Related Experiment Video

Updated: Jun 26, 2026

Detection and Visualization of DNA Damage-induced Protein Complexes in Suspension Cell Cultures Using the Proximity Ligation Assay
13:10

Detection and Visualization of DNA Damage-induced Protein Complexes in Suspension Cell Cultures Using the Proximity Ligation Assay

Published on: June 9, 2017

TEGDMA-induced oxidative DNA damage and activation of ATM and MAP kinases

Alexander Eckhardt1, Nicol Gerstmayr, Karl-Anton Hiller

  • 1Department of Operative Dentistry and Periodontology, University of Regensburg, Regensburg, Germany.

Biomaterials
|January 14, 2009
PubMed

Insights

Triethylene glycol dimethacrylate (TEGDMA) resin monomers cause oxidative stress and DNA damage in oral cells. N-acetylcysteine (NAC) partially protects cells by inhibiting ATM and MAPK signaling pathways.

Area of Science:

  • Biomaterials Science
  • Molecular Biology
  • Toxicology

Background:

  • Resin monomers in dental materials can harm oral tissues.
  • Understanding molecular mechanisms of toxicity is crucial for developing protective strategies.
  • Oxidative stress and DNA damage are key factors in cellular injury.

Purpose of the Study:

  • To investigate oxidative DNA damage, ATM activation, and MAPK signaling induced by triethylene glycol dimethacrylate (TEGDMA).
  • To assess the protective effects of N-acetylcysteine (NAC) against TEGDMA-induced toxicity.
  • To elucidate the role of oxidative stress in TEGDMA's effects on oral cells.

Main Methods:

  • Exposure of THP-1 cells to varying concentrations of TEGDMA.
  • Measurement of cell viability and 8-oxoguanine (8-oxoG) levels.
  • Analysis of cell cycle progression, ATM activation, and MAPK phosphorylation (p38, ERK1/2).
  • Evaluation of NAC's protective effects.

Main Results:

  • TEGDMA (3-5 mM) reduced cell viability and increased 8-oxoG levels, indicating DNA damage.
  • TEGDMA caused cell cycle arrest in G1 and G2 phases.
  • Activation of ATM and phosphorylation of p38 and ERK1/2 were observed, suggesting oxidative stress.
  • NAC partially mitigated TEGDMA's toxicity and inhibited signaling pathway activation.

Conclusions:

  • TEGDMA induces oxidative stress, DNA damage, and activates ATM and MAPK signaling pathways in oral cells.
  • These pathways are involved in regulating cell survival and apoptosis.
  • NAC demonstrates potential as a protective agent against resin monomer-induced oral tissue damage.

More Related Videos

Visualizing the DNA Damage Response in Purkinje Cells Using Cerebellar Organotypic Cultures08:41

Visualizing the DNA Damage Response in Purkinje Cells Using Cerebellar Organotypic Cultures

Published on: December 27, 2024

Visualization of DNA Repair Proteins Interaction by Immunofluorescence07:55

Visualization of DNA Repair Proteins Interaction by Immunofluorescence

Published on: June 26, 2020

Related Concept Videos

DNA Damage can Stall the Cell Cycle02:36

DNA Damage can Stall the Cell Cycle

In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
DNA Damage Can Stall the Cell Cycle02:36

DNA Damage Can Stall the Cell Cycle

In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
MAPK Signaling Cascades01:07

MAPK Signaling Cascades

Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...
Spontaneous and Induced Mutations01:30

Spontaneous and Induced Mutations

Spontaneous mutations arise infrequently during DNA replication due to errors in the process. A key factor behind these errors is tautomeric shifts in nitrogenous bases, where bases transition from keto to enol forms or amino to imino forms. This shift can alter base-pairing rules, leading to mutations. Additionally, reactive oxygen species (ROS) arising from aerobic metabolism can damage DNA, resulting in depurination (loss of a purine base) or depyrimidination (loss of a pyrimidine base).
TGF - β Signaling Pathway01:16

TGF - β Signaling Pathway

The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors are of three kinds RI, RII, and RIII. The RI...
PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a rapamycin-insensitive companion...