CYP1A and POR gene mediated mitochondrial membrane damage induced by carbon nanoparticle in human mesenchymal stem cells
CYP1A and POR gene mediated mitochondrial membrane damage induced by carbon nanoparticle in human mesenchymal stem cells
复制标题
DOI：
10.1016/j.etap.2013.03.009
复制
发表时间：
2013-07-01
影响因子：
4.3
通讯作者：
Lei, K. A.
中科院分区：
文献类型：
--
作者：
Alshatwi, Ali A.;Periasamy, Vaiyapuri Subbarayan;Lei, K. A.
纳米颗粒（NP）会引起呼吸系统和心血管问题，此外，小的羧基聚苯乙烯纳米颗粒会引起溶血、激活血小板并诱发人体血液炎症。已知碳纳米颗粒（CNP）会干扰细胞代谢、特定细胞功能，此外还可能引起细胞毒性。我们的目的是研究 CNP 对人间充质干细胞 (hMSC) 氧化应激、线粒体膜损伤和细胞内基因表达的影响。 CNP 在 50 至 400 μg/mL 的剂量范围内引起 hMSC 的剂量和时间依赖性生长抑制。与对照相比，暴露有毒剂量的 CNP，即 50 μg/mL (D1) 和 100 μg/mL (D2) 会降低细胞内线粒体膜电位。通过碘化丙啶染色和荧光显微镜分析证实，CNP 处理的细胞由于细胞膜损伤而失去形态。与对照相比，氧化应激反应基因如 GSTM3 和 GSR1 的表达增加了一倍，但 SOD 和 GPx 暂时没有观察到变化。我们发现 CYP1A 和 POR 基因的表达增加了至少 2 倍，这与线粒体跨膜电位有关。总之，CNP 与 hMSC 的常规和高暴露会增加氧化应激和线粒体膜损伤。 (C) 2013 Elsevier B.V. 保留所有权利。
Nanoparticles (NPs) can cause respiratory and cardiovascular problems, furthermore small carboxyl polystyrene NPs induce hemolysis, activate platelets and induce inflammation in human blood. Carbon nanoparticles (CNPs) are known to interfere with cellular metabolism, specific cellular functions and moreover may cause cellular toxicity. We aimed to study the influence of CNPs on oxidative stress, mitochondrial membrane damage and intracellular gene expression in human mesenchymal stem cells (hMSCs). CNPs cause a dose and time dependent growth inhibition in hMSCs at a dose range from 50 to 400 mu g/mL. Exposure of CNPs toxic doses viz., 50 mu g/mL (D1) and 100 mu g/mL (D2) decreased intracellular mitochondrial membrane potential compared to control. CNPs treated cells were found to lose their morphology due to cell membrane damage have been confirmed by propidium iodide staining and fluorescence microscopic analysis. Oxidative stress responsive genes like GSTM3 and GSR1 expression have increased a fold when compared to control, interim there is no change were observed in SOD and GPx. We found an increased expression of CYP1A and POR genes by at least 2- fold, which is involved in mitochondrial trans-membrane potential. In conclusion, routine and high exposure of CNPs to hMSCs increased oxidative stress and mitochondrial membrane damage. (C) 2013 Elsevier B.V. All rights reserved.