Combined Effect of Silica Nanoparticles and Benzo[a]pyrene on Cell Cycle Arrest Induction and Apoptosis in Human Umbilical Vein Endothelial Cells.
Combined Effect of Silica Nanoparticles and Benzo[a]pyrene on Cell Cycle Arrest Induction and Apoptosis in Human Umbilical Vein Endothelial Cells.
复制标题
二氧化硅纳米颗粒和苯并[a]芘对人脐静脉内皮细胞细胞周期阻滞诱导和凋亡的联合作用
DOI：
10.3390/ijerph14030289
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发表时间：
2017-03-09
影响因子：
--
通讯作者：
Sun Z
中科院分区：
文献类型：
--
作者：
Asweto CO;Wu J;Hu H;Feng L;Yang X;Duan J;Sun Z
超细颗粒物（UFP）等颗粒物（PM）和多环芳烃（PAH）等有机化合物污染物在环境中广泛存在。 UFP和PAH存在于空气中，它们的存在可能会增强它们各自对人类健康的不利影响。然而，它们联合相互作用对人体细胞的机制和影响尚不清楚。我们研究了二氧化硅纳米颗粒（SiNPs）（UFP）和苯并[a]芘（B[a]P）（PAH）对人内皮细胞的联合毒性。将人脐血管内皮细胞 (HUVEC) 暴露于 SiNP 或 B[a]P，或 SiNP 和 B[a]P 的组合。通过评估细胞氧化应激、DNA 损伤、细胞周期停滞和细胞凋亡来研究毒性。我们的结果表明 SiNPs 能够诱导活性氧 (ROS) 的产生。 B[a]P单独作用时没有毒性作用。然而，SiNPs 和 B[a]P 的共同暴露协同诱导 DNA 损伤、氧化应激、细胞周期在 G2/M 检查点停滞和细胞凋亡。共同暴露通过 Chk1 的上调和 Cdc25C、细胞周期蛋白 B1 的下调诱导 G2/M 停滞。联合暴露还上调了促凋亡蛋白 bax、caspase-3 和 caspase-9，同时下调了抗凋亡蛋白 bcl-2。这些结果表明 SiNP 和 B[a]P 之间的相互作用协同增强对 HUVEC 的毒理学作用。这些信息应该有助于我们进一步了解 PAH 和 UFP 的联合毒性。
Particulate matter (PM) such as ultrafine particulate matter (UFP) and the organic compound pollutants such as polycyclic aromatic hydrocarbon (PAH) are widespread in the environment. UFP and PAH are present in the air, and their presence may enhance their individual adverse effects on human health. However, the mechanism and effect of their combined interactions on human cells are not well understood. We investigated the combined toxicity of silica nanoparticles (SiNPs) (UFP) and Benzo[a]pyrene (B[a]P) (PAH) on human endothelial cells. Human umbilical vascular endothelial cells (HUVECs) were exposed to SiNPs or B[a]P, or a combination of SiNPs and B[a]P. The toxicity was investigated by assessing cellular oxidative stress, DNA damage, cell cycle arrest, and apoptosis. Our results show that SiNPs were able to induce reactive oxygen species generation (ROS). B[a]P, when acting alone, had no toxicity effect. However, a co-exposure of SiNPs and B[a]P synergistically induced DNA damage, oxidative stress, cell cycle arrest at the G2/M check point, and apoptosis. The co-exposure induced G2/M arrest through the upregulation of Chk1 and downregulation of Cdc25C, cyclin B1. The co-exposure also upregulated bax, caspase-3, and caspase-9, the proapoptic proteins, while down-regulating bcl-2, which is an antiapoptotic protein. These results show that interactions between SiNPs and B[a]P synergistically potentiated toxicological effects on HUVECs. This information should help further our understanding of the combined toxicity of PAH and UFP.