Polycyclic aromatic hydrocarbons (PAHs) may cause lipid peroxidation via reactive oxygen species generation. 15-F2t-isoprostane (IsoP), an oxidative stress marker, is formed from arachidonic acid (AA) by a free-radical induced oxidation. AA may also be converted to prostaglandins (PG) by prostaglandin-endoperoxide synthase (PTGS) induced by NF-κB. We treated human embryonic lung fibroblasts (HEL12469) with benzo[a]pyrene (B[a]P), 3-nitrobenzanthrone (3-NBA) and extractable organic matter (EOM) from ambient air particulate matter <2.5 µm for 4 and 24 h. B[a]P and 3-NBA induced expression of PAH metabolising, but not antioxidant enzymes. The concentrations of IsoP decreased, whereas the levels of AA tended to increase. Although the activity of NF-κB was not detected, the tested compounds affected the expression of prostaglandin-endoperoxide synthase 2 (PTGS2). The levels of prostaglandin E2 (PGE2) decreased following exposure to B[a]P, whereas 3-NBA exposure tended to increase PGE2 concentration. A distinct response was observed after EOM exposure: expression of PAH-metabolising enzymes was induced, IsoP levels increased after 24-h treatment but AA concentration was not affected. The activity of NF-κB increased after both exposure periods, and a significant induction of PTGS2 expression was found following 4-h treatment. Similarly to PAHs, the EOM exposure was associated with a decrease of PGE2 levels. In summary, exposure to PAHs with low pro-oxidant potential results in a decrease of IsoP levels implying 'antioxidant' properties. For such compounds, IsoP may not be a suitable marker of lipid peroxidation.

中文翻译：

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与人类胚胎肺成纤维细胞中脂质过氧化有关的过程，用多环芳烃和颗粒物质的有机提取物处理。

多环芳烃（PAH）可能会通过活性氧的产生而引起脂质过氧化。15-F2t-异前列腺素（IsoP），一种氧化应激标记，是由花生四烯酸（AA）通过自由基诱导的氧化作用形成的。AA也可以通过NF-κB诱导的前列腺素内过氧化物合酶（PTGS）转化为前列腺素（PG）。我们用苯并[a] py（B [a] P），3-硝基苯并蒽醌（3-NBA）和可从环境空气中颗粒物<2.5 µm提取的有机物（EOM）处理人类胚胎肺成纤维细胞（HEL12469）4和24 H。B [a] P和3-NBA诱导PAH代谢的表达，但不诱导抗氧化酶的表达。IsoP的浓度降低，而AA的水平则趋于增加。尽管未检测到NF-κB的活性，所测试的化合物影响前列腺素-过氧化物合酶2（PTGS2）的表达。暴露于B [a] P后，前列腺素E2（PGE2）的水平降低，而3-NBA暴露则倾向于增加PGE2的浓度。EOM暴露后观察到明显的反应：诱导PAH代谢酶的表达，处理24小时后IsoP水平升高，但不影响AA浓度。在两个暴露时期后，NF-κB的活性均增加，并且在4小时的治疗后发现PTGS2表达的显着诱导。与PAH相似，EOM暴露与PGE2水平降低有关。总之，暴露于低促氧化剂电位的PAHs会导致IsoP水平降低，这意味着“抗氧化剂”特性。对于这类化合物，