Effects of low dose chlorhexidine mouthrinses on oral bacteria and salivary microflora including those producing hydrogen sulfide

2004 ◽  
Vol 19 (5) ◽  
pp. 309-313 ◽  
Author(s):  
P. K. Sreenivasan ◽  
E. Gittins
2014 ◽  
Vol 80 (14) ◽  
pp. 4184-4188 ◽  
Author(s):  
Jumpei Washio ◽  
Yuko Shimada ◽  
Masakazu Yamada ◽  
Ryouichi Sakamaki ◽  
Nobuhiro Takahashi

ABSTRACTIndigenous oral bacteria in the tongue coating such asVeillonellahave been identified as the main producers of hydrogen sulfide (H2S), one of the major components of oral malodor. However, there is little information on the physiological properties of H2S production by oralVeillonellasuch as metabolic activity and oral environmental factors which may affect H2S production. Thus, in the present study, the H2S-producing activity of growing cells, resting cells, and cell extracts of oralVeillonellaspecies and the effects of oral environmental factors, including pH and lactate, were investigated. Type strains ofVeillonella atypica,Veillonella dispar, andVeillonella parvulawere used. TheseVeillonellaspecies produced H2S during growth in the presence ofl-cysteine. Resting cells of these bacteria produced H2S froml-cysteine, and the cell extracts showed enzymatic activity to convertl-cysteine to H2S. H2S production by resting cells was higher at pH 6 to 7 and lower at pH 5. The presence of lactate markedly increased H2S production by resting cells (4.5- to 23.7-fold), while lactate had no effect on enzymatic activity in cell extracts. In addition to H2S, ammonia was produced in cell extracts of all the strains, indicating that H2S was produced by the catalysis of cystathionine γ-lyase (EC 4.4.1.1). Serine was also produced in cell extracts ofV. atypicaandV. parvula, suggesting the involvement of cystathionine β-synthase lyase (EC 4.2.1.22) in these strains. This study indicates thatVeillonellaproduce H2S froml-cysteine and that their H2S production can be regulated by oral environmental factors, namely, pH and lactate.


2014 ◽  
Vol 70 (a1) ◽  
pp. C454-C454
Author(s):  
Yuichiro Kezuka ◽  
Yasuo Yoshida ◽  
Takamasa Nonaka

Hydrogen sulfide (H2S) is one of the predominant volatile sulfur compounds that are primarily responsible for oral malodor and contribute to the progress of periodontal disease. H2S in the human oral cavity is generally produced by enzymatic actions of oral bacteria.Fusobacterium nucleatum, a Gram negative periodontal pathogen, is known to be one of the heaviest H2S producers [1]. For now, four genes (fn0625,fn1055,fn1220, andfn1419) encoding pyridoxal-5′-phosphate (PLP)-dependent H2S-producing enzymes have been identified and characterized inF. nucleatumATCC 25586. Of the four enzymes, Fn1055 protein is a unique H2S-producing enzyme, which produces H2S and L-serine from L-cysteine [2]. Therefore, Fn1055 might play important roles in L-serine biosynthesis in addition to H2S production in this periodontal pathogen. Crystal structures of recombinant Fn1055 and its site-directed mutant complex with L-cysteine (a substrate) were determined at 2.1 Å resolution. The enzyme forms a homodimer whose subunits are related by a two-fold axis. The subunit is composed of two domains with α/β structure. The PLP cofactor forms a covalent internal aldimine linkage with the ε-amino group of Lys46 at the bottom of active site cleft between the domains, in the absence of substrate. On the other hand, in the cocrystal of mutant with L-cysteine, the introduced L-cysteine was found to be covalently bound to PLP, instead of Lys46. This covalent intermediate was identified as an α-aminoacrylate, which is the key species of PLP-dependent-enzyme catalysis, by spectrophotometric measurement. Along with the intermediate formation, closure of active site cleft was also observed. Furthermore, we found an amino acid residue acting as a base and confirmed its indispensability for catalysis by enzymatic analyses. These results support that H2S production by Fn1055 proceeds through the β-elimination of L-cysteine, and enable us to propose a detailed catalytic mechanism of Fn1055.


2020 ◽  
Vol 9 (8) ◽  
pp. 2484 ◽  
Author(s):  
Katarzyna Hampelska ◽  
Marcelina Maria Jaworska ◽  
Zuzanna Łucja Babalska ◽  
Tomasz M. Karpiński

Halitosis is a common ailment concerning 15% to 60% of the human population. Halitosis can be divided into extra-oral halitosis (EOH) and intra-oral halitosis (IOH). The IOH is formed by volatile compounds, which are produced mainly by anaerobic bacteria. To these odorous substances belong volatile sulfur compounds (VSCs), aromatic compounds, amines, short-chain fatty or organic acids, alcohols, aliphatic compounds, aldehydes, and ketones. The most important VSCs are hydrogen sulfide, dimethyl sulfide, dimethyl disulfide, and methyl mercaptan. VSCs can be toxic for human cells even at low concentrations. The oral bacteria most related to halitosis are Actinomyces spp., Bacteroides spp., Dialister spp., Eubacterium spp., Fusobacterium spp., Leptotrichia spp., Peptostreptococcus spp., Porphyromonas spp., Prevotella spp., Selenomonas spp., Solobacterium spp., Tannerella forsythia, and Veillonella spp. Most bacteria that cause halitosis are responsible for periodontitis, but they can also affect the development of oral and digestive tract cancers. Malodorous agents responsible for carcinogenesis are hydrogen sulfide and acetaldehyde.


