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首页> 外文期刊>Journal of Cellular Physiology >Chromium (VI) inhibits heme oxygenase-1 expression in vivo and in arsenic-exposed human airway epithelial cells.
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Chromium (VI) inhibits heme oxygenase-1 expression in vivo and in arsenic-exposed human airway epithelial cells.

机译：铬(VI)抑制血红素oxygenase-1表达式在体内和arsenic-exposed人工气道上皮细胞。

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Inhaled hexavalent chromium (Cr(VI)) promotes lung injury and pulmonary diseases through poorly defined mechanisms. One hypothesis for this lung pathogenesis is that Cr(VI) silences induction of cytoprotective genes, such as heme oxygenase-1 (HO-1), whose total lung mRNA levels were reduced 21 days after nasal instillation of potassium dichromate in C57BL/6 mice. To investigate the mechanisms for this inhibition, Cr(VI) effects on basal and arsenic (As(III))-induced HO-1 expression were examined in cultured human bronchial epithelial (BEAS-2B) cells. An effect of Cr(VI) on the low basal HO-1 mRNA and protein levels in BEAS-2B cells was not detectible. In contrast, Cr(VI) added to the cells before As(III), but not simultaneously with As(III), attenuated As(III)-induced HO-1 expression. Transient transfection with luciferase reporter gene constructs controlled by the full length ho-1 promoter or deletion mutants demonstrated that this inhibition occurred in the E1 enhancer region containing critical antioxidant response elements (ARE). Cr(VI) pretreatment inhibited As(III)-induced activity of a transiently expressed reporter construct regulated by three ARE tandem repeats. The mechanism for this Cr(VI)-attenuated transactivation appeared to be Cr(VI) reduction of the nuclear levels of the transcription factor Nrf2 and As(III)-stimulated Nrf2 transcriptional complex binding to the ARE cis element. Finally, exposing cells to Cr(VI) prior to co-exposure with As(III) synergized for apoptosis and loss of membrane integrity. These data suggest that Cr(VI) silences induction of ARE-driven genes required for protection from secondary insults. The data also have important implications for understanding the toxic mechanisms of low level, mixed metal exposures in the lung.
机译：吸入六价铬(铬(VI))促进肺通过差损伤和肺疾病定义机制。发病机制是铬(VI)沉默的感应cytoprotective基因,如血红素oxygenase-1(HO-1),其肺总mRNA水平降低鼻腔滴注法的钾后21天C57BL / 6小鼠重铬酸。这种抑制机制、铬(VI)的影响全身的基底和砷((3))HO-1表达在人工培养的研究支气管上皮细胞(BEAS-2B)。低铬(VI)的基底HO-1信使rna和蛋白质水平BEAS-2B细胞没有可发觉的。相反,铬(VI)添加到细胞(3),但不像(3)同时,全身的减毒(III) HO-1表达式。瞬时转染与荧光素酶的记者全长基因构造控制ho-1发起人或删除突变体这种抑制作用发生在E1增强剂区域包含关键抗氧化反应元素(是)。(3)全身的活动是暂时性的记者表示构造由三个串联重复序列。铬(VI)减毒transactivation似乎铬(VI)减少核的水平转录因子Nrf2以及(III)刺激Nrf2转录复杂的绑定独联体元素。一氧化碳暴露之前(III)主体性细胞凋亡以及膜完整性的损失。数据表明,铬(VI)沉默的感应驱动保护所需的基因次要的侮辱。对理解毒性的影响机制的低水平,混合金属接触肺。

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