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A Fulvic Acid-like Substance Participates in the Pro-inflammatory Effects of Cigarette Smoke and Wood Smoke Particles.
Chemical Research in Toxicology ( IF 4.1 ) Pub Date : 2020-03-27 , DOI: 10.1021/acs.chemrestox.0c00036
David H Gonzalez 1 , Joleen M Soukup 2 , Michael C Madden 2 , Michael Hays 2 , Jon Berntsen 3 , Suzanne E Paulson 1 , Andrew J Ghio 2
Affiliation  

We tested the postulates that (1) a fulvic acid (FA)-like substance is included in cigarette smoke and wood smoke particles (WSP) and (2) cell exposure to this substance results in a disruption of iron homeostasis, associated with a deficiency of the metal and an inflammatory response. The fluorescence excitation-emission matrix spectra of the water-soluble components of cigarette smoke condensate and WSP (Cig-WS and Wood-WS) approximated those for the standard reference materials, Suwanee River and Nordic fulvic acids (SRFA and NFA). Fourier transform infrared spectra for the FA fraction of cigarette smoke and WSP (Cig-FA and Wood-FA), SRFA, and NFA also revealed significant similarities (O-H bond in alcohols, phenols, and carboxylates, C═O in ketones, aldehydes, and carboxylates, and a significant carboxylate content). After exposure to Cig-WS and Wood-WS and the FA standards, iron was imported by respiratory epithelial cells, reflecting a functional iron deficiency. The release of pro-inflammatory mediators interleukin (IL)-8 and IL-6 by respiratory epithelial cells also increased following exposures to Cig-WS, Wood-WS, SRFA, and NFA. Co-exposure of the respiratory epithelial cells with iron decreased supernatant concentrations of the ILs relative to exposures to Cig-WS, Wood-WS, SRFA, and NFA alone. It is concluded that (1) a FA-like substance is included in cigarette smoke and WSP and (2) respiratory epithelial cell exposure to this substance results in a disruption of iron homeostasis associated with both a cell deficiency of the metal and an inflammatory response.

中文翻译:

黄腐酸样物质参与卷烟和木烟颗粒的促炎作用。

我们测试了以下假设:(1)卷烟烟雾和木烟颗粒(WSP)中包含类富黄酸(FA)类物质,以及(2)细胞暴露于该物质会导致铁稳态破坏,并伴有缺乏金属和炎症反应。香烟烟雾冷凝物和WSP(Cig-WS和Wood-WS)的水溶性组分的荧光激发发射矩阵光谱近似于标准参考物质Suwanee River和北欧富富酸(SRFA和NFA)的光谱。香烟烟雾和WSP的FA组分(Cig-FA和Wood-FA),SRFA和NFA的傅里叶变换红外光谱也显示出显着的相似性(醇,酚和羧酸盐中的OH键,酮,醛,和羧酸盐,以及相当大的羧酸盐含量)。暴露于Cig-WS和Wood-WS以及FA标准后,铁通过呼吸道上皮细胞输入,反映出功能性铁缺乏症。暴露于Cig-WS,Wood-WS,SRFA和NFA后,呼吸道上皮细胞释放促炎性介质白介素(IL)-8和IL-6的数量也增加。相对于单独暴露于Cig-WS,Wood-WS,SRFA和NFA,呼吸道上皮细胞与铁的共同暴露降低了IL的上清液浓度。结论是:(1)卷烟烟雾和WSP中包含FA类物质,(2)呼吸上皮细胞暴露于该物质会导致与金属细胞缺乏和炎症反应相关的铁稳态破坏。 。反映功能性铁缺乏症。暴露于Cig-WS,Wood-WS,SRFA和NFA后,呼吸道上皮细胞释放促炎性介质白介素(IL)-8和IL-6的数量也增加。相对于单独暴露于Cig-WS,Wood-WS,SRFA和NFA,呼吸道上皮细胞与铁的共同暴露降低了IL的上清液浓度。结论是:(1)卷烟烟雾和WSP中包含FA类物质,并且(2)呼吸上皮细胞暴露于该物质会导致与金属细胞缺乏和炎性反应有关的铁稳态破坏。 。反映功能性铁缺乏症。暴露于Cig-WS,Wood-WS,SRFA和NFA后,呼吸道上皮细胞释放促炎性介质白介素(IL)-8和IL-6的数量也增加。相对于单独暴露于Cig-WS,Wood-WS,SRFA和NFA,呼吸道上皮细胞与铁的共同暴露降低了IL的上清液浓度。结论是:(1)卷烟烟雾和WSP中包含FA类物质,并且(2)呼吸上皮细胞暴露于该物质会导致与金属细胞缺乏和炎性反应有关的铁稳态破坏。 。相对于单独暴露于Cig-WS,Wood-WS,SRFA和NFA,呼吸道上皮细胞与铁的共同暴露降低了IL的上清液浓度。结论是:(1)卷烟烟雾和WSP中包含FA类物质,并且(2)呼吸上皮细胞暴露于该物质会导致与金属细胞缺乏和炎性反应有关的铁稳态破坏。 。相对于单独暴露于Cig-WS,Wood-WS,SRFA和NFA,呼吸道上皮细胞与铁的共同暴露降低了IL的上清液浓度。结论是:(1)卷烟烟雾和WSP中包含FA类物质,(2)呼吸上皮细胞暴露于该物质会导致与金属细胞缺乏和炎症反应相关的铁稳态破坏。 。
更新日期:2020-04-23
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