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Impact of Acrylamide on Cellular Senescence Response and Cell Cycle Distribution Via an In-Vitro Study Publisher



Mahdizade E1, 2 ; Baeeri M2, 3 ; Hodjat M4 ; Rahimifard M3 ; Navaeinigjeh M3 ; Haghiaminjan H5 ; Moeininodeh S3 ; Hassani S2, 3 ; Dehghan G1 ; Hosseinpourfeizi MA1 ; Abdollahi M2, 3
Authors
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Authors Affiliations
  1. 1. Department of Biology, Faculty of Natural Sciences, University of Tabriz, Tabriz, Iran
  2. 2. Department of Toxicology and Pharmacology, Faculty of Pharmacy, Tehran University of Medical Sciences, Tehran, Iran
  3. 3. Toxicology and Diseases Group, Pharmaceutical Sciences Research Center (PSRC), The Institute of Pharmaceutical Sciences (TIPS), Tehran University of Medical Sciences, Tehran, Iran
  4. 4. Dental Research Center, Dentistry Research Institute, Tehran University of Medical Sciences, Tehran, Iran
  5. 5. Pharmaceutical Sciences Research Center, Ardabil University of Medical Sciences, Ardabil, Iran

Source: Iranian Journal of Pharmaceutical Research Published:2021


Abstract

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. © 2021, Briefland. All rights reserved.
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