PMID- 16376982
OWN - NLM
STAT- MEDLINE
DCOM- 20070110
LR  - 20181201
IS  - 0109-5641 (Print)
IS  - 0109-5641 (Linking)
VI  - 22
IP  - 12
DP  - 2006 Dec
TI  - Involvement of oxidative stress in mutagenicity and apoptosis caused by dental 
      resin monomers in cell cultures.
PG  - 1086-92
AB  - OBJECTIVE: This investigation studied the possibility that apoptosis as well as 
      mutagenicity induced by resin monomers are mediated by oxidative stress. METHODS: 
      A range of dilutions of three resin monomers (GMA, TEGDMA, and HEMA) was added to 
      culture medium (DMEM/10% FBS), of V79-4 fibroblasts and RPC-C2A pulp cells for 24 
      h. Their cytotoxic effects were measured by a colorimetric functional assay 
      (MTT). Chromosomal aberration induced by the resin monomers was investigated by 
      counting micronuclei in V79-4 cells. The effects of the resin monomers on DNA 
      fragmentation were viewed by agarose gel electrophoresis of DNA, isolated from 
      RPC-C2A pulp cells that were treated by resin compounds. Resin monomer-induced 
      apoptosis was further confirmed by flow cytometry (staining with both annexin 
      V-FITC and PI). RESULTS: All monomers exhibited a dose-dependent cytotoxic 
      effect, and the ranking of the cytotoxicity based on TC50 was GMA > TEGDMA > 
      HEMA. The resin monomer-induced cytotoxicity was significantly decreased by 
      co-treatment with N-acetylcystein (NAC), an antioxidant. The authors also 
      confirmed a dose-dependent genotoxicity of the resin monomers that had induced 
      micronucleated cells in V79-4 fibroblasts. Similar to the effects on 
      cytotoxicity, NAC reduced the numbers of micronuclei in comparison with those 
      generated by the resin monomers. The preventive effects of NAC were also observed 
      in monomer-induced apoptosis in RPC-C2A cells. A DNA ladder pattern, 
      characteristic of apoptosis, was shown at cytotoxic concentrations, but NAC 
      blocked the resin monomer-mediated DNA fragmentation. The preventive effects of 
      NAC on apoptosis were confirmed by Annexin V staining. Cells exposed to 300 
      microM GMA, 7 mM TEGDMA, or 14 mM HEMA for 24 h showed a significant increase in 
      apoptotic cells, while NAC co-treatment caused a reduction in apoptotic cells 
      compared to controls. SIGNIFICANCE: These findings suggest that glutathione 
      depletion and oxidative stress are responsible for GMA, TEGDMA, and HEMA-induced 
      mutagenicity and apoptosis.
FAU - Lee, Dong Hee
AU  - Lee DH
AD  - Department of Dental Biomaterials Science and Dental Research Institute, College 
      of Dentistry, Seoul National University, 28 Yeonkun-dong, Chongro-ku, Seoul 
      110-749, South Korea.
FAU - Lim, Bum-Soon
AU  - Lim BS
FAU - Lee, Yong-Keun
AU  - Lee YK
FAU - Ahn, Sug-Joon
AU  - Ahn SJ
FAU - Yang, Hyeong-Cheol
AU  - Yang HC
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20060110
PL  - England
TA  - Dent Mater
JT  - Dental materials : official publication of the Academy of Dental Materials
JID - 8508040
RN  - 0 (Composite Resins)
RN  - 0 (Epoxy Compounds)
RN  - 0 (Methacrylates)
RN  - 0 (Polymethacrylic Acids)
RN  - 0 (Reactive Oxygen Species)
RN  - 14I47YJ5EY (triethylene glycol dimethacrylate)
RN  - 3WJQ0SDW1A (Polyethylene Glycols)
RN  - 6E1I4IV47V (hydroxyethyl methacrylate)
RN  - R8WN29J8VF (glycidyl methacrylate)
MH  - Animals
MH  - Apoptosis
MH  - Cells, Cultured
MH  - Composite Resins/chemistry/*toxicity
MH  - Cricetinae
MH  - Cricetulus
MH  - DNA Damage
MH  - Dental Pulp/cytology/*drug effects
MH  - Epoxy Compounds/toxicity
MH  - Fibroblasts/drug effects
MH  - Lung/cytology/drug effects
MH  - Methacrylates/*toxicity
MH  - Mutagenicity Tests
MH  - *Oxidative Stress
MH  - Polyethylene Glycols/toxicity
MH  - Polymethacrylic Acids/toxicity
MH  - Rats
MH  - Reactive Oxygen Species/metabolism
EDAT- 2005/12/27 09:00
MHDA- 2007/01/11 09:00
CRDT- 2005/12/27 09:00
PHST- 2005/03/21 00:00 [received]
PHST- 2005/09/08 00:00 [revised]
PHST- 2005/09/22 00:00 [accepted]
PHST- 2005/12/27 09:00 [pubmed]
PHST- 2007/01/11 09:00 [medline]
PHST- 2005/12/27 09:00 [entrez]
AID - S0109-5641(05)00328-3 [pii]
AID - 10.1016/j.dental.2005.09.002 [doi]
PST - ppublish
SO  - Dent Mater. 2006 Dec;22(12):1086-92. doi: 10.1016/j.dental.2005.09.002. Epub 2006 
      Jan 10.