Dental adhesive compounds alter glutathione levels but not glutathione redox balance in human THP-1 monocytic cells

M. Noda, J. C. Wataha, J. B. Lewis, M. Kaga, P. E. Lockwood, Regina L W Messer, H. Sano

Research output: Contribution to journalArticle

27 Citations (Scopus)

Abstract

The use of hydrophilic dental monomers in dentin bonding agents has vastly improved resin-dentin bond strengths, but incomplete polymerization of these monomers and their leaching into adjacent (pulpal) oral tissues has raised concerns about their biocompatibility. The sublethal effects of these resins are virtually unknown, but their electrophilic nature led to the hypothesis that they may alter cellular oxidative stress pathways. Glutathione balance between reduced (GSH) and oxidized (GSSG) is a major mechanism by which cells maintain redox balance and was therefore the focus of the current investigation. THP-1 human monocytic cells were exposed to hydroxyethyl methacrylate (HEMA), benzoyl peroxide (BPO), camphorquinone (CQ), or triethyelene glycol dimethacrylate (TEGDMA) for 24 h at sublethal doses, then GSH and GSSG levels were measured by means of Ellman's method adapted for cell culture. The results indicate that these dental resin compounds act at least partly via oxidative stress by increasing GSH levels at sublethal concentrations. However, the GSH-GSSG ratio was relatively unaffected. Only BPO altered the GSH-GSSG ratio at 24 h, again at sublethal levels (7.5-15 μmol/L). The results support the hypothesis that resin monomers act, at least in part, via oxidative stress, and that oxidative-stress pathways should be one focus of future investigations of monomer biocompatibility.

Original languageEnglish (US)
Pages (from-to)308-314
Number of pages7
JournalJournal of Biomedical Materials Research - Part B Applied Biomaterials
Volume73
Issue number2
DOIs
StatePublished - May 1 2005

Fingerprint

Dental Cements
Oxidative stress
Glutathione Disulfide
Oxidation-Reduction
Glutathione
Adhesives
Oxidative Stress
Resins
Monomers
Benzoyl Peroxide
Benzoyl peroxide
Biocompatibility
Dentin-Bonding Agents
Synthetic Resins
Glycols
Bond strength (materials)
Dentin
Cell culture
Polymerization
Leaching

Keywords

  • Biocompatibility
  • Composites
  • Electrophiles
  • Oxidative stress

ASJC Scopus subject areas

  • Biomaterials
  • Biomedical Engineering

Cite this

Dental adhesive compounds alter glutathione levels but not glutathione redox balance in human THP-1 monocytic cells. / Noda, M.; Wataha, J. C.; Lewis, J. B.; Kaga, M.; Lockwood, P. E.; Messer, Regina L W; Sano, H.

In: Journal of Biomedical Materials Research - Part B Applied Biomaterials, Vol. 73, No. 2, 01.05.2005, p. 308-314.

Research output: Contribution to journalArticle

@article{12bd301254cc45099737db9ae2b855dd,
title = "Dental adhesive compounds alter glutathione levels but not glutathione redox balance in human THP-1 monocytic cells",
abstract = "The use of hydrophilic dental monomers in dentin bonding agents has vastly improved resin-dentin bond strengths, but incomplete polymerization of these monomers and their leaching into adjacent (pulpal) oral tissues has raised concerns about their biocompatibility. The sublethal effects of these resins are virtually unknown, but their electrophilic nature led to the hypothesis that they may alter cellular oxidative stress pathways. Glutathione balance between reduced (GSH) and oxidized (GSSG) is a major mechanism by which cells maintain redox balance and was therefore the focus of the current investigation. THP-1 human monocytic cells were exposed to hydroxyethyl methacrylate (HEMA), benzoyl peroxide (BPO), camphorquinone (CQ), or triethyelene glycol dimethacrylate (TEGDMA) for 24 h at sublethal doses, then GSH and GSSG levels were measured by means of Ellman's method adapted for cell culture. The results indicate that these dental resin compounds act at least partly via oxidative stress by increasing GSH levels at sublethal concentrations. However, the GSH-GSSG ratio was relatively unaffected. Only BPO altered the GSH-GSSG ratio at 24 h, again at sublethal levels (7.5-15 μmol/L). The results support the hypothesis that resin monomers act, at least in part, via oxidative stress, and that oxidative-stress pathways should be one focus of future investigations of monomer biocompatibility.",
keywords = "Biocompatibility, Composites, Electrophiles, Oxidative stress",
author = "M. Noda and Wataha, {J. C.} and Lewis, {J. B.} and M. Kaga and Lockwood, {P. E.} and Messer, {Regina L W} and H. Sano",
year = "2005",
month = "5",
day = "1",
doi = "10.1002/jbm.b.30257",
language = "English (US)",
volume = "73",
pages = "308--314",
journal = "Journal of Biomedical Materials Research - Part A",
issn = "0021-9304",
publisher = "Heterocorporation",
number = "2",

