Acrylamide induces accelerated endothelial ...
Type de document :
Article dans une revue scientifique
PMID :
URL permanente :
Titre :
Acrylamide induces accelerated endothelial aging in a human cell model
Auteur(s) :
Sellier, Cyril [Auteur]
Lille Inflammation Research International Center - U 995 [LIRIC]
Boulanger, Eric [Auteur]
Lille Inflammation Research International Center - U 995 [LIRIC]
Maladry, Francois [Auteur]
Lille Inflammation Research International Center - U 995 [LIRIC]
Tessier, Frederic [Auteur]
Lille Inflammation Research International Center - U 995 [LIRIC]
Lorenzi, Rodrigo [Auteur]
Lille Inflammation Research International Center - U 995 [LIRIC]
Nevière, Rémi [Auteur]
Lille Inflammation Research International Center - U 995 [LIRIC]
Desreumaux, Pierre [Auteur]
Lille Inflammation Research International Center - U 995 [LIRIC]
BEUSCART, Jean-Baptiste [Auteur]
Evaluation des technologies de santé et des pratiques médicales - ULR 2694 [METRICS]
Puisieux, Francois [Auteur]
Evaluation des technologies de santé et des pratiques médicales - ULR 2694 [METRICS]
Grossin, Nicolas [Auteur]
Lille Inflammation Research International Center - U 995 [LIRIC]
Lille Inflammation Research International Center - U 995 [LIRIC]
Boulanger, Eric [Auteur]

Lille Inflammation Research International Center - U 995 [LIRIC]
Maladry, Francois [Auteur]
Lille Inflammation Research International Center - U 995 [LIRIC]
Tessier, Frederic [Auteur]

Lille Inflammation Research International Center - U 995 [LIRIC]
Lorenzi, Rodrigo [Auteur]
Lille Inflammation Research International Center - U 995 [LIRIC]
Nevière, Rémi [Auteur]
Lille Inflammation Research International Center - U 995 [LIRIC]
Desreumaux, Pierre [Auteur]

Lille Inflammation Research International Center - U 995 [LIRIC]
BEUSCART, Jean-Baptiste [Auteur]

Evaluation des technologies de santé et des pratiques médicales - ULR 2694 [METRICS]
Puisieux, Francois [Auteur]

Evaluation des technologies de santé et des pratiques médicales - ULR 2694 [METRICS]
Grossin, Nicolas [Auteur]
Lille Inflammation Research International Center - U 995 [LIRIC]
Titre de la revue :
Food and chemical toxicology
Nom court de la revue :
Food Chem. Toxicol.
Numéro :
83
Pagination :
140-145
Date de publication :
2015-09-01
ISSN :
0278-6915
Mot(s)-clé(s) :
Mesh:Carcinogens/toxicity*
Mesh:Cell Proliferation/drug effects
Mesh:Biomarkers/metabolism
Mesh:Carcinogens/metabolism
Mesh:Acrylamide/metabolism
Mesh:Cell Survival/drug effects
Mesh:Cells
Mesh:Cultured
Mesh:Cellular Senescence/drug effects*
Mesh:Endothelium
Mesh:Vascular/cytology
Mesh:Endothelium
Mesh:Vascular/drug effects*
Mesh:Endothelium
Mesh:Vascular/metabolism
Mesh:Epoxy Compounds/metabolism
Mesh:Epoxy Compounds/toxicity*
Mesh:Human Umbilical Vein Endothelial Cells/cytology
Mesh:Humans
Mesh:Maillard Reaction
Mesh:Osmolar Concentration
Mesh:Telomere Shortening/drug effects
Mesh:Toxicity Tests
Mesh:Subchronic
Mesh:beta-Galactosidase/metabolism
Mesh:Apoptosis/drug effects
Mesh:Acrylamide/toxicity*
Telomere length shortening
Hayflick''s limit
Senescence
Endothelial cell
Acrylamide
Mesh:Cell Proliferation/drug effects
Mesh:Biomarkers/metabolism
Mesh:Carcinogens/metabolism
Mesh:Acrylamide/metabolism
Mesh:Cell Survival/drug effects
Mesh:Cells
Mesh:Cultured
Mesh:Cellular Senescence/drug effects*
Mesh:Endothelium
Mesh:Vascular/cytology
Mesh:Endothelium
Mesh:Vascular/drug effects*
Mesh:Endothelium
Mesh:Vascular/metabolism
Mesh:Epoxy Compounds/metabolism
Mesh:Epoxy Compounds/toxicity*
Mesh:Human Umbilical Vein Endothelial Cells/cytology
Mesh:Humans
Mesh:Maillard Reaction
Mesh:Osmolar Concentration
Mesh:Telomere Shortening/drug effects
Mesh:Toxicity Tests
Mesh:Subchronic
Mesh:beta-Galactosidase/metabolism
Mesh:Apoptosis/drug effects
Mesh:Acrylamide/toxicity*
Telomere length shortening
Hayflick''s limit
Senescence
Endothelial cell
Acrylamide
Discipline(s) HAL :
Sciences du Vivant [q-bio]
Résumé en anglais : [en]
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 ...
Lire la suite >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.Lire moins >
Lire la suite >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.Lire moins >
Langue :
Anglais
Audience :
Internationale
Vulgarisation :
Non
Établissement(s) :
Inserm
Université de Lille
CHU Lille
Université de Lille
CHU Lille
Équipe(s) de recherche :
Inflammatory digestive disease : pathophysiology and therapeutic targets developement
Glycation from inflammation to aging
Glycation from inflammation to aging
Date de dépôt :
2019-03-01T15:06:01Z
2020-03-12T11:26:38Z
2020-03-12T11:26:38Z