Department of Biology, Jackson State University, Jackson, MS 39217, USA.
Sci Total Environ. 2010 Mar 15;408(8):1812-7. doi: 10.1016/j.scitotenv.2010.01.035. Epub 2010 Feb 18.
In this study, we used a systematic approach to study and compare the in vitro cytotoxicity of selected engineered carbon nanotubes (CNTs) to test cell lines including human skin keratinocytes, lung cells and lymphocytes. Results of fluorescein diacetate (FDA) uptake in T4 lymphocyte A3 cells indicated cytotoxicity caused by single-walled carbon nanotubes (SWCNTs) at concentrations of 2, 5 and 10ppm. At 2ppm, the SWCNT treatment group retained 71.3% viability compared to the PBS control group. At 10ppm, cellular viability further decreased to 56.5% of the PBS control group. In the skin keratinocyte HaCaT cells and lung MSTO-211H cells, the SWCNT did not demonstrate any cytotoxicity at concentrations of 2 and 5ppm but slightly inhibited HaCaT cells and caused significant toxicity to MSTO-211H cells at 10ppm. Multi-walled carbon nanotube (MWCNT) testing showed significant cytotoxicity to A3 cells in a dose-dependent manner. At 10ppm the viability of the cells decreased to 89.1% compared to the PBS control. In MSTO-211H cells, MWCNT caused significant toxicity at concentrations of 2ppm and higher. By comparison, HaCaT cells were inhibited significantly only at 10ppm. Overall, the test CNTs inhibited cellular viabilities in a concentration, cell type, and CNT type-dependent pattern. The viabilities of the MWCNT-impacted cells are higher than the corresponding SWCNT groups. We speculate that on a per volume basis, the greater availability of defects and contaminants for cellular interaction may contribute to the higher cytotoxicity of SWCNT in this study. The interaction between the SWCNTs and A3 lymphocytes was also observed by scanning electron microscopy. The mechanism for causing cell death in this study was attributed to apoptosis and necrosis after physical penetration by CNTs and oxidative stress via formation of reactive oxygen species.
在这项研究中，我们采用系统的方法研究和比较了选定的工程化碳纳米管（CNT）的体外细胞毒性，以测试包括人皮肤角质细胞、肺细胞和淋巴细胞在内的细胞系。T4 淋巴细胞 A3 细胞中荧光素二乙酸（FDA）摄取的结果表明，在 2、5 和 10ppm 浓度下，单壁碳纳米管（SWCNT）具有细胞毒性。在 2ppm 时，SWCNT 处理组与 PBS 对照组相比保持了 71.3%的活力。在 10ppm 时，细胞活力进一步下降至 PBS 对照组的 56.5%。在皮肤角质细胞 HaCaT 细胞和肺 MSTO-211H 细胞中，SWCNT 在 2 和 5ppm 浓度下没有表现出任何细胞毒性，但略微抑制了 HaCaT 细胞，并在 10ppm 时对 MSTO-211H 细胞造成显著毒性。多壁碳纳米管（MWCNT）测试显示，A3 细胞的细胞毒性呈剂量依赖性。在 10ppm 时，细胞活力与 PBS 对照组相比下降到 89.1%。在 MSTO-211H 细胞中，MWCNT 在 2ppm 及更高浓度下引起显著毒性。相比之下，仅在 10ppm 时 HaCaT 细胞受到显著抑制。总的来说，测试 CNT 以浓度、细胞类型和 CNT 类型依赖的方式抑制细胞活力。MWCNT 影响细胞的活力高于相应的 SWCNT 组。我们推测，在每单位体积中，细胞相互作用的缺陷和污染物的更大可用性可能导致在这项研究中 SWCNT 具有更高的细胞毒性。通过扫描电子显微镜也观察到了 SWCNT 与 A3 淋巴细胞之间的相互作用。本研究中导致细胞死亡的机制归因于 CNT 物理穿透引起的细胞凋亡和坏死以及活性氧形成引起的氧化应激。
