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The processes associated with lipid peroxidation in human embryonic lung fibroblasts, treated with polycyclic aromatic hydrocarbons and organic extract from particulate matter.
Mutagenesis ( IF 2.5 ) Pub Date : 2019-05-29 , DOI: 10.1093/mutage/gez004
Pavel Rossner 1 , Helena Libalova 1 , Tereza Cervena 1, 2 , Kristyna Vrbova 1 , Fatima Elzeinova 1 , Alena Milcova 1 , Andrea Rossnerova 1 , Zuzana Novakova 1 , Miroslav Ciganek 3 , Michaela Pokorna 1 , Antonin Ambroz 1 , Jan Topinka 1
Affiliation  

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:

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,
更新日期:2019-11-01
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