Selenoenzymes, whose activity depends on adequate selenium (Se) supply, and phase II enzymes, encoded by target genes of nuclear factor erythroid 2-related factor 2 (Nrf2), take part in governing cellular redox homeostasis. Their interplay is still not entirely understood. Here, we exposed HepG2 hepatoma cells cultured under Se-deficient, Se-adequate, or Se-supranutritional conditions to the Nrf2 activators sulforaphane, cardamonin, or diethyl maleate. Nrf2 protein levels and intracellular localization were determined by immunoblotting, and mRNA levels of Nrf2 target genes and selenoproteins were assessed by qRT-PCR. Exposure to electrophiles resulted in rapid induction of Nrf2 and its enrichment in the nucleus, independent of the cellular Se status. All three electrophilic compounds caused an enhanced expression of Nrf2 target genes, although with differences regarding extent and time course of their induction. Whereas Se status did not significantly affect mRNA levels of the Nrf2 target genes, gene expression of selenoproteins with a low position in the cellular “selenoprotein hierarchy”, such as glutathione peroxidase 1 (GPX1) or selenoprotein W (SELENOW), was elevated under Se-supplemented conditions, as compared to cells held in Se-deficient media. In conclusion, no major effect of Se status on Nrf2 signalling was observed in HepG2 cells.

中文翻译：

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亲电试剂对Nrf2的激活在很大程度上与HepG2细胞的硒状态无关

硒酶的活性取决于充足的硒（Se）供应，而II期酶则由核因子红系2相关因子2（Nrf2）的靶基因编码，参与控制细胞的氧化还原稳态。它们之间的相互作用仍不完全清楚。在这里，我们将在缺硒，富硒或富硒条件下培养的HepG2肝癌细胞暴露于Nrf2激活剂萝卜硫烷，豆蔻素或马来酸二乙酯。通过免疫印迹测定Nrf2蛋白水平和细胞内定位，并通过qRT-PCR评估Nrf2靶基因和硒蛋白的mRNA水平。接触亲电子试剂会导致Nrf2的快速诱导及其在细胞核中的富集，而与细胞硒状态无关。所有这三种亲电子化合物均导致Nrf2靶基因表达增强，尽管在归纳的程度和时间上存在差异。硒的状态对Nrf2靶基因的mRNA水平没有明显影响，而硒下谷胱甘肽过氧化物酶1（GPX1）或硒蛋白W（SELENOW）等在细胞“硒蛋白层次”中位置低的硒蛋白的基因表达却升高了。 -与硒缺乏培养基中保存的细胞相比-补充的条件 总之，在HepG2细胞中未观察到Se状态对Nrf2信号的重大影响。与在缺乏硒的培养基中保存的细胞相比，在富含硒的条件下细胞中的汞升高。总之，在HepG2细胞中未观察到Se状态对Nrf2信号的重大影响。与在缺乏硒的培养基中保存的细胞相比，在富含硒的条件下细胞中的汞升高。总之，在HepG2细胞中未观察到Se状态对Nrf2信号的重大影响。