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通过体外研究探讨丙烯酰胺对细胞衰老反应和细胞周期分布的影响。

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

作者信息

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

机构信息

Department of Biology, Faculty of Natural Sciences, University of Tabriz, Tabriz, Iran.

Department of Toxicology and Pharmacology, Faculty of Pharmacy, Tehran University of Medical Sciences, Tehran, Iran.

出版信息

Iran J Pharm Res. 2021 Fall;20(4):165-177. doi: 10.22037/ijpr.2021.115117.15206.

DOI:10.22037/ijpr.2021.115117.15206
PMID:35194437
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8842627/
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.

摘要

已表明接触某些环境毒素主要通过诱导氧化应激和对细胞系统的影响与细胞衰老相关。丙烯酰胺（ACR）因其对人类饮食暴露具有高风险的有害影响而引起全球关注。尽管有大量证据表明ACR具有致癌性，但关于其对细胞衰老影响的研究有限。在胚胎成纤维细胞暴露于ACR后，评估了β-半乳糖苷酶（SA-β-gal）活性水平、细胞周期分布以及衰老相关基因和炎症标志物的表达。暴露于不同浓度的ACR后，SA-β-gal活性显著升高，同时活性氧水平和脂质过氧化水平大幅增加。经ACR处理的细胞总抗氧化能力和硫醇分子水平明显下降。此外，在5 mM ACR的高浓度下，包括p38、p53和p21在内的细胞衰老相关基因的表达显著上调。ACR还诱导胚胎成纤维细胞出现G0/G1期阻滞。当前研究结果表明，接触ACR可增强衰老反应，导致氧化应激增加和细胞损伤。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1365/8842627/e0fde9a2fc06/ijpr-20-165-g007.jpg
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