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Impact of Acrylamide on Cellular Senescence Response and Cell Cycle Distribution via an In-vitro Study

Exposure to certain environmental toxins has been shown to be associated with cellular senescence mainly through induction of oxidative stress and impact on cellular systems. Acrylamide (ACR) has raised worldwide concerns regarding the high risk of human dietary exposure to its hazardous effect. Alt...

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Autores principales: Mahdizade, Elahe, Baeeri, Maryam, Hodjat, Mahshid, Rahimifard, Mahban, Navaei-Nigjeh, Mona, Haghi-Aminjan, Hamed, Moeini-Nodeh, Shermineh, Hassani, Shokoufeh, Dehghan, Gholamreza, Hosseinpour-Feizi, Mohammad Ali, Abdollahi, Mohammad
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Shaheed Beheshti University of Medical Sciences 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8842627/
https://www.ncbi.nlm.nih.gov/pubmed/35194437
http://dx.doi.org/10.22037/ijpr.2021.115117.15206
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author Mahdizade, Elahe
Baeeri, Maryam
Hodjat, Mahshid
Rahimifard, Mahban
Navaei-Nigjeh, Mona
Haghi-Aminjan, Hamed
Moeini-Nodeh, Shermineh
Hassani, Shokoufeh
Dehghan, Gholamreza
Hosseinpour-Feizi, Mohammad Ali
Abdollahi, Mohammad
author_facet Mahdizade, Elahe
Baeeri, Maryam
Hodjat, Mahshid
Rahimifard, Mahban
Navaei-Nigjeh, Mona
Haghi-Aminjan, Hamed
Moeini-Nodeh, Shermineh
Hassani, Shokoufeh
Dehghan, Gholamreza
Hosseinpour-Feizi, Mohammad Ali
Abdollahi, Mohammad
author_sort Mahdizade, Elahe
collection PubMed
description Exposure to certain environmental toxins has been shown to be associated with cellular senescence mainly through induction of oxidative stress and impact on cellular systems. Acrylamide (ACR) has raised worldwide concerns regarding the high risk of human dietary exposure to its hazardous effect. Although there is ample evidence about the carcinogenicity of ACR, limited studies have focused on its impact on cellular aging. The levels of β-galactosidase (SA-β-gal) activity, cell cycle distribution, and the expression of the senescence-associated gene and inflammatory markers were evaluated following exposure of embryonic fibroblast cells to ACR. A significant elevation in SA-β-gal activity after exposure to different concentrations of ACR was accompanied by a considerably increased level of reactive oxygen species and lipid peroxidation. ACR-treated cells showed a noticeable decline in the total antioxidant capacity and thiol molecules. Moreover, the expression of cellular senescence-related genes including p38, p53, and p21 significantly upregulated at the high concentration of 5 mM ACR. ACR also induced G0/G1 phase arrest in embryonic fibroblast cells. The current study results revealed that exposure to ACR could enhance senescence response, contributing to increased oxidative stress and cellular damage. 
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spelling pubmed-88426272022-02-21 Impact of Acrylamide on Cellular Senescence Response and Cell Cycle Distribution via an In-vitro Study Mahdizade, Elahe Baeeri, Maryam Hodjat, Mahshid Rahimifard, Mahban Navaei-Nigjeh, Mona Haghi-Aminjan, Hamed Moeini-Nodeh, Shermineh Hassani, Shokoufeh Dehghan, Gholamreza Hosseinpour-Feizi, Mohammad Ali Abdollahi, Mohammad Iran J Pharm Res Original Article Exposure to certain environmental toxins has been shown to be associated with cellular senescence mainly through induction of oxidative stress and impact on cellular systems. Acrylamide (ACR) has raised worldwide concerns regarding the high risk of human dietary exposure to its hazardous effect. Although there is ample evidence about the carcinogenicity of ACR, limited studies have focused on its impact on cellular aging. The levels of β-galactosidase (SA-β-gal) activity, cell cycle distribution, and the expression of the senescence-associated gene and inflammatory markers were evaluated following exposure of embryonic fibroblast cells to ACR. A significant elevation in SA-β-gal activity after exposure to different concentrations of ACR was accompanied by a considerably increased level of reactive oxygen species and lipid peroxidation. ACR-treated cells showed a noticeable decline in the total antioxidant capacity and thiol molecules. Moreover, the expression of cellular senescence-related genes including p38, p53, and p21 significantly upregulated at the high concentration of 5 mM ACR. ACR also induced G0/G1 phase arrest in embryonic fibroblast cells. The current study results revealed that exposure to ACR could enhance senescence response, contributing to increased oxidative stress and cellular damage.  Shaheed Beheshti University of Medical Sciences 2021 /pmc/articles/PMC8842627/ /pubmed/35194437 http://dx.doi.org/10.22037/ijpr.2021.115117.15206 Text en https://creativecommons.org/licenses/by/3.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution License, (http://creativecommons.org/licenses/by/3.0/ (https://creativecommons.org/licenses/by/3.0/) ) which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Article
Mahdizade, Elahe
Baeeri, Maryam
Hodjat, Mahshid
Rahimifard, Mahban
Navaei-Nigjeh, Mona
Haghi-Aminjan, Hamed
Moeini-Nodeh, Shermineh
Hassani, Shokoufeh
Dehghan, Gholamreza
Hosseinpour-Feizi, Mohammad Ali
Abdollahi, Mohammad
Impact of Acrylamide on Cellular Senescence Response and Cell Cycle Distribution via an In-vitro Study
title Impact of Acrylamide on Cellular Senescence Response and Cell Cycle Distribution via an In-vitro Study
title_full Impact of Acrylamide on Cellular Senescence Response and Cell Cycle Distribution via an In-vitro Study
title_fullStr Impact of Acrylamide on Cellular Senescence Response and Cell Cycle Distribution via an In-vitro Study
title_full_unstemmed Impact of Acrylamide on Cellular Senescence Response and Cell Cycle Distribution via an In-vitro Study
title_short Impact of Acrylamide on Cellular Senescence Response and Cell Cycle Distribution via an In-vitro Study
title_sort impact of acrylamide on cellular senescence response and cell cycle distribution via an in-vitro study
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8842627/
https://www.ncbi.nlm.nih.gov/pubmed/35194437
http://dx.doi.org/10.22037/ijpr.2021.115117.15206
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