Fluoride, triclosan and organic weak acids as modulators of the arginine deiminase system in biofilms and suspension cells of oral streptococci.

Fluoride, triclosan and organic weak acids as modulators of the arginine deiminase system in biofilms and suspension cells of oral streptococci.
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氟化物、三氯生和有机弱酸作为口腔链球菌生物膜和悬浮细胞中精氨酸脱亚胺酶系统的调节剂。

DOI:
10.1111/j.1399-302x.2008.00502.x
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发表时间:
2009
影响因子:
--
通讯作者:
Marquis,RE
Marquis,RE
中科院分区:
--
文献类型:
--
作者:
Barboza-Silva,E;Castro,ACD;Marquis,RE

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Introduction:The arginine deiminase system (ADS) of oral bacteria is a major generator of alkali (ammonia) in dental plaque and is considered to have anticaries effects. However, many of the antimicrobial agents used in oral care products may reduce alkali production by the ADS. The objective of our work was to assess the sensitivity of the ADS of oral streptococci to commonly used antimicrobials, fluoride, triclosan and organic weak acids.Methods:Streptococcus sanguinisNCTC 10904 andStreptococcus rattiFA‐1 were grown in suspension cultures and mono‐organism biofilms. ADS activity at pH values of 4, 5 and 6 was assessed, and the actions of the agents was determined in terms of reduced production of alkali from arginine, inhibition of ADS enzymes and changes in uptake of arginine.Results:ADS activity was not greatly affected by pH changes between 4 and 6 and was greater per unit of biomass for cell suspensions than for biofilms. NaF was a poor inhibitor, while triclosan was highly effective with a 50% inhibitory dose for the two organisms between 0.03 and 0.05 and between 0.10 and 0.15 mm‐h for suspension cells and biofilms, respectively. The weak acid indomethacin was nearly as potent at pH 4.0 as triclosan, while capric and lauric acids were less potent, especially for biofilms. The methyl ester of lauric acid was slightly stimulatory. The major targets for the inhibitors appeared to be transport systems for arginine uptake, although carbamate kinase was a secondary target.Conclusion:Triclosan, indomethacin, caprate and laurate can reduce ADS activity in dental plaque.