Institute of Toxicology and Genetics, Karlsruhe Institute of Technology, Eggenstein-Leopoldshafen, Germany.
Anal Bioanal Chem. 2011 Dec;401(10):3197-212. doi: 10.1007/s00216-011-5102-4. Epub 2011 May 28.
Combustion-derived nanoparticles as constituents of ambient particulate matter have been shown to induce adverse health effects due to inhalation. However, the components inducing these effects as well as the biological mechanisms are still not fully understood. The fine fraction of fly ash particles collected from the electrostatic precipitator of a municipal solid waste incinerator was taken as an example for real particles with complex composition released into the atmosphere to study the mechanism of early biological responses of BEAS-2B human lung epithelial cells. The studies include the effects of the water-soluble and -insoluble fractions of the fly ash and the well-studied carbon black nanoparticles were used as a reference. Fly ash induced reactive oxygen species (ROS) and increased the total cellular glutathione (tGSH) content. Carbon black also induced ROS generation; however, in contrast to the fly ash, it decreased the intracellular tGSH. The fly ash-induced oxidative stress was correlated with induction of the anti-oxidant enzyme heme oxygenase-1 and increase of the redox-sensitive transcription factor Nrf2. Carbon black was not able to induce HO-1. ROS generation, tGSH increase and HO-1 induction were only induced by the insoluble fraction of the fly ash, not by the water-soluble fraction. ROS generation and HO-1 induction were markedly inhibited by pre-incubation of the cells with the anti-oxidant N-acetyl cysteine which confirmed the involvement of oxidative stress. Both effects were also reduced by the metal chelator deferoxamine indicating a contribution of bioavailable transition metals. In summary, both fly ash and carbon black induce ROS but only fly ash induced an increase of intracellular tGSH and HO-1 production. Bioavailable transition metals in the solid water-insoluble matrix of the fly ash mostly contribute to the effects.
燃烧衍生的纳米颗粒作为环境颗粒物的组成部分，已被证明由于吸入而导致不良健康影响。然而，引起这些效应的成分以及生物机制仍未完全了解。以从城市固体废物焚烧厂静电除尘器收集的飞灰颗粒的细颗粒为例，研究了复杂成分的实际颗粒释放到大气中对 BEAS-2B 人肺上皮细胞早期生物学反应的机制。这些研究包括飞灰的水溶性和不溶性部分的影响，以及经过充分研究的碳黑纳米颗粒被用作参考。飞灰诱导活性氧（ROS）并增加总细胞谷胱甘肽（tGSH）含量。碳黑也诱导 ROS 的产生；然而，与飞灰相反，它降低了细胞内 tGSH。飞灰诱导的氧化应激与抗氧化酶血红素加氧酶-1的诱导和氧化还原敏感转录因子 Nrf2 的增加相关。碳黑不能诱导 HO-1。ROS 的产生、tGSH 的增加和 HO-1 的诱导仅由飞灰的不溶性部分诱导，而不由水溶性部分诱导。细胞用抗氧化剂 N-乙酰半胱氨酸预先孵育可明显抑制 ROS 的产生和 HO-1 的诱导，证实了氧化应激的参与。两种作用也被金属螯合剂去铁胺减少，表明生物可利用的过渡金属的贡献。总之，飞灰和碳黑都诱导 ROS，但只有飞灰诱导细胞内 tGSH 和 HO-1 产生增加。飞灰固体水不溶性基质中生物可利用的过渡金属主要促成了这些作用。
