The oxidative stress: endoplasmic reticulum stress axis in cadmium toxicity
The oxidative stress: endoplasmic reticulum stress axis in cadmium toxicity
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DOI：
10.1007/s10534-010-9296-2
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发表时间：
2010-10-01
期刊：
影响因子：
3.5
通讯作者：
Hiramatsu, Nobuhiko
中科院分区：
文献类型：
--
作者：
Kitamura, Masanori;Hiramatsu, Nobuhiko
镉优先积累在肾脏中，这是镉相关毒性的主要目标。有几种潜在的机制被认为是组织损伤的关键介质，而活性氧(ROS)被认为是组织损伤的重要介质。除了氧化应激，我们最近发现内质网(ER)应激也起着关键作用。镉在体内和体外引起内质网应激，并介导靶组织细胞凋亡的诱导。在这篇文章中，我们描述了内质网应激和未折叠蛋白反应(UPR)的特定分支在镉引发的组织损伤中的作用，特别是肾毒性。我们还讨论了氧化应激和内质网应激之间的关系，以及选择性ROS参与UPR促凋亡分支的诱导。
Cadmium preferentially accumulates in the kidney, the major target for cadmium-related toxicity. Several underlying mechanisms are postulated, and reactive oxygen species (ROS) have been considered as crucial mediators for tissue injuries. In addition to oxidative stress, we recently disclosed that endoplasmic reticulum (ER) stress also plays a critical role. Cadmium causes ER stress in vitro and in vivo and mediates induction of apoptosis in target tissues. In this article, we describe a role for ER stress and involvement of particular branches of the unfolded protein response (UPR) in cadmium-triggered tissue injury, especially nephrotoxicity. We also discuss relationship between oxidative stress and ER stress, and involvement of selective ROS in the induction of pro-apoptotic branches of the UPR.