Endoplasmic reticulum stress and oxidative stress drive endothelial dysfunction induced by high selenium

<p></p><div> <p>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....

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Main Author: Matshediso Zachariah (13878830) (author)
Other Authors: Hatem Maamoun (14778730) (author), Larissa Milano (14133591) (author), Margaret P. Rayman (14778733) (author), Lisiane B. Meira (14778736) (author), Abdelali Agouni (181926) (author)
Published: 2023
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_version_ 1864513565255270400
author Matshediso Zachariah (13878830)
author2 Hatem Maamoun (14778730)
Larissa Milano (14133591)
Margaret P. Rayman (14778733)
Lisiane B. Meira (14778736)
Abdelali Agouni (181926)
author2_role author
author
author
author
author
author_facet Matshediso Zachariah (13878830)
Hatem Maamoun (14778730)
Larissa Milano (14133591)
Margaret P. Rayman (14778733)
Lisiane B. Meira (14778736)
Abdelali Agouni (181926)
author_role author
dc.creator.none.fl_str_mv Matshediso Zachariah (13878830)
Hatem Maamoun (14778730)
Larissa Milano (14133591)
Margaret P. Rayman (14778733)
Lisiane B. Meira (14778736)
Abdelali Agouni (181926)
dc.date.none.fl_str_mv 2023-03-16T06:23:34Z
dc.identifier.none.fl_str_mv 10.1002/jcp.30175
dc.relation.none.fl_str_mv https://figshare.com/articles/journal_contribution/Endoplasmic_reticulum_stress_and_oxidative_stress_drive_endothelial_dysfunction_induced_by_high_selenium/22258207
dc.rights.none.fl_str_mv CC BY 4.0
info:eu-repo/semantics/openAccess
dc.subject.none.fl_str_mv Biological sciences
Biochemistry and cell biology
Cell Biology
Clinical Biochemistry
Physiology
dc.title.none.fl_str_mv Endoplasmic reticulum stress and oxidative stress drive endothelial dysfunction induced by high selenium
dc.type.none.fl_str_mv Text
Journal contribution
info:eu-repo/semantics/publishedVersion
text
contribution to journal
description <p></p><div> <p>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.</p></div><p></p><h2>Other Information</h2> <p> Published in: Journal of Cellular Physiology<br> License: <a href="http://creativecommons.org/licenses/by/4.0/" target="_blank">http://creativecommons.org/licenses/by/4.0/</a><br>See article on publisher's website: <a href="http://dx.doi.org/10.1002/jcp.30175" target="_blank">http://dx.doi.org/10.1002/jcp.30175</a></p>
eu_rights_str_mv openAccess
id Manara2_68603fcc35ee005be167153d263c47af
identifier_str_mv 10.1002/jcp.30175
network_acronym_str Manara2
network_name_str Manara2
oai_identifier_str oai:figshare.com:article/22258207
publishDate 2023
repository.mail.fl_str_mv
repository.name.fl_str_mv
repository_id_str
rights_invalid_str_mv CC BY 4.0
spelling Endoplasmic reticulum stress and oxidative stress drive endothelial dysfunction induced by high seleniumMatshediso Zachariah (13878830)Hatem Maamoun (14778730)Larissa Milano (14133591)Margaret P. Rayman (14778733)Lisiane B. Meira (14778736)Abdelali Agouni (181926)Biological sciencesBiochemistry and cell biologyCell BiologyClinical BiochemistryPhysiology<p></p><div> <p>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.</p></div><p></p><h2>Other Information</h2> <p> Published in: Journal of Cellular Physiology<br> License: <a href="http://creativecommons.org/licenses/by/4.0/" target="_blank">http://creativecommons.org/licenses/by/4.0/</a><br>See article on publisher's website: <a href="http://dx.doi.org/10.1002/jcp.30175" target="_blank">http://dx.doi.org/10.1002/jcp.30175</a></p>2023-03-16T06:23:34ZTextJournal contributioninfo:eu-repo/semantics/publishedVersiontextcontribution to journal10.1002/jcp.30175https://figshare.com/articles/journal_contribution/Endoplasmic_reticulum_stress_and_oxidative_stress_drive_endothelial_dysfunction_induced_by_high_selenium/22258207CC BY 4.0info:eu-repo/semantics/openAccessoai:figshare.com:article/222582072023-03-16T06:23:34Z
spellingShingle Endoplasmic reticulum stress and oxidative stress drive endothelial dysfunction induced by high selenium
Matshediso Zachariah (13878830)
Biological sciences
Biochemistry and cell biology
Cell Biology
Clinical Biochemistry
Physiology
status_str publishedVersion
title Endoplasmic reticulum stress and oxidative stress drive endothelial dysfunction induced by high selenium
title_full Endoplasmic reticulum stress and oxidative stress drive endothelial dysfunction induced by high selenium
title_fullStr Endoplasmic reticulum stress and oxidative stress drive endothelial dysfunction induced by high selenium
title_full_unstemmed Endoplasmic reticulum stress and oxidative stress drive endothelial dysfunction induced by high selenium
title_short Endoplasmic reticulum stress and oxidative stress drive endothelial dysfunction induced by high selenium
title_sort Endoplasmic reticulum stress and oxidative stress drive endothelial dysfunction induced by high selenium
topic Biological sciences
Biochemistry and cell biology
Cell Biology
Clinical Biochemistry
Physiology