Triclosan affects steroidogenesis in mouse primary astrocytes in vitro with engagement of Sirtuin 1 and 3.

Triclosan (TCS) is a widely used antimicrobial, antifungal, and antiviral agent. To date, it has been reported that TCS can enter the human body and disrupt hormonal homeostasis. Therefore, the aim of our paper was to evaluate the impact of TCS on astrocytes, i.e. a crucial population of cells responsible for steroid hormone production. Our data showed that, in mouse primary astrocyte cultures, TCS can act as an endocrine disrupting chemical through destabilization of the production or secretion of progesterone (P4), testosterone (T), and estradiol (E2). TCS affects the mRNA expression of enzymes involved in neurosteroidogenesis, such as Cyp17a1, 17ß-Hsd, and Cyp19a1. Our data showed that a partial PPARγ agonist (honokiol) prevented changes in Cyp17a1 mRNA expression caused by TCS. Similarly, honokiol inhibited TCS-stimulated P4 release. However, rosiglitazone (classic PPARγ agonist) or GW9662 (PPARγ antagonist) had a much stronger effect. Therefore, we believe that the changes observed in the P4, T, and E2 levels are a result of dysregulation of the activity of the aforementioned enzymes, whose expression can be affected by TCS through a Pparγ-dependent pathway. TCS was found to decrease the aryl hydrocarbon receptor (AhR) and Sirtuin 3 protein levels, which may be the result of the activation of the these proteins. Since our study showed dysregulation of the production or secretion of neurosteroids in astrocytes, it can be concluded that TCS reaching the brain may contribute to the development of neurodegenerative diseases in which an abnormal amount of neurosteroids is observed.

Triclosan administration to humanized UDP-glucuronosyltransferase 1 neonatal mice induces UGT1A1 through a dependence on PPARα and ATF4.

Triclosan (TCS) is an antimicrobial toxicant found in a myriad of consumer products and has been detected in human tissues, including breastmilk. We have evaluated the impact of lactational TCS on UDP-glucuronosyltransferase 1A1 (UGT1A1) expression and bilirubin metabolism in humanized UGT1 (hUGT1) neonatal mice. In hUGT1 mice, expression of the hepatic UGT1A1 gene is developmentally delayed resulting in elevated total serum bilirubin (TSB) levels. We found that newborn hUGT1 mice breastfed or orally treated with TCS presented lower TSB levels along with induction of hepatic UGT1A1. Lactational and oral treatment by gavage with TCS leads to the activation of hepatic nuclear receptors constitutive androstane receptor (CAR), peroxisome proliferator-activated receptor alpha (PPARα), and stress sensor, activating transcription factor 4 (ATF4). When CAR-deficient hUGT1 mice (hUGT1/Car-/-) were treated with TCS, TSB levels were reduced with a robust induction of hepatic UGT1A1, leaving us to conclude that CAR is not tied to UGT1A1 induction. Alternatively, when PPARα-deficient hUGT1 mice (hUGT1/Pparα-/-) were treated with TCS, hepatic UGT1A1 was not induced. Additionally, we had previously demonstrated that TCS is a potent inducer of ATF4, a transcriptional factor linked to the integrated stress response. When ATF4 was deleted in liver of hUGT1 mice (hUGT1/Atf4ΔHep) and these mice treated with TCS, we observed superinduction of hepatic UGT1A1. Oxidative stress genes in livers of hUGT1/Atf4ΔHep treated with TCS were increased, suggesting that ATF4 protects liver from excessive oxidative stress. The increase oxidative stress may be associated with superinduction of UGT1A1. The expression of ATF4 in neonatal hUGT1 hepatic tissue may play a role in the developmental repression of UGT1A1.

Antimicrobial Activity of Antibacterial Sutures in Oral Surgery: A Scoping Review.

