Dental adhesive compounds alter glutathione levels but not glutathione redox balance in human THP-1 monocytic cells.
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 micromol/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.
Noda
M
M
Oral Rehabilitation, Center for Dental Clinics, Hokkaido University Hospital, Sapporo, Japan.
Wataha
J C
JC
Lewis
J B
JB
Kaga
M
M
Lockwood
P E
PE
Messer
R L W
RL
Sano
H
H
D019328:Buthionine Sulfoximine / Q000494:pharmacology; D002460:Cell Line; D003188:Composite Resins / Q000494:pharmacology; D017220:Dentin-Bonding Agents / Q000494:pharmacology*; D005978:Glutathione / Q000378:metabolism*; D019803:Glutathione Disulfide / Q000378:metabolism; D005980:Glutathione Reductase / Q000378:metabolism; D006801:Humans; D008689:Methacrylates / Q000494:pharmacology; D009000:Monocytes / Q000187:drug effects / Q000502:physiology*; D010084:Oxidation-Reduction; D018384:Oxidative Stress / Q000502:physiology*; D011092:Polyethylene Glycols / Q000494:pharmacology; D011109:Polymethacrylic Acids / Q000494:pharmacology
D003188:Composite Resins; D017220:Dentin-Bonding Agents; D008689:Methacrylates; D011109:Polymethacrylic Acids; C020946:triethylene glycol dimethacrylate; D011092:Polyethylene Glycols; D019328:Buthionine Sulfoximine; C005044:hydroxyethyl methacrylate; D005980:Glutathione Reductase; D005978:Glutathione; D019803:Glutathione Disulfide