2009 ◽  
Vol 80 (11) ◽  
pp. 1845-1851 ◽  
Author(s):  
Akihiro Yoshida ◽  
Mamiko Yoshimura ◽  
Naoya Ohara ◽  
Shigeru Yoshimura ◽  
Shiori Nagashima ◽  
...  

2009 ◽  
Vol 87 (7) ◽  
pp. 531-538 ◽  
Author(s):  
Liping Fang ◽  
Hong Li ◽  
Chaoshu Tang ◽  
Bin Geng ◽  
Yongfen Qi ◽  
...  

The present study investigated the role of the endogenous cystathionine γ-lyase (CSE) / hydrogen sulfide pathway in the pathogenesis of pulmonary fibrosis. Rats treated with intratracheal bleomycin were exposed either to the H2S donor NaHS or to saline. The results on day 7 showed that plasma H2S concentration and pulmonary CSE activity (H2S production rate) were significantly lower in rats treated with bleomycin and saline (fibrosis-alone) than in controls, whereas on day 28 plasma H2S concentration was higher and pulmonary CSE activity was the same as that of controls. The relative CSE mRNA level in the lungs of rats treated with bleomycin was significantly higher than control values on days 7 and 28. After exposure to NaHS, the total lung hydroxyproline content and the malondialdehyde (MDA) content were both significantly lower, with no difference observed between NaHS high-dose and low-dose treatments. Further, MDA formation stimulated by the free radical-generating system (FRGS) in vitro was lower in lung tissue incubated with NaHS than it was in tissue incubated with FRGS alone. These results suggest that NaHS administration ameliorated the pulmonary fibrosis induced by bleomycin in rats and that this protective effect of H2S may be mediated by its antioxidative action.


1990 ◽  
Vol 5 (4) ◽  
pp. 195-201 ◽  
Author(s):  
Sten Persson ◽  
Maj-Britt Edlund ◽  
Rolf Claesson ◽  
Jan Carlsson

1971 ◽  
Vol 49 (10) ◽  
pp. 1677-1682 ◽  
Author(s):  
C. Willis ◽  
A. W. Boyd ◽  
O. A. Miller

Gaseous H2S has been irradiated with electron pulses from a Febetron 705 at a dose rate of ~2 × 1027 eV g−1 s−1. For single pulse experiments, the yield of hydrogen is G(H2) = 12.0 ± 0.5, independent of pressure from at least 350 to 1600 Torr. Addition of SF6 reduces the yield to G(H2) = 7.9 ± 0.3 which is fairly close to that observed for pure H2S at low dose rates. The reduction, ΔG(H2) = 4.1 ± 0.3, agrees very well with the ion pair yield based on a W value of 25.3 eV.In multi-pulse irradiations, for pure H2S, the yield falls off with dose giving a limiting yield close to G(H2) = 8.0. No similar fall-off is observed for H2S–SF6 mixtures. It is proposed that at high absorbed doses and at low dose rates, there is no contribution to the hydrogen yield from neutralization processes; and that this is due to neutralization of H3S+ by an ion of the type Sn− rather than a free electron.


2020 ◽  
Author(s):  
Katy Goyak ◽  
R. Jeffrey Lewis

Acute exposure to hydrogen sulfide initiates a series of hallmark biological effects that occur progressively at increasing exposure levels: odor perception, conjunctivitis, olfactory paralysis, “knockdown”, pulmonary edema, and paralysis of breathing. Although effects of exposure to high concentrations of hydrogen sulfide are clear, effects associated with chronic, low-level exposure in humans is under debate, leading to uncertainty in the critical effect used in regulatory risk assessments addressing low dose exposures. This study integrates experimental animal, observational epidemiology, and occupational exposure evidence by applying a pathway-based approach. A hypothesized adverse outcome pathway (AOP) network was developed from 34 studies, comprised of 5 AOPs sharing 2 molecular initiating events (MIEs) and culminating in 5 adverse outcomes. A comparative assessment of effect levels and weight of evidence identified an AOP leading to a biologically-plausible, low-dose outcome relative to the other outcomes (nasal lesions, 30 ppm vs neurological effects, >80 ppm; pulmonary edema, >80 ppm; cardiovascular related mortality, >400 ppm; mortality via central nervous system depression, >400 ppm). This AOP (i.e., AOP1) consists of the following key events: cytochrome oxidase inhibition (>10 ppm), neuronal cell loss (>30 ppm), and olfactory nasal lesions (defined as both neuronal cell loss and basal cell hyperplasia; >30 ppm) in rodents or olfactory paralysis (>100 ppm) in humans. The key event relationships in this pathway were supported by high empirical evidence and have high biological plausibility due to known mechanistic understanding and consistency in observations for diverse chemicals. Based on assessment using the human relevance framework, this biological pathway (or, mode of action) is qualitatively possible in humans and is likely to share the same set of key event leading to olfactory paralysis in humans. This approach provides a basis to link the known observations in humans with the subchronic animal data, reducing the overall uncertainty of the human health risk assessment of H2S.


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