OBJECTIVE: The aim of this scoping review was to explore and synthesise the current evidence on the antimicrobial activity of antibacterial suture materials used in oral surgery. METHODS: The review was conducted following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) Extension for Scoping Reviews. A bibliographic search was carried out in the PubMed and Scopus databases to retrieve all human clinical studies that investigated the antimicrobial efficacy of antibacterial-coated sutures used in oral surgery. Included studies were screened and extracted independently by 2 examiners. Data were tabulated and qualitatively described. RESULTS: The search initially returned 150 articles and resulted in 5 included studies after the duplicates' removal and the full-text screening. Selected studies were published from 2014 to 2019. Three studies (60%) were randomised clinical trials, whilst the remaining studies did not report information on randomisation. The antimicrobial agents for coated sutures included triclosan and chlorhexidine. In almost all the studies, antibacterial-coated sutures exhibited lower bacterial retention compared to those without coating. CONCLUSIONS: Within limitations, the antimicrobial-coated sutures employed in oral surgery exhibited good results in terms of their microbicidal activity when compared with sutures that were not coated. Considering the high variability and confounding factors identified in the included studies, more high-quality research is needed to confirm these results. Antimicrobial-coated sutures could represent a promising and clinically valid strategy to reduce microbial colonisation in oral surgery. The reduced bacterial adherence is likely to improve the clinical success of the surgical procedures. Yet, the cost-benefit ratio of antimicrobial-coated sutures should be assessed in larger clinical trials to confirm their efficacy over conventional noncoated sutures.

Comparison of bacterial colonization on absorbable non-coated suture with Triclosan- or Chlorhexidine-coated sutures: a randomized controlled study.

OBJECTIVE: The oral cavity is a colossal reservoir for the bacteria. The healing of tissues is compromised after flap surgery, particularly in the presence of sutures, as they can act as repositories for bacteria, ultimately leading to surgical site infections. Hence, antibacterial-coated sutures have been considered as an alternative to reduce the risk of these infections and further improve the wound healing of the tissues after flap surgery. Since minimal information is available on the effect of antibacterial-coated sutures on periodontal tissues, this study aims to clinically and microbiologically assess the antibacterial efficacy of Triclosan (TCS) and Chlorhexidine-coated sutures (CCS) on periodontal tissues compared to non-coated sutures (NCS). PATIENTS AND METHODS: A total of 75 subjects with moderate to severe periodontitis were included in the study and randomly allocated to one of the three groups, (TCS, CCS, and NCS groups) equally. Suture removal was performed on postoperative day 8, and parameters such as wound healing and post-operative pain were evaluated. The retrieved suture samples were subjected to microbiological analysis and the bacteria were identified quantitatively and qualitatively. RESULTS: Intragroup analysis of the wound healing index and post-operative pain for all the groups showed a significant improvement (p<0.01), from day 8 to day 30. Intergroup analysis of the wound healing index revealed significant wound healing (p<0.05) on day 15 and day 30. For post-operative pain, intergroup analyses showed significantly low pain scores (p<0.01) for the TCS group. Microbiologic analysis of aerobic colony counts in both anterior and posterior regions revealed significantly (p<0.01) least colony counts in TCS and highest colony counts in NCS groups, respectively. Although anaerobic colony counts were not statistically significant, relatively fewer colony counts were identified in the TCS group. Whereas, relatively higher anaerobic colony counts were seen in the CCS group in the anterior region and in the NCS group in the posterior region. Qualitative assessment revealed higher amounts of Streptococcus and Staphylococcus species in all the three groups (TCS, CCS, and NCS groups). CONCLUSIONS: Antibacterial-coated sutures, particularly Triclosan-coated sutures, are effective in reducing bacterial accumulation compared to non-coated sutures. Therefore, these sutures can be effectively utilized in periodontal flap surgery.

Staphylococcus aureus Adhesion and Biofilm Formation on Vascular Polyester Grafts are Inhibited In Vitro by Triclosan.

OBJECTIVE: This study evaluated Staphylococcus aureus adhesion and biofilm formation on vascular grafts, which has seldom been investigated. METHODS: Adhesion and biofilm formation capabilities of three methicillin susceptible S. aureus strains (one biofilm forming reference strain and two clinical isolates) on five different vascular biomaterials were evaluated in vitro, including polyester (P), P + gelatin (PG), P + collagen (PC), PC + silver (PCS), and PCS + triclosan (PCST). Staphylococcus aureus adhesion on grafts was evaluated after one hour of culture and biofilm formation after 24 hours of culture by four different methods: spectrophotometry after crystal violet staining; sonicate fluid culture; metabolic assay; and scanning electron microscopy (SEM). Optical density was compared using Mann-Whitney pairwise test, and bacterial counts using Wilcoxon pairwise test. RESULTS: PCST grafts were most efficient in preventing S. aureus adhesion and biofilm formation, regardless of the method used. Bacterial counts and metabolic activity were significantly lower on PCST grafts after 24 hours (5.65 vs. 9.24 [PCS], 8.99 [PC], 8.82 [PG], and 10.44 log10 CFU/mL [P]; p < .015), and only PCST grafts were bactericidal. Biofilm formation was significantly diminished on PCST grafts compared with all other grafts (p < .001). Bacterial viability and metabolic activity after 24 hours were more impaired on PG compared with PC graft, and were surprisingly higher on PCS compared with PC grafts. Biofilm biomass formed after exposure to P, PG, PC, and PCS grafts was also reduced after 24 hours of incubation with PCST grafts (p < .001). After 24 hours, few bacteria were visible by SEM on PCST grafts, whereas bacterial biofilm colonies were clearly identified on other graft surfaces. CONCLUSION: Triclosan impregnated PCST grafts appeared to interfere with S. aureus adhesion from early stages of biofilm formation in vitro. Silver impregnation was not efficient in preventing biofilm formation, and collagen coating promoted S. aureus biofilm formation more than gelatin coating.

