Acrylamide induces accelerated endothelial aging in a human cell model

Food Chem Toxicol. 2015 Sep;83:140-5. doi: 10.1016/j.fct.2015.05.021. Epub 2015 Jun 10.


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.

Keywords: Acrylamide; Endothelial cell; Hayflick's limit; Senescence; Telomere length shortening.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acrylamide / metabolism
  • Acrylamide / toxicity*
  • Apoptosis / drug effects
  • Biomarkers / metabolism
  • Carcinogens / metabolism
  • Carcinogens / toxicity*
  • Cell Proliferation / drug effects
  • Cell Survival / drug effects
  • Cells, Cultured
  • Cellular Senescence / drug effects*
  • Endothelium, Vascular / cytology
  • Endothelium, Vascular / drug effects*
  • Endothelium, Vascular / metabolism
  • Epoxy Compounds / metabolism
  • Epoxy Compounds / toxicity*
  • Human Umbilical Vein Endothelial Cells / cytology
  • Humans
  • Maillard Reaction
  • Osmolar Concentration
  • Telomere Shortening / drug effects
  • Toxicity Tests, Subchronic
  • beta-Galactosidase / metabolism


  • Biomarkers
  • Carcinogens
  • Epoxy Compounds
  • Acrylamide
  • glycidamide
  • GLB1 protein, human
  • beta-Galactosidase