Acrylamide induces accelerated endothelial aging in a human cell model. (September 2015)

• Record Type: Journal Article
• Authors: Sellier, Cyril; Boulanger, Eric; Maladry, François; Tessier, Frédéric J.; Lorenzi, Rodrigo; Nevière, Rémi; Desreumaux, Pierre; Beuscart, Jean-Baptiste; Puisieux, François; Grossin, Nicolas
• Is Part Of: Food and chemical toxicology. Volume 83(2015)
• Page Start: 140
• Page End: 145
• Publication Date: 2015-09
• Subjects: Acrylamide -- Endothelial cell -- Senescence -- Hayflick's limit -- Telomere length shortening; AAM acrylamide -- C12FDG d-galactopyranoside -- CPD cumulative population doubling -- DiOC6-[3] 3, 3′-dihexyloxacarbocyanine iodide -- GA glycidamide -- HUVEC human umbilical vein endothelial cell -- PI propidium iodide -- SA-β-gal senescence-associated β-galactosidase -- SIPS stress-induced premature senescence -- TL telomere length; Toxicology -- Periodicals; Food poisoning -- Periodicals; Food Poisoning -- Periodicals; Toxicology -- Periodicals; Toxicologie -- Périodiques; Intoxications alimentaires -- Périodiques; Food poisoning; Toxicology; Periodicals; Electronic journals; 615.9
• DOI: 10.1016/j.fct.2015.05.021
• Languages: English
• ISSNs: 0278-6915

Abstract

Abstract: Acrylamide (AAM) has been recently discovered in food as a Maillard reaction product. AAM and glycidamide (GA), its metabolite, have been described as probably carcinogenic to humans. It is widely established that senescence and carcinogenicity are closely related. In vitro, endothelial aging is characterized by replicative senescence in which primary cells in culture lose their ability to divide. Our objective was to assess the effects of AAM and GA on human endothelial cell senescence. Human umbilical vein endothelial cells (HUVECs) cultured in vitro were used as model. HUVECs were cultured over 3 months with AAM or GA (1, 10 or 100 μM) until growth arrest. To analyze senescence, β-galactosidase activity and telomere length of HUVECs were measured by cytometry and semi-quantitative PCR, respectively. At all tested concentrations, AAM or GA reduced cell population doubling compared to the control condition ( p < 0.001). β-galactosidase activity in endothelial cells was increased when exposed to AAM (≥10 μM) or GA (≥1 μM) ( p < 0.05). AAM (≥10 μM) or GA (100 μM) accelerated telomere shortening in HUVECs ( p < 0.05). In conclusion, in vitro chronic exposure to AAM or GA at low concentrations induces accelerated senescence. This result suggests that an exposure to AAM might contribute to endothelial aging. Highlights: Chronic exposure to acrylamide in vitro has never been explored before. This work is the first one to investigate the vascular toxicity of AAM. Acrylamide could induce an accelerated endothelial aging.