Weak acid effects and fluoride inhibition of glycolysis byStreptococcus mutansGS-5

Canadian Journal of Microbiology - Tập 41 Số 9 - Trang 785-791 - 1995
Wesley A. Belli1, Daniel H. Buckley, Robert E. Marquis
1Department of Microbiology and Immunology, University of Rochester Medical Center, NY 14642-8672, USA.

Tóm tắt

Fluoride and a variety of other weak acids acted to reduce reversibily the acid tolerance of glycolysis by intact cells of Streptococcus mutans GS-5 as shown by higher final pH values in acid-drop experiments with glucose in excess. The order of effectiveness was fluoride > indomethacin > ibuprofen > ketoprofen > salicylate > sorbate > cinnamate > p-hydroxybenzoate > benzoate > ascorbate. Only fluoride also acted as an inhibitor of the glycolytic enzyme enolase. However, enolase in permeabilized cells was also inhibited by acidification with a sharp drop-off in activity between pH 6 and 5. It was proposed that the weak acids, including fluoride, acted to reduce glycolytic acid tolerance by enhancing cytoplasmic acidification and thereby inhibiting enzymes such as enolase. The potencies of the acids could not be predicted accurately from knowledge of pKavalues, octanol–water partition coefficients, and molecular weights. It was concluded that their modes of action in acid sensitization involved perturbations of membrane function in addition to their acting as transmembrane carriers of protons. Methylparaben (methyl ester of p-hydroxybenzoate) was also a sensitizer but was less effective than the parent acid.Key words: fluoride, weak acids, enolase, Streptococcus mutans, glycolysis.

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Tài liệu tham khảo

Belli W.A., 1991, Appl. Environ. Microbiol., 57, 1134, 10.1128/AEM.57.4.1134-1138.1991

Bender G.R., 1985, J. Dent. Res., 64, 90, 10.1177/00220345850640021701

Bender G.R., 1986, Infect. Immun., 53, 331, 10.1128/IAI.53.2.331-338.1986

Bunick F. J., 1981, Infect. Immun., 34, 856, 10.1128/IAI.34.3.856-863.1981

Casiano-Colbn A., 1988, Appl. Environ. Microbiol, 54, 1318, 10.1128/AEM.54.6.1318-1324.1988

Curran T.M., 1994, FEMS Microbiol. Lett., 119, 283, 10.1111/j.1574-6968.1994.tb06902.x

Eisenberg A.D., 1981, Antimicrob. Agents Chemother., 19, 807, 10.1128/AAC.19.5.807

Gutknecht J., 1988, J. Membr. Biol., 106, 83, 10.1007/BF01871769

Gutknecht J., 1981, Biochim. Biophys. Acta, 644, 153, 10.1016/0005-2736(81)90071-7

Hiither F.-J., 1990, Infect. Immun., 58, 1043, 10.1128/IAI.58.4.1043-1047.1990

Kanapka J.A., 1971, Arch. Biochem. Biophys., 146, 167, 10.1016/S0003-9861(71)80053-X

Kashket E.R., 1987, FEMS Microbiol. Rev., 46, 233, 10.1111/j.1574-6968.1987.tb02463.x

Kashket S., 1985, Infect. Immun., 48, 19, 10.1128/IAI.48.1.19-22.1985

Kaufmann M., 1992, Caries Res., 26, 110, 10.1159/000261494

Marquis R.E., 1990, J. Dent. Res., 69, 672, 10.1177/00220345900690S130

Salmond C.V., 1984, J. Gen. Microbiol., 130, 2845

Sheu C.W., 1975, Antimicrob. Agents Chemother., 7, 349, 10.1128/AAC.7.3.349

Sikkema J. J., 1994, J. Biol. Chem., 269, 8022, 10.1016/S0021-9258(17)37154-5