Use of monofilament sutures and triclosan coating to protect against surgical site infections in spinal surgery: a laboratory-based study.

PURPOSE: We investigated bacterial propagation through multifilament, monofilament sutures and whether sutures coated with triclosan would exhibit a different phenomenon. METHODS: One centimetre (cm) wide trenches were cut in the middle of Columbia blood Agar plates. We tested a 6 cm length of two Triclosan-coated (PDS plus®, Vicryl plus®) and two uncoated (PDS ®, Vicryl ®) sutures. Each suture was inoculated with a bacterial suspension containing methicillin-sensitive Staphylococcus aureus (MSSA), Escherichia coli (E. coli), Staphylococcus epidermidis, methicillin-resistant Staphylococcus aureus (MRSA) at one end of each suture. The plates were incubated at 36C for 48 h, followed by room temperature for a further 5 days. We established bacterial propagation by observing for any bacterial growth on the Agar on the opposite side of the trench. RESULTS: Bacterial propagation was observed on the opposite side of the trench with both suture types, monofilament PDS and multifilament Vicryl, when tested with the motile bacterium (E. coli). Propagation was not observed on the other side of the trench with the monofilament PDS suture following incubation with MSSA and S. epidermidis, and in 66% of MRSA. With multifilament suture Vicryl, propagation was observed on the other side of the trench in 90% (MSSA), 80% (S. epidermidis), and 100% (MRSA) of plates tested. No bacterial propagation was observed in any of the triclosan-coated sutures (monofilament or multifilament). CONCLUSIONS: Monofilament sutures are associated in vitro with less bacterial propagation along their course when compared to multifilament sutures. Inhibition in both sutures can be further enhanced with a triclosan coating.

Resistance-driven innovations in the discovery of bactericides: novel triclosan derivatives decorating isopropanolamine moiety as promising anti-biofilm agents against destructive plant bacterial diseases.

BACKGROUND: Controlling bacterial infections in plants is a major challenge owing to the appearance of resistant strains. As a physical barrier, the bacterial biofilm helps bacterial infections acquire drug resistance by enabling bacteria to accommodate complex and volatile environmental conditions and avoid bactericidal effects. Thus, developing new antibacterial agents with antibiofilm potency is imperative. RESULTS: A series of simple triclosan derivatives containing isopropanolamine moiety were elaborately designed and assessed for their antibacterial behavior. Bioassay results showed that some title compounds had excellent bioactivity against three destructive bacteria Xanthomonas oryzae pv. oryzae (Xoo), Xanthomonas axonopodis pv. citri (Xac) and Pseudomonas syringae pv. actinidiae (Psa). Notably, compound C8 displayed high bioactivities toward Xoo and Xac, with EC50 values were 0.34 and 2.11 µg mL-1 , respectively. In vivo trials revealed that compound C8 exhibited excellent protective activities against rice bacterial blight and citrus bacterial canker at 200 µg mL-1 , with control effectivenesses of 49.57% and 85.60%, respectively. Compound A4 had remarkably inhibitory activity toward Psa, with an EC50 value of 2.63 µg mL-1 , and demonstrated outstanding protective activity with a value of 77.23% against Psa in vivo. Antibacterial mechanisms indicated that compound C8 dose-dependently prevented biofilm formation and extracellular polysaccharide production. C8 also significantly weakened the motility and pathogenicity of Xoo. CONCLUSION: This study contributes to the development and excavation of novel bactericidal candidates with broad-spectrum antibacterial activity by targeting bacterial biofilm to control refractory plant bacterial diseases. © 2023 Society of Chemical Industry.

