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LDH activity of S. mutans with nicotine. S. mutans was treated with 0-4 mg/ml nicotine for 24 h in TSBS. Biofilm was washed and processed for LDH assay. The manufacturer's protocol was followed. Panel A demonstrates the overall biofilm LDH activity. Since nicotine stimulates S. mutans biofilm formation (Huang et al. 11 ), crystal violet assay was used to estimate the amount of biofilm in each treatment (data not shown). Panel B demonstrates the ratio of LDH assay over the crystal violet assay data. This represents unit cell LDH activity. Asterisks indicate significant difference between nicotine treated and non-treated. * P < 0.05, and ** P < 0.01.

LDH activity of S. mutans with nicotine. S. mutans was treated with 0-4 mg/ml nicotine for 24 h in TSBS. Biofilm was washed and processed for LDH assay. The manufacturer's protocol was followed. Panel A demonstrates the overall biofilm LDH activity. Since nicotine stimulates S. mutans biofilm formation (Huang et al. 11 ), crystal violet assay was used to estimate the amount of biofilm in each treatment (data not shown). Panel B demonstrates the ratio of LDH assay over the crystal violet assay data. This represents unit cell LDH activity. Asterisks indicate significant difference between nicotine treated and non-treated. * P < 0.05, and ** P < 0.01.

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Several epidemiology studies have reported a positive relationship between smoking and dental caries. Nicotine, an alkaloid component of tobacco, has been demonstrated to stimulate biofilm formation and metabolic activity of Streptococcus mutans, one of the most important pathogens of dental caries. The first aim of the present study was to explore...

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... mutans biofilm overall LDH activity was significantly increased at 1, 2 and 4 mg/ml nicotine (Fig. 4). However, after adjustment by the biofilm volume, which was determined by crystal violet assay (data not shown), there was no difference among those groups. This indicates nicotine does not directly affect LDH activity of S. mutans, but with the increased bacterial cell number by nicotine treatment, the overall biofilm LDH activity was ...
Context 2
... in a pH range of 5 to 6.2. 36 LDH deficiency is lethal to S. mutans due to accumulated toxic intermediate products such as pyruvate. 38,39 Since LDH activity is directly related to S. mutans lactic acid production, LDH is considered one of S. mutans major virulence factors. Although nicotine does not directly regulate S. mutans LDH activity (Fig. 4, panel B), nicotine increases total bacterial cells in the biofilm, the overall LDH activity is increased (Fig. 4, panel A). S. mutans biofilm lactate generation was significantly increased with 1 mg/ml nicotine treatment (unpublished ...
Context 3
... such as pyruvate. 38,39 Since LDH activity is directly related to S. mutans lactic acid production, LDH is considered one of S. mutans major virulence factors. Although nicotine does not directly regulate S. mutans LDH activity (Fig. 4, panel B), nicotine increases total bacterial cells in the biofilm, the overall LDH activity is increased (Fig. 4, panel A). S. mutans biofilm lactate generation was significantly increased with 1 mg/ml nicotine treatment (unpublished ...

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... These findings are further supported by the results of a meta-analysis conducted by Jiang et al. in which 10 of the 11 studies included in survey have found a positive correlation between smoking and dental caries [7]. The most probable cause for this should be the effect of cigarette smoke components, especially nicotine, on the proliferation, dental biofilm accumulation and metabolism of cariogenic bacteria, which was confirmed by several studies [8][9][10][11]). Results from an in vitro research by Huang et al. suggest that nicotine, depending on its concentration level, can have an inhibitory or stimulating effect on the proliferation and metabolic activity of Streptococcus mutans [8] The same study group conducted further research on the effect of nicotine on S. mutans in which they found that nicotine stimulates higher production rates of extracellular polysaccharides, promotes the activity of the bacterial enzyme lactate dehydrogenase in vitro. ...
... Results from an in vitro research by Huang et al. suggest that nicotine, depending on its concentration level, can have an inhibitory or stimulating effect on the proliferation and metabolic activity of Streptococcus mutans [8] The same study group conducted further research on the effect of nicotine on S. mutans in which they found that nicotine stimulates higher production rates of extracellular polysaccharides, promotes the activity of the bacterial enzyme lactate dehydrogenase in vitro. Furthermore, the exposure to nicotine stimulated bacterial cell aggregation and formation of a thicker biofilm [9]. A similar study was conducted on electric cigarettes (vaping), which compared their effect on S. mutans growth, adhesion, and biofilm formation with the effect that cigarette smoke has on the same factors. ...
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... 89,90 The influence of nicotine on the activity of lactate dehydrogenase (LDH) was also assessed. 91 Lactate dehydrogenase is an enzyme that catalyzes the last step in the bacterial glycolytic pathway, converting pyruvate to lactate. 92 Although nicotine does not directly affect LDH, it indirectly enhances its activity by increasing the total amount of bacteria. ...
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... Nicotine, an alkaloid component in cigarette smoking, stimulates biofilm formation and metabolic activity of Streptococcus mutans, one of the most important pathogens of [5] dental caries. ...
... Nicotine stimulates Streptococcus mutans planktonic cell glucosyltransferase (Gtf) synthesis and glucan-binding protein (Gbp) expression as a mechanism to increase planktonic cell attachment to biofilm matrix leading to an increased number of cells in the biofilm which causes the [5] development of more carious lesions in smoker. ...
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Full-text available
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Background SCH-79797 was recently shown to be a broad-spectrum antibacterial agent with a dual-bactericidal mechanism. However, its anti-biofilm effect remains unknown. Purpose To investigate the effect of SCH-79797 on the biofilm formation of the cariogenic Streptococcus mutans Methods and Results Crystal violet staining, colony forming units count and MTT assays (for cell metabolic activity) revealed that S. mutans biofilm formation was significantly suppressed. In addition, virulence factors, including extracellular polysaccharides (investigated by bacterial/exopolysaccharide staining and the anthrone method) and acid production (investigated by lactic acid and supernatant pH detection) were also inhibited significantly. Moreover, the biofilm inhibitory effect of SCH-79797 was mediated through its repression of bacterial growth and not by a bactericidal effect, which was verified by growth curve and bacterial live/ dead staining, respectively. Quantitative real-time PCR results disclosed that SCH-79797 affected bacterial acid production and tolerance, polysaccharide synthesis and remodeling, biofilm formation and quorum sensing-related gene expression. In addition, SCH-79797 showed good biocompatibility as determined by cytotoxicity assays. Conclusion SCH-79797 had an anti-biofilm effect and showed application prospects in the control of dental caries.