Mutagenicity of ethanolic extracts of used acrylic dentures.

The in vivo physicochemical sorption of mutagenic substances onto acrylic polymers was investigated in worn acrylic dentures. Thus, ethanolic extracts of acrylic dentures from 41 of a total of 69 human donors (60%), were found mutagenic in the standard plate incorporation Salmonella mutagenicity test against either TA98 or TA100 strains. Denture extracts from smokers produced mutagenicity more often than the ones from non-smokers (75% vs. 45%, P 0.01). Mutagenicity was preferentially directed against TA98 (TA98:TA100 = 2.9:1, P < 0.0005). Predilection for TA98 was more pronounced in denture extracts from non-smokers (4.7:1) than from smokers (2.0:1). When direct mutagenicity was observed, it was reduced by the rat-liver S9. Induced mutant yields were 6.1 +/- 3.9 and 7.0 +/- 8.9 times higher than the spontaneous for TA98 and TA100 respectively (smokers, 50-cm2 denture surface area eq./plate+S9). Denture extracts from smokers induced higher levels of mutation than the ones from non-smokers (TA98 + S9, smoker:non-smoker = 2:1, P < 0.01). Mutagenicity was associated with longer periods of denture usage (P 0.007). Thus, denture poly(methyl methacrylate) base material can adsorb mutagenic substances, possibly from diet and tobacco, which are extractable by ethanol. Theoretically, the in situ alcoholic desorption and recirculation of carcinogenic mutagens may have a contributory role in certain cases of intra-oral and upper alimentary tract carcinogenesis.

Mutagenicity of 4-aminoantipyrine and 4-nitrosoantipyrine, the C-nitroso derivative of antipyrine.

The drug antipyrine and its 4-substituted analogs, 4-aminoantipyrine, 4-dimethylaminoantipyrine (aminopyrine) and 4-nitrosoantipyrine were tested for mutagenicity against the screening array of Salmonella typhimurium tester strains TA100, TA98, TA97, TA102 and TA104. Antipyrine and aminopyrine were nonmutagenic to all 5 tester strains even in the presence of S9. 4-Aminoantipyrine was directly mutagenic to TA97 only and the presence of S9 slightly increased its activity. 4-Nitrosoantipyrine was directly mutagenic to all tester strains used and S9 decreased its activity except with strain TA102. The possible long-term hazards of C-nitroso compounds derived from drugs and dietary constituents are discussed in view of their pluripotent direct genotoxicity.

Activation of rutin by human oral bacterial isolates to the carcinogen-mutagen quercetin.

Oral streptococci, isolated from the mouths of 2 healthy subjects, hydrolysed innocuous rutin, a flavonoid glycoside, to its genotoxic aglycon quercetin, in vitro. The isolates were identified as Streptococcus milleri. The glycosidase, rutinase, was studied in cell-free extracts derived from one of the isolates, grown anaerobically in batch cultures by the use of a bioassay, the Ames test, in which S-9 was replaced by the cell-free extracts. This streptococcal rutinase was: constitutive, partly inducible, cytosolic, most active for rutin and most active at pH 6.5. Type-culture collection strains of other oral streptococci (Streptococcus salivarius ATCC 25975 and Streptococcus mutans strain 6715-10) showed no capacity for rutin degradation. A hypothesis for a novel role of the oral microflora in a disease process other than caries and periodontal disease, namely intra-oral cancer, is presented. The possibility of a bacterial liberation of the genotoxic quercetin in situ could be but one example of its involvement in the local carcinogenic process.