Acrylamide induces accelerated endothelial aging in a human cell model
| Autor: | Rodrigo Lorenzi, Cyril Sellier, Eric Boulanger, Pierre Desreumaux, Nicolas Grossin, François Puisieux, Remi Neviere, Frédéric J. Tessier, Jean-Baptiste Beuscart, François Maladry |
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| Přispěvatelé: | Lille Inflammation Research International Center (LIRIC), Institut Pasteur de Lille, Réseau International des Instituts Pasteur (RIIP)-Réseau International des Instituts Pasteur (RIIP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lille-Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille), Expression de Gènes et régulation Epigénétique par l'ALiment (EGEAL), Institut Polytechnique LaSalle Beauvais, Santé publique : épidémiologie et qualité des soins-EA 2694 (CERIM), Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille)-Université de Lille, Pôle de gérontologie [CHRU de Lille], Hôpital Roger Salengro-Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille), This study was supported by the GLYCACHIC Program (Nord-Pas de Calais and Picardie Regions 2011_00202/00219-00221 and European Union 2011_00190/00198-00199) with additional assistance provided by the Nutrition-Health-Longevity (Nutrition-Santé-Longévité) Cluster (Lille, France). The authors are also grateful to Lille Métropole Communauté Urbaine and to Digestscience Foundation for financial support., Université de Lille-Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille), Lille Inflammation Research International Center - U 995 (LIRIC), Evaluation des technologies de santé et des pratiques médicales - ULR 2694 (METRICS), Hôpital Roger Salengro [Lille]-Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille), Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lille-Institut Pasteur de Lille, Réseau International des Instituts Pasteur (RIIP)-Réseau International des Instituts Pasteur (RIIP) |
| Jazyk: | angličtina |
| Rok vydání: | 2015 |
| Předmět: |
[SDV]Life Sciences [q-bio]
Apoptosis MESH: Epoxy Compounds/metabolism MESH: Acrylamide/metabolism Toxicology MESH: Acrylamide/toxicity Umbilical vein 0302 clinical medicine MESH: Osmolar Concentration MESH: Cell Proliferation/drug effects Endothelial cell MESH: Epoxy Compounds/toxicity MESH: Telomere Shortening/drug effects MESH: Carcinogens/metabolism Hayflick's limit Cells Cultured Cellular Senescence Telomere Shortening 0303 health sciences Acrylamide Chemistry MESH: Carcinogens/toxicity General Medicine Endothelial stem cell medicine.anatomical_structure Biochemistry MESH: Endothelium Vascular/metabolism 030220 oncology & carcinogenesis Cell aging MESH: Cells Cultured Senescence Telomere length shortening MESH: Apoptosis/drug effects Endothelium MESH: Endothelium Vascular/cytology Cell Survival MESH: Maillard Reaction MESH: Toxicity Tests Subchronic 03 medical and health sciences parasitic diseases Human Umbilical Vein Endothelial Cells medicine Humans Cell Proliferation 030304 developmental biology MESH: Humans Cell growth MESH: Endothelium Vascular/drug effects MESH: Biomarkers/metabolism Osmolar Concentration Toxicity Tests Subchronic beta-Galactosidase Molecular biology Maillard Reaction Telomere MESH: Human Umbilical Vein Endothelial Cells/cytology Carcinogens Epoxy Compounds MESH: Cellular Senescence/drug effects Endothelium Vascular MESH: beta-Galactosidase/metabolism MESH: Cell Survival/drug effects Biomarkers Food Science |
| Zdroj: | Food and Chemical Toxicology Food and Chemical Toxicology, Elsevier, 2015, Food and chemical toxicology, 83, pp.140-145. ⟨10.1016/j.fct.2015.05.021⟩ Food and Chemical Toxicology, 2015, Food and chemical toxicology, 83, pp.140-145. ⟨10.1016/j.fct.2015.05.021⟩ |
| ISSN: | 0278-6915 |
| DOI: | 10.1016/j.fct.2015.05.021⟩ |
| Popis: | International audience; 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.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. |
| Databáze: | OpenAIRE |
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