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商业级炭火烤肉操作产生的排放物会在人支气管上皮细胞中引发氧化应激和炎症反应。

Emissions from commercial-grade charbroiling meat operations induce oxidative stress and inflammatory responses in human bronchial epithelial cells.

作者信息

Li Ning, Bhattacharya Poulomi, Karavalakis Georgios, Williams Keisha, Gysel Nicholas, Rivera-Rios Nachamari

机构信息

Department of Pathobiology and Diagnostic Investigation, College of Veterinary Medicine, Michigan State University, East Lansing, MI, USA.

Center for Environmental Research and Technology, Bourns College of Engineering, University of California Riverside, Riverside, CA, USA.

出版信息

Toxicol Rep. 2014 Oct 2;1:802-811. doi: 10.1016/j.toxrep.2014.09.015. eCollection 2014.

DOI:10.1016/j.toxrep.2014.09.015
PMID:28962293
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5598377/
Abstract

Commercial charbroiling emissions are a significant source of ambient particulate matter (PM) in urban settings. The objective of this study was to determine whether organic extract of PM emissions from commercial charbroiling meat operations could induce an inflammatory response in human bronchial epithelial cells and whether this effect was mediated by oxidative stress. PM samples were collected during cooking hamburgers on a commercial-grade under-fired charbroiler and sequentially extracted with water and methanol to obtain the aqueous PM suspension (AqPM) and organic extract (OE). The pro-oxidative and pro-inflammatory effects of OE were assessed using human bronchial epithelial cell line BEAS-2B. While AqPM did not have any effect, OE effectively induced the expression of heme oxygennase-1 and cyclooxygenase-2 in BEAS-2B cells. OE also up-regulated the levels of IL-6, IL-8, and prostaglandin E2. OE-induced cellular inflammatory response could be effectively suppressed by the antioxidant N-acetyl cysteine, nuclear factor (erythroid-derived 2)-like 2 activator sulforaphane and p38 MAPK inhibitor SB203580. In conclusion, organic chemicals emitted from commercial charbroiling meat operations could induce an inflammatory response in human bronchial epithelial cells, which was mediated by oxidative stress and p38 MAPK.

摘要

在城市环境中,商业烤炙排放是环境颗粒物(PM)的一个重要来源。本研究的目的是确定商业烤炙肉类操作产生的PM排放物的有机提取物是否能在人支气管上皮细胞中诱导炎症反应,以及这种效应是否由氧化应激介导。在商用级欠火烤架上烹饪汉堡包期间收集PM样本,依次用水和甲醇提取,以获得水性PM悬浮液(AqPM)和有机提取物(OE)。使用人支气管上皮细胞系BEAS-2B评估OE的促氧化和促炎作用。虽然AqPM没有任何作用,但OE有效地诱导了BEAS-2B细胞中血红素加氧酶-1和环氧化酶-2的表达。OE还上调了IL-6、IL-8和前列腺素E2的水平。抗氧化剂N-乙酰半胱氨酸、核因子(红系衍生2)样2激活剂萝卜硫素和p38丝裂原活化蛋白激酶抑制剂SB203580可有效抑制OE诱导的细胞炎症反应。总之,商业烤炙肉类操作排放的有机化学物质可在人支气管上皮细胞中诱导炎症反应,这是由氧化应激和p38丝裂原活化蛋白激酶介导的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f817/5598377/326eaeee732c/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f817/5598377/74effe0fe0eb/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f817/5598377/5c862953596e/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f817/5598377/375a52d2777e/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f817/5598377/061e2c492766/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f817/5598377/909aa291d1e9/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f817/5598377/326eaeee732c/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f817/5598377/74effe0fe0eb/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f817/5598377/5c862953596e/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f817/5598377/375a52d2777e/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f817/5598377/061e2c492766/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f817/5598377/909aa291d1e9/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f817/5598377/326eaeee732c/gr6.jpg

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