unknown mechanism. This study aimed at investigating the toxicity caused due to long-term co-exposure to SiNPs and B[a]P on pulmonary systems at low dose using human bronchial epithelial (BEAS-2B) cells. The characterizations of SiNPs and B[a]P were done by transmission electron microscopy (TEM) and zeta potential granulometry. Cytotoxicity is evaluated using cell counting kit-8 (CCK-8) assay and lactate dehydrogenase (LDH) activity; oxidative stress, cell cycle and apoptosis were assessed by flow cytometry, and inflammatory factors were detected using a Luminex xMAP system. Results show an obvious inhibition of cell proliferation and a marked increase in the LDH expression in the BEAS-2B cells after long-term co-exposure. Furthermore, long-term co-exposure is the most potent in generating intracellular ROS, thus causing inflammation. Cellular apoptotic rate is enhanced in the co-exposed group at low dose. Moreover, the long-term co-exposure induces significant cell cycle arrest, increasing the proportion of cells at the G2/M phase, while decreasing those at the G0/G1 phase. This study is the first attempt to reveal the severe synergistic and additive toxic effects induced by SiNPs and B[a]P co-exposure for long-term in BEAS-2B cells even at low dose.

中文翻译:

无定形二氧化硅纳米粒子和低剂量苯并[a]芘共同暴露对人支气管上皮BEAS-2B细胞的慢性影响。

作为细颗粒物(PM2.5)的主要成分,纳米二氧化硅(SiNPs)和苯并[ a ]芘(B[ a ]P)近年来引起了越来越多的关注。然而,同时接触 SiNPs 和 B[ a ]P 会通过未知机制加重毒性,从而导致肺损伤。本研究旨在利用人支气管上皮 (BEAS-2B) 细胞研究低剂量长期共同暴露于 SiNPs 和 B[ a ]P 对肺系统造成的毒性。SiNPs 和 B[ a ]P的表征通过透射电子显微镜 (TEM) 和 zeta 电位粒度测定法完成。使用细胞计数试剂盒 8 (CCK-8) 测定和乳酸脱氢酶 (LDH) 活性评估细胞毒性;通过流式细胞术评估氧化应激、细胞周期和细胞凋亡,并使用 Luminex xMAP 系统检测炎症因子。结果显示,长期共暴露后,BEAS-2B细胞增殖明显受到抑制,LDH表达明显增加。此外,长期共同暴露最能有效地产生细胞内活性氧,从而引起炎症。低剂量联合暴露组细胞凋亡率增加。此外,长期共同暴露会诱导显着的细胞周期停滞,增加 G2/M 期细胞的比例,同时减少 G0/G1 期细胞的比例。这项研究首次尝试揭示 SiNPs 和 B[ a ]P 长期共同暴露在 BEAS-2B 细胞中(即使是低剂量)也会产生严重的协同和累加毒性效应。
更新日期:2019-08-12
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