}

TY - JOUR

T1 - Dental adhesive compounds alter glutathione levels but not glutathione redox balance in human THP-1 monocytic cells

AU - Noda, M.

AU - Wataha, J. C.

AU - Lewis, J. B.

AU - Kaga, M.

AU - Lockwood, P. E.

AU - Messer, Regina L W

AU - Sano, H.

PY - 2005/5/1

Y1 - 2005/5/1

N2 - The use of hydrophilic dental monomers in dentin bonding agents has vastly improved resin-dentin bond strengths, but incomplete polymerization of these monomers and their leaching into adjacent (pulpal) oral tissues has raised concerns about their biocompatibility. The sublethal effects of these resins are virtually unknown, but their electrophilic nature led to the hypothesis that they may alter cellular oxidative stress pathways. Glutathione balance between reduced (GSH) and oxidized (GSSG) is a major mechanism by which cells maintain redox balance and was therefore the focus of the current investigation. THP-1 human monocytic cells were exposed to hydroxyethyl methacrylate (HEMA), benzoyl peroxide (BPO), camphorquinone (CQ), or triethyelene glycol dimethacrylate (TEGDMA) for 24 h at sublethal doses, then GSH and GSSG levels were measured by means of Ellman's method adapted for cell culture. The results indicate that these dental resin compounds act at least partly via oxidative stress by increasing GSH levels at sublethal concentrations. However, the GSH-GSSG ratio was relatively unaffected. Only BPO altered the GSH-GSSG ratio at 24 h, again at sublethal levels (7.5-15 μmol/L). The results support the hypothesis that resin monomers act, at least in part, via oxidative stress, and that oxidative-stress pathways should be one focus of future investigations of monomer biocompatibility.

AB - The use of hydrophilic dental monomers in dentin bonding agents has vastly improved resin-dentin bond strengths, but incomplete polymerization of these monomers and their leaching into adjacent (pulpal) oral tissues has raised concerns about their biocompatibility. The sublethal effects of these resins are virtually unknown, but their electrophilic nature led to the hypothesis that they may alter cellular oxidative stress pathways. Glutathione balance between reduced (GSH) and oxidized (GSSG) is a major mechanism by which cells maintain redox balance and was therefore the focus of the current investigation. THP-1 human monocytic cells were exposed to hydroxyethyl methacrylate (HEMA), benzoyl peroxide (BPO), camphorquinone (CQ), or triethyelene glycol dimethacrylate (TEGDMA) for 24 h at sublethal doses, then GSH and GSSG levels were measured by means of Ellman's method adapted for cell culture. The results indicate that these dental resin compounds act at least partly via oxidative stress by increasing GSH levels at sublethal concentrations. However, the GSH-GSSG ratio was relatively unaffected. Only BPO altered the GSH-GSSG ratio at 24 h, again at sublethal levels (7.5-15 μmol/L). The results support the hypothesis that resin monomers act, at least in part, via oxidative stress, and that oxidative-stress pathways should be one focus of future investigations of monomer biocompatibility.

KW - Biocompatibility

KW - Composites

KW - Electrophiles

KW - Oxidative stress

UR - http://www.scopus.com/inward/record.url?scp=18244397184&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=18244397184&partnerID=8YFLogxK

U2 - 10.1002/jbm.b.30257

DO - 10.1002/jbm.b.30257

M3 - Article

VL - 73

SP - 308

EP - 314

JO - Journal of Biomedical Materials Research - Part A

JF - Journal of Biomedical Materials Research - Part A

SN - 0021-9304

IS - 2

ER -