An in vitro reporter gene assay based on human breast cancer T47D cells (ER-CALUX) was applied to examine the ability of diesel exhaust to induce or inhibit estrogen receptor (ER)-mediated gene expression. Exhaust from a heavy-duty diesel engine was either treated by iron- or copper/iron-catalyzed diesel particulate filters (DPFs) or studied as unfiltered exhaust. Collected samples included particle-bound and semivolatile constituents of diesel exhaust. Our findings show that all of the samples contained compounds that were able to induce ER-mediated gene expression as well as compounds that suppressed the activity of the endogenous hormone 17beta-estradiol (E2). Estrogenic activity prevailed over antiestrogenic activity. We found an overall ER-mediated activity of 1.63 +/- 0.31 ng E2 CALUX equivalents (E2-CEQs) per m(3) of unfiltered exhaust. In filtered exhaust, we measured 0.74 +/- 0.07 (iron-catalyzed DPF) and 0.55 +/- 0.09 ng E2-CEQ m(-3) (copper/iron-catalyzed DPF), corresponding to reductions in estrogenic activity of 55 and 66%, respectively. Our study demonstrates that both catalytic DPFs lowered the ER-mediated endocrine-disrupting potential of diesel exhaust.
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机译:基于人乳腺癌T47D细胞(ER-CALUX)的体外报道基因测定被应用于检查柴油机排气诱导或抑制雌激素受体(ER)介导的基因表达的能力。重型柴油发动机的废气通过铁或铜/铁催化的柴油机微粒过滤器(DPF)进行处理,或作为未过滤的废气进行研究。收集的样品包括柴油机废气中颗粒结合和半挥发性成分。我们的发现表明,所有样品均包含能够诱导ER介导的基因表达的化合物,以及抑制内源激素17β-雌二醇(E2)活性的化合物。雌激素活性胜过抗雌激素活性。我们发现,每m(3)未过滤的废气中总的ER介导活性为1.63 +/- 0.31 ng E2 CALUX当量(E2-CEQs)。在过滤后的废气中,我们测得0.74 +/- 0.07(铁催化的DPF)和0.55 +/- 0.09 ng E2-CEQ m(-3)(铜/铁催化的DPF),对应于雌激素活性降低55和分别为66%。我们的研究表明,两种催化性DPF都降低了ER介导的内分泌扰乱柴油机排气的潜力。
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