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Updated: Jul 2, 2026
Induction and Validation of Cellular Senescence in Primary Human Cells
Published on: June 20, 2018
Dicarbonyl-induced accelerated aging in vitro in human skin fibroblasts
Henrik Sejersen1, Suresh I S Rattan
1Laboratory of Cellular Ageing, Department of Molecular Biology, University of Aarhus, Gustav Wieds Vej 10-C, 8000, Aarhus, Denmark. Henrik.Sejersen@agrsci.dk
Abstract:
Dicarbonyls glyoxal (GO) and methylglyoxal (MGO) produced during the autoxidation of reducing sugars are a source of macromolecular damage in cells. Since an accumulation of damaged macromolecules is a universal characteristic of aging, we have tested whether GO and MGO which cause oxidative damage to proteins and other macromolecules can bring about accelerated aging in normal human skin fibroblasts in vitro. A treatment of cells with 1.0 mM GO or 400 microM MGO leads to the appearance of senescent phenotype within 3 days, as judged by the following criteria: morphological phenotype, irreversible growth arrest and G2 arrest, increased senescence-associated beta-galactosidase (SABG) activity, increased H2O2 level, increased Nxi-(carboxymethyl)-lysine (CML) protein level, and altered activities of superoxide dismutase and catalase antioxidant enzymes. This experimental model of accelerated cellular aging in vitro can be useful for studies on testing the effects of various physical, chemical and biological conditions, including natural and synthetic molecules, for the modulation of aging.
Insights
Glyoxal (GO) and methylglyoxal (MGO) can accelerate cellular aging in human skin fibroblasts. This study demonstrates their role in inducing a senescent phenotype, offering a model for aging research.
Area of Science:
- Cellular Biology
- Aging Research
- Biochemistry
Background:
- Dicarbonyls like glyoxal (GO) and methylglyoxal (MGO) arise from sugar autoxidation and cause macromolecular damage.
- Accumulation of damaged macromolecules is a hallmark of cellular aging.
Purpose of the Study:
- To investigate if GO and MGO induce accelerated aging in normal human skin fibroblasts in vitro.
- To establish a cellular model for studying aging modulation.
Main Methods:
- Treatment of human skin fibroblasts with GO or MGO.
- Assessment of cellular aging criteria including morphology, growth arrest, senescence-associated beta-galactosidase (SABG) activity, hydrogen peroxide (H2O2) levels, N-(carboxymethyl)-lysine (CML) protein levels, and antioxidant enzyme activities.
Main Results:
- Treatment with 1.0 mM GO or 400 microM MGO induced a senescent phenotype within 3 days.
- Observed changes included morphological alterations, irreversible growth and G2 arrest, increased SABG activity, elevated H2O2 and CML levels, and modified superoxide dismutase and catalase activities.
Conclusions:
- GO and MGO can accelerate cellular aging in human skin fibroblasts.
- This in vitro model is valuable for testing interventions that modulate aging processes.
