Suppr超能文献

无机砷在培养的角质形成细胞中激活转录因子Nrf2:过氧化氢的作用。

Transcription factor Nrf2 activation by inorganic arsenic in cultured keratinocytes: involvement of hydrogen peroxide.

作者信息

Pi Jingbo, Qu Wei, Reece Jeffrey M, Kumagai Yoshito, Waalkes Michael P

机构信息

Inorganic Carcinogenesis Section, Laboratory of Comparative Carcinogenesis, NCI at NIEHS, National Institutes of Health, Research Triangle Park, NC 27709, USA.

出版信息

Exp Cell Res. 2003 Nov 1;290(2):234-45. doi: 10.1016/s0014-4827(03)00341-0.

Abstract

Inorganic arsenic is a well-documented human carcinogen that targets the skin. The induction of oxidative stress, as shown with arsenic, may have a bearing on the carcinogenic mechanism of this metalloid. The transcription factor Nrf2 is a key player in the regulation of genes encoding for many antioxidative response enzymes. Thus, the effect of inorganic arsenic (as sodium arsenite) on Nrf2 expression and localization was studied in HaCaT cells, an immortalized human keratinocyte cell line. We found, for the first time, that arsenic enhanced cellular expression of Nrf2 at the transcriptional and protein levels and activated expression of Nrf2-related genes in these cells. In addition, arsenic exposure caused nuclear accumulation of Nrf2 in association with downstream activation of Nrf2-mediated oxidative response genes. Arsenic simultaneously increased the expression of Keap1, a regulator of Nrf2 activity. The coordinated induction of Keap1 expression and nuclear Nrf2 accumulation induced by arsenic suggests that Keap1 is important to arsenic-induced Nrf2 activation. Furthermore, when cells were pretreated with scavengers of hydrogen peroxide (H(2)O(2)) such as catalase-polyethylene glycol (PEG-CAT) or Tiron, arsenic-induced nuclear Nrf2 accumulation was suppressed, whereas CuDIPSH, a cell-permeable superoxide dismutase (SOD) mimic compound that produces H(2)O(2) from superoxide (*O(2)(-)), enhanced Nrf2 nuclear accumulation. These results indicate that H(2)O(2), rather than *O(2)(-), is the mediator of nuclear Nrf2 accumulation. Additional study showed that arsenic causes increased cellular H(2)O(2) production and that H(2)O(2) itself has the ability to increase Nrf2 expression at both the transcription and protein levels in HaCaT cells. Taken together, these data clearly show that arsenic increases Nrf2 expression and activity at multiple levels and that H(2)O(2) is one of the mediators of this process.

摘要

无机砷是一种有充分文献记载的可靶向皮肤的人类致癌物。如砷所显示的那样,氧化应激的诱导可能与这种类金属的致癌机制有关。转录因子Nrf2是许多抗氧化反应酶编码基因调控中的关键因子。因此,在永生化的人角质形成细胞系HaCaT细胞中研究了无机砷(以亚砷酸钠形式)对Nrf2表达和定位的影响。我们首次发现,砷在转录和蛋白质水平上增强了Nrf2的细胞表达,并激活了这些细胞中Nrf2相关基因的表达。此外,砷暴露导致Nrf2在细胞核中积累,并伴有Nrf2介导的氧化反应基因的下游激活。砷同时增加了Nrf2活性调节因子Keap1的表达。砷诱导的Keap1表达和细胞核Nrf2积累的协同作用表明,Keap1对砷诱导的Nrf2激活很重要。此外,当细胞用过氧化氢(H₂O₂)清除剂如过氧化氢酶 - 聚乙二醇(PEG - CAT)或替诺福韦预处理时,砷诱导的细胞核Nrf2积累受到抑制,而CuDIPSH,一种可透过细胞的超氧化物歧化酶(SOD)模拟化合物,能将超氧化物(O₂⁻)转化为H₂O₂,增强了Nrf2的细胞核积累。这些结果表明,是H₂O₂而非O₂⁻介导了细胞核Nrf2的积累。进一步的研究表明,砷会导致细胞内H₂O₂生成增加,并且H₂O₂本身具有在HaCaT细胞中在转录和蛋白质水平上增加Nrf2表达的能力。综上所述,这些数据清楚地表明,砷在多个水平上增加了Nrf2的表达和活性,并且H₂O₂是这一过程的介导因子之一。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验