Toxicities of triclosan, phenol, and copper sulfate in activated sludge

The effect of toxicants on the BOD degradation rate constant was used to quantitatively establish the toxicity of triclosan, phenol, and copper (II) against activated sludge microorganisms. Toxicities were tested over the following ranges of concentrations: 0-450 mg/L for phenol, 0-2 mg/L for triclosan, and 0-35 mg/L for copper sulfate (pentahydrate). According to the EC(50) values, triclosan was the most toxic compound tested (EC(50) = 1.82 +/- 0.1 mg/L), copper (II) had intermediate toxicity (EC(50) = 18.3 +/- 0.37 mg/L), and phenol was the least toxic (EC(50) = 270 +/- 0.26 mg/L). The presence of 0.2% DMSO had no toxic effect on the activated sludge. The toxicity evaluation method used was simple, reproducible, and directly relevant to activated sludge wastewater treatment processes.     

Novel in vitro model for studying ureteric stent‐induced cell injury

OBJECTIVE

To develop a novel in vitro model for the study of bladder and kidney epithelial cell injury akin to stent movement, as ureteric stents are associated with urinary tract complications that can significantly add to patient morbidity. These sequelae may be linked to inflammation triggered by stent‐mediated mechanical injury to the urinary tract.

MATERIALS AND METHODS

T24 bladder and A498 kidney cell line monolayers were damaged mechanically by segments of either Percuflex Plus® (PP) or Triumph® (triclosan‐eluting) stents (both from Boston Scientific Corporation Inc. Natick, MA, USA) and the resulting expression profiles of several pro‐inflammatory cytokines and growth factors were analysed.

RESULTS

After control injury using the PP stent, supernatants of both cell lines had significantly increased levels of interleukin (IL)‐6, IL‐8, basic fibroblast growth factor and platelet‐derived growth factor BB, and A498 cells also had increased tumour necrosis factor α. In almost all cases, the presence of triclosan within the media abrogated the pro‐inflammatory cytokine increases, while its effects on growth factors varied.

CONCLUSION

This study suggests that stent‐related symptoms in the bladder and kidney may be partially due to a local inflammatory response to epithelial damage caused by the presence and movement of the stent. Future stent design should take these inflammatory responses, with respect to physical injury, into consideration, using either more biocompatible materials or anti‐inflammatory compounds such as triclosan.     

A rapid procedure to ascertain the antimicrobial efficacy of oral care formulations

A rapid method examining the antimicrobial efficacy of oral care formulations with alamar blue, an oxidation-reduction dye with fluorescent end-points, is described. Significant correlations between increasing viable plate counts of the oral bacteria Actinomyces viscosus, Streptococcus sanguis, Streptococcus mutans and Actinobacillus actinomycetemcomitans and increased alamar fluorescence were noted. Metabolically active bacteria reduced alamar with the reduced dye found in the cell-free filtrate. Insignificant alamar reductions were noted in the absence of bacteria or by spent culture supernatants. The efficacy of mouthrinses with clinically proven antiplaque agents such as chlorhexidine or cetylpyridinium chloride were determined by alamar blue. In a model system with A. viscosus, triclosan dentifrices demonstrate a dose-dependent effect on bacteria. Human salivary bacteria demonstrate increasing alamar fluorescence with increasing plate counts. A clinical study examined the effects of rinsing with chlorhexidine or cetylpyridinium chloride mouthrinses in comparison with a placebo mouthrinse and water on salivary bacteria. Rinsing with chlorhexidine resulted in the least number of bacteria by alamar and plate count methods. In summary, the current study demonstrates the utility of alamar blue to examine the antimicrobial effects of oral care formulations in laboratory and clinical studies.     

Interaction of triclosan with eukaryotic membrane lipids

The possibility that triclosan and PVM/MA (polyvinylmethyl ether/maleic acid) copolymer, additives to dentrifrices, could interact with eukaryotic membrane lipids was studied by two methods: first, by determining the pressure/molecular area isotherms at 37 degrees C of glycerophospholipid monolayers, using the Langmuir technique; and second, by phase-transition parameters in liposomes of the same lipids, using differential scanning calorimetry (DSC). Triclosan interacted, in a concentration-independent manner, with monolayers of saturated phosphatidylcholines (PC; i.e. markers of the outer membrane leaflet of eukaryotic cells). Triclosan and PVM/MA copolymer mixtures were shown to clearly interact in a concentration-dependent manner with PC. Triclosan was found to interact with liposomes of saturated and unsaturated phosphatidylcholines and phosphatidylserines (PS; i.e. markers of the inner membrane leaflet of eukaryotic cells), and saturated ethanolamines (PE; i.e. markers of the inner membrane leaflet of eukaryotic cells), resulting in a decrease of the lipid melting temperature (Tm). PVM/MA copolymer changed the Tm of PS, PC, and PE in different manners. By adding PVM/MA or triclosan-PVM/MA copolymer mixtures to 1-stearoyl-2-oleoyl-sn-glycero-3-phosphoserine (SOPS) no lipid transitions were detected. A biphasic change of the PC transition temperature resulted when triclosan or triclosan PVM/MA copolymer mixtures were added, indicating domain formation and change of the lipid polymorphism.     

