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AuthorZachariah, Matshediso
AuthorMaamoun, Hatem
AuthorMilano, Larissa
AuthorRayman, Margaret P.
AuthorMeira, Lisiane B.
AuthorAgouni, Abdelali
Available date2020-12-21T10:45:19Z
Publication Date2020-01-01
Publication NameJournal of Cellular Physiologyen_US
Identifierhttp://dx.doi.org/10.1002/jcp.30175
CitationZachariah, M, Maamoun, H, Milano, L, Rayman, MP, Meira, LB, Agouni, A. Endoplasmic reticulum stress and oxidative stress drive endothelial dysfunction induced by high selenium. J Cell Physiol. 2020; 1– 12. https://doi.org/10.1002/jcp.30175
ISSN00219541
URIhttps://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85096647041&origin=inward
URIhttp://hdl.handle.net/10576/17227
AbstractSelenium 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.
Languageen
PublisherWiley
Subjectapoptosis
Subjectendoplasmic-reticulum stress
Subjectendothelial dysfunction
Subjectoxidative stress
Subjectselenium
TitleEndoplasmic reticulum stress and oxidative stress drive endothelial dysfunction induced by high selenium
TypeArticle
elsevier.identifier.scopusid SCOPUS_ID:85096647041


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