期刊
JOURNAL OF CELLULAR PHYSIOLOGY
卷 236, 期 6, 页码 4348-4359出版社
WILEY
DOI: 10.1002/jcp.30175
关键词
apoptosis; endoplasmic‐ reticulum stress; endothelial dysfunction; oxidative stress; selenium
资金
- Qatar National Research Fund [UREP24-016-3-004]
- Qatar National Library
- Royal Society [RG120480]
- Qatar University [QUCG-CPH-20/21-3]
Selenium is an essential trace element for human health, but a balanced intake is crucial for maximizing its health benefits. High selenium intake above physiological levels may increase diabetes risk and result in endothelial dysfunction. Selenium induces cancer cell apoptosis via endoplasmic reticulum stress, but its role in endothelial dysfunction remains unknown.
Selenium is an essential trace element important for human health. A balanced intake is, however, crucial to maximize the health benefits of selenium. At physiological concentrations, selenium mediates antioxidant, anti-inflammatory, and pro-survival actions. However, supra-nutritional selenium intake was associated with increased diabetes risk leading potentially to endothelial dysfunction, the initiating step in atherosclerosis. High selenium causes apoptosis in cancer cells via endoplasmic reticulum (ER) stress, a mechanism also implicated in endothelial dysfunction. Nonetheless, whether ER stress drives selenium-induced endothelial dysfunction, remains unknown. Here, we investigated the effects of increasing concentrations of selenium on endothelial cells. High selenite reduced nitric oxide bioavailability and impaired angiogenesis. High selenite also induced ER stress, increased reactive oxygen species (ROS) production, and apoptosis. Pretreatment with the chemical chaperone, 4-phenylbutyrate, prevented the toxic effects of selenium. Our findings support a model where high selenite leads to endothelial dysfunction through activation of ER stress and increased ROS production. These results highlight the importance of tailoring selenium supplementation to achieve maximal health benefits and suggest that prophylactic use of selenium supplements as antioxidants may entail risk.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据