含三氯羟基二苯醚消毒液中检出木糖氧化无色杆菌

目的　观察 5 %三氯羟基二苯醚消毒液中细菌存活情况。方法　进行细菌的鉴定分离及中和剂选择试验和定量杀菌试验。结果　在使用前含 5 %三氯羟基二苯醚 (三氯散 )的消毒液中检出 1株木糖氧化无色杆菌 ,生长菌落数为 5 .5 0× 1 0 5CFU/mL。受污染消毒液经加温杀菌后 ,对大肠埃希菌、金黄色葡萄球菌仍具有较好杀灭效果 ,而对取自该样液的木糖氧化无色杆菌仍无杀灭作用。结论　木糖氧化无色杆菌可抵抗较高浓度的三氯羟基二苯醚     

含Triclosan和Sodium Monofluorophosphate 新型牙膏对牙菌斑量和唾液中变异链球菌数的影响

目的评价一种含0．3％Triclosan和1．1％sodium monofluorophosphate(SMFP)新型牙膏抑制牙菌斑和唾液中变异链球菌数的效果。方法对239名12-13岁学生进行为期6个月的临床检查,在首次及以后的第3个月和第6个月进行。检查内容包括牙菌斑计数和唾液中变异链球菌数的检测。结果(1)与对照组相比较,实验组3个月和6个月后的牙菌斑计数有很明显的降低,两组间有显著性差异(P分别为0．016和0．047)。(2)两组唾液中变异链球菌数在6月后均有明显降低,但无显著性差异(P=0．41)。结论含0．3％triclosan和1．1％SMFP新型牙膏能显著抑制牙菌斑的形成。     

Triclosan-containing mouthwashes—does the nature of the solvent influence their clinical effect?

The effect of triclosan on plaque inhibition was studied with various solvents. Eight subjects used the solutions as moulhwashes twice daily for 4 days while refraining from any other form of oral hygiene. Bacteriologic tests were also done with the same solutions. The study showed that the nature of the substance used to dissolve triclosan may be of clinical significance. Solutions of triclosan in polyethylene glycol, glycerol, or 3% sodium lauryl sulfate (SLS) alone showed marked antiplaque effect. (The first two solutions both contained 1.5% SLS.) However, triclosan dissolved in Tween 80 had only a negligible clinical effect. In vitro experiment showed that antibacterial tests did not correlate well with clinical data. It is proposed that the nature of the micelles of the detergents which are used to dissolve iriclosan is of significant importance. Strongly charged micelles such as SLS show clinical effect, whereas less charged micelles of SLS/Tween 80 or uncharged micelles of Tween 80 alone appear not to have this effect.     

Severe contact dermatitis as a result of an antiseptic bath oil

Siblings aged 7 and 5 years developed extensive truncal and flexural inflammation and desquamation unresponsive to standard eczema therapy. After delays in diagnosis, subsequent history revealed prior use of an antiseptic bath oil in a much stronger concentration than recommended. The case illustrates the severe irritant contact dermatitis that can arise following inadequate dilution of antiseptic bath oils, presumably as a result of skin contact with benzalkonium chloride and triclosan. Features that may direct attention to such irritant dermatitis are flexural predominance with superficial desquamation and rapid improvement after avoidance of exposure to the antiseptic solution.     

Triclosan inhibits the activation of human periodontal ligament fibroblasts induced by lipopolysaccharide from Porphyromonas gingivalis

Periodontitis is a highly prevalent, chronic, non-specific, and immunologically devastating disease of periodontal tissues, caused by microbial infection. This study aims to examine the efficacy and protective mechanism of triclosan (TCS), a bisphenolic, non-cationic component of oral care products, against periodontal inflammation induced by lipopolysaccharide purified from Porphyromonas gingivalis (LPS-PG). TCS markedly downregulated interleukin-6 (IL-6), IL-8, and IL-15 in human periodontal ligament fibroblasts (HPDLFs) treated with LPS-PG. By using a liquid chromatography-tandem mass spectrometry (LC-MS/MS) approach, 318 differentially expressed proteins (161 upregulated and 157 downregulated) were identified in TCS-pretreated HPDLFs. TCS upregulated HSPA5 and HSP90B1 but downregulated HSPA2. Besides, TCS upregulated miR-548i in HPDLFs, which downregulated IL-15. These results indicate that TCS attenuates the activation of HPDLFs and downregulates the inflammatory cytokines through various mechanisms, thus highlighting its protective role in periodontal inflammation.     

Antimicrobial agent triclosan suppresses mast cell signaling via phospholipase D inhibition

Humans are exposed to the antimicrobial agent triclosan (TCS) through use of TCS‐containing products. Exposed tissues contain mast cells, which are involved in numerous biological functions and diseases by secreting various chemical mediators through a process termed degranulation. We previously demonstrated that TCS inhibits both Ca²⁺ influx into antigen‐stimulated mast cells and subsequent degranulation. To determine the mechanism linking the TCS cytosolic Ca²⁺ depression to inhibited degranulation, we investigated the effects of TCS on crucial signaling enzymes activated downstream of the Ca²⁺ rise: protein kinase C (PKC; activated by Ca²⁺ and reactive oxygen species [ROS]) and phospholipase D (PLD). We found that TCS strongly inhibits PLD activity within 15 minutes post‐antigen, a key mechanism of TCS mast cell inhibition. In addition, experiments using fluorescent constructs and confocal microscopy indicate that TCS delays antigen‐induced translocations of PKCβII, PKCδ and PKC substrate myristoylated alanine‐rich C‐kinase. Surprisingly, TCS does not inhibit PKC activity or overall ability to translocate, and TCS actually increases PKC activity by 45 minutes post‐antigen; these results are explained by the timing of both TCS inhibition of cytosolic Ca²⁺ (~15+ minutes post‐antigen) and TCS stimulation of ROS (~45 minutes post‐antigen). These findings demonstrate that it is incorrect to assume that all Ca²⁺‐dependent processes will be synchronously inhibited when cytosolic Ca²⁺ is inhibited by a toxicant or drug. The results offer molecular predictions of the effects of TCS on other mammalian cell types, which share these crucial signal transduction elements and provide biochemical information that may underlie recent epidemiological findings implicating TCS in human health problems.