Effects of zinc and/or fluoride on growth, glycolysis and survival of Streptococcus mutans GS-5 were examined in vitro. Zinc inhibited growth and glycolysis, and enhanced the antimetabolic activity of fluoride. Zinc alone had little effect on cell survival. During cell growth without pH control a protection from cell death was mediated by fluoride, which appeared to be caused by a higher final pH in the culture medium. When cell death was observed under controlled pH conditions in a lactate-acetate buffer at pH 6.5, 5.0 or 4.0, fluoride was bactericidal only at pH 4.0. However, the combination of zinc plus fluoride was strongly bactericidal at all pH values that were tested.

Adenosine 5′-triphosphate (ATP) content and viability of Streptococcus mutans GS-5 were studied in a lactate-acetate buffer at pH 6.5, 5.0 and 4.0 with or without added NaF. Reductions in cellular ATP occurred at all pH values tested, but were most pronounced at pH 4.0 and 5.0 with added fluoride and at pH 4.0 alone. Fluoride at pH 4.0 resulted in the lowest ATP content and was strongly bactericidal, while under all other conditions, no or very delayed cell death was observed. Our findings support the idea that fluoride-mediated transmembrane proton conduction is an important mechanism in the antimicrobial activity of fluoride and that this activity at low pH may be involved in the cariostatic action of fluoride.

The effects of low concentrations (1.0 mmol/l of selenite and seleno-dl-cystine were tested alone, or in combination with NaF, on growth, glycolysis, and survival of Streptococcus mutans GS-5. In batch culture, both selenium-containing compounds (1.0 mmol/l) inhibited the growth rate and final cell yield by 92% or greater; glycolysis, however, was not affected. The observed bactericidal action of selenite at 0.1 mmol/l was pH-dependent. Fluoride reduced the killing effect of SeO₃ in the culture medium and in a lactate-acetate buffer system at pH 6.5, 5.0 and 4.0. These data indicate that selenium-containing compounds exert an antibacterial action on cells of S. mutans in a manner which leaves glycolysis unaffected.