Xylitol is a five-carbon sugar alcohol that reduces the incidence of caries by inhibiting the growth of oral streptococci, including Streptococcus mutans. Since xylitol is transported via the fructose phosphotransferase system, we hypothesized that it could also affect the growth of other oral bacteria strains. We tested the effects of xylitol against non-periodontopathogenic oral bacteria frequently found in healthy subjects as well as periodontopathogens including Porphyromonas gingivalis, Treponema denticola, and Tannerella forsythia. With 5% xylitol, Streptococcus vestibularis and Gemella morbillorum showed marked growth inhibition. With 10% xylitol, all of the tested periodontopathogens and Actinomyces naeslundii showed marked growth inhibition, whereas the growth inhibition of Neisseria mucosa, Neisseria sicca and Veillonella parvula was mild only. Xylitol is a widely used sweetener and the concentration used in our experiment is easily achieved in the oral cavity. If xylitol reduces the growth of periodontopathogens more preferentially, it could also reduce the prevalence of these pathogens and have clinical utility in the prevention or treatment of periodontal disease.
Actinomyces ; Bacteria* ; Forsythia ; Fructose ; Gemella ; Incidence ; Mouth ; Neisseria mucosa ; Neisseria sicca ; Periodontal Diseases ; Porphyromonas gingivalis ; Prevalence ; Streptococcus ; Streptococcus mutans ; Sweetening Agents ; Treponema denticola ; Veillonella ; Xylitol*

Xylitol is a five-carbon sugar alcohol that inhibits the growth of oral streptococci, including Streptococcus mutans. In this study, we tested xylitol sensitivity among the oral streptococci. We also compared nucleotide homology of putative fructose phosphotransferase system (PTS) and xylitol sensitivity, since xylitol is transported via the fructose PTS. Among the tested Streptococci, S. pneumonia showed the highest resistance to xylitol while S. gordonii and S. sanguinis showed the most sensitive growth inhibition. These streptococci could be grouped according to their xylitol sensitivity. S. mutans and S. salivarius showed similar bacterial growth inhibition by xylitol. S. mitis, S. oralis, S. pneumonia, S. intermedius and S. anginosus showed relatively low sensitivity to xylitol. When the genetic homologies of five fructose PTSs were compared among the tested streptococci, closely related streptococci showed similar sensitivity to xylitol. Taken together, fructose PTSs may mediate the sensitivity to xylitol in oral streptococci.
Fructose ; Pneumonia ; Streptococcus ; Streptococcus mutans ; Xylitol*

BACKGROUND/AIMS: Most pesticide formulations contain both chief and additive ingredients. But, the additives may not have been tested as thoroughly as the chief ingredients. The surfactant, nonyl phenoxypolyethoxylethanol (NP40), is an additive frequently present in pesticide formulations. We investigated the effects of NP40 and other constituents of a validamycin pesticide formulation on cell viability and on the expression of genes involved in cell damage pathways. METHODS: The effects of validamycin pesticide ingredients on cell viability and of NP40 on the mRNA expression of 80 genes involved in nine key cellular pathways were examined in the human neuroblastoma SK-N-SH cell line. RESULTS: The chemicals present in the validamycin pesticide formulation were cytotoxic to SK-N-SH cells and NP40 showed the greatest cytotoxicity. A range of gene expression changes were identified, with both up- and down-regulation of genes within the same pathway. However, all genes tested in the necrosis signaling pathway were down-regulated and all genes tested in the cell cycle checkpoint/arrest pathway were up-regulated. The median fold-change in gene expression was significantly higher in the cell cycle checkpoint/arrest pathway than in the hypoxia pathway category (p = 0.0064). The 70 kDa heat shock protein 4 gene, within the heat shock protein/unfolded protein response category, showed the highest individual increase in expression (26.1-fold). CONCLUSIONS: NP40 appeared to be particularly harmful, inducing gene expression changes that indicated genotoxicity, activation of the cell death (necrosis signaling) pathway, and induction of the 70 kDa heat shock protein 4 gene.
Aged ; Cell Cycle Checkpoints/drug effects/genetics ; Cell Line, Tumor ; Cell Survival/drug effects ; Dose-Response Relationship, Drug ; Female ; Gene Expression Regulation/drug effects ; Genes, cdc ; HSP110 Heat-Shock Proteins/genetics/metabolism ; Humans ; Inositol/*analogs & derivatives/chemistry/poisoning ; Necrosis ; Neurons/*drug effects/metabolism/pathology ; Nonoxynol/chemistry/*toxicity ; Pesticides/chemistry/*poisoning ; RNA, Messenger/metabolism ; Signal Transduction/drug effects ; Surface-Active Agents/chemistry/*toxicity