The mutagenic activity of unpolymerized resin monomers in Salmonella typhimurium and V79 cells

Abstract

Dimethacrylate derivatives are used as monomers to polymerize dental composite materials and for a great variety of other industrial resins. Occupational exposure is likely in various ways because of the many areas of methacrylate application. Here, the mutagenicity of the monomers, bisphenol A-diglycidyl dimethacrylate (Bis-GMA), urethane dimethacrylate (UDMA), triethylene glycol dimethacrylate (TEGDMA), Bisphenol A (BPA), glycidyl methacrylate (GMA), methyl methacrylate (MMA), and 2-hydroxyethyl methacrylate (HEMA) was studied in a bacterial (Ames test) and a mammalian gene mutation assay (V79/HPRT assay). Mutagenicity was determined in different Salmonella typhimurium strains (TA97a, TA98, TA100, TA102) and in V79 cells in the presence and in the absence of a metabolically active microsomal fraction from rat liver (S9). No mutagenic effects were observed with Bis-GMA and UDMA, methyl methacrylate, 2-hydroxyethyl methacrylate and bisphenol A. Glycidyl methacrylate (GMA) was mutagenic in a dose-dependent manner in three Salmonella tester strains. The number of mutants was increased by a factor of 2 to 3 with strains TA97a and TA102 in the absence of S9. Moreover, the numbers of mutants induced in S. typhimurium TA100 were about 8-fold higher than in solvent controls. GMA also induced an increase of mutants in V79 cells in the absence of S9. However, GMA was inactivated by microsomal enzymes. Triethylenglycol dimethacrylate (TEGDMA) was not mutagenic in any S. typhimurium. In contrast, the compound induced a dose-dependent rise in mutant frequencies in V79 cell cultures. It is concluded that TEGDMA acted through a clastogenic mechanism which is not detected by Ames tester strains.