Do Antiseptic Coated Sutures Reduce Colo-Colonic Anastomotic Leaks?

BACKGROUND: Colorectal anastomotic leaks remain one of the most significant complications following colorectal surgery. Various interventions to reduce anastomotic leaks have been investigated, however few have resulted in a significant improvement. To date antiseptic coated monofilament sutures for sutured bowel anastomoses have not been assessed, hence this study was undertaken to investigate whether or not triclosan impregnated polydioxanone suture material (PDS) results in fewer anastomotic leaks. METHODS: A rabbit colo-colonic anastomotic model was developed to compare the tensile strength and local inflammatory response between triclosan coated PDS and uncoated PDS. RESULTS: Of the 42 anastomoses there were 4 (9.5%) leaks. Of the remaining 38 anastomoses neither the leak pressures, degree of bowel wall inflammation or fibrosis were statistically different (P = .11; .813 and .658 respectively) when comparing the two suture materials. CONCLUSIONS: In an animal model, triclosan coated PDS is as safe as uncoated PDS in performing colo-colonic anastomosis.

Evaluation of Microbial Adherence on Antibacterial Suture Materials during Intraoral Wound Healing: A Prospective Comparative Study.

AIM: To assess the efficacy of antiseptic-coated silk sutures with triclosan-coated polyglactin 910 suture in reducing bacterial colonization after oral surgical procedures. MATERIALS AND METHODS: The patients who required multiple sutures after surgical procedures in the mandible were the study subjects. The sites of suturing were divided into three groups. Group A - surgical site receiving black-braided silk suture (control group). Group B - surgical site receiving triclosan-coated Polyglactin 910 suture (experimental group). Group C - surgical site receiving antiseptic-coated silk suture (experimental group). Evaluation was done on the 3rd postoperative and 7th postoperative day. Microbial adherence was evaluated by microbiological study. RESULTS: The mean comparison of microbial count between 3rd and 7th post-op day in the three groups shows an increased microbial colonization in the control group when compared with the experimental groups. The combined mean microbial adherence in the three groups showed microbial count in the uncoated silk suture (group A) as 10.35 ± 3.74, triclosan-coated suture (group B) as 6.28 ± 2.17 and iodoform + calendula oil-coated suture (group C) as 7.1 ± 2.02 which is statistically significant (p < 0.05). CONCLUSION: The present research concluded that the pomade-coated silk suture is as efficient as triclosan-coated VICRYL PLUS Polyglactin 910 sutures in reducing the bacterial colonization in intraoral wound healing. CLINICAL SIGNIFICANCE: The pomade (iodoform + calendula oil) may be advocated in the field of oral and maxillofacial surgery for impregnating the suture materials which act as an antiseptic agent and a promoter of wound healing which is easily accessible and also cost-effective.

Three-Dimensional Mass Spectrometry Imaging Reveals Distributions of Lipids and the Drug Metabolite Associated with the Enhanced Growth of Colon Cancer Cell Spheroids Treated with Triclosan.

The application of mass spectrometry imaging (MSI) to explore the responses of cancer cell spheroids (CCS) after treatment of exogenous molecules has attracted growing attention. Increasing studies have utilized MSI to image the two-dimensional distributions of exogenous and endogenous molecules in planar CCS sections. However, because CCS are volumetric and heterogenous, maintaining their three-dimensional (3D) information is essential for acquiring a better understanding of the tumor microenvironment and mechanisms of action of exogenous molecules. Here, an established method of 3D MSI was applied to distinguish the distributions of triclosan sulfate and endogenous lipids in three microregions of colon CCS with an enhanced growth induced by the treatment of triclosan, a common antimicrobial agent. The results of 3D MSI showed that triclosan sulfate gradually accumulated from the periphery to the entire structure of CCS and finally localized in the core region. Spatial lipidomics analysis revealed that the upregulated phosphatidylethanolamine (fold change (FD) = 1.26, p = 0.0021), phosphatidylinositol (FD = 1.17, p = 0.0180), and phosphatidylcholine (FD = 1.22, p = 0.0178) species mainly distributed in the outer proliferative region, while the upregulated sphingomyelin (FD = 1.18, p = 0.024) species tended to distribute in the inner necrotic region. Our results suggest that a competitive mechanism between inhibiting and promoting CCS growth might be responsible for the proliferation of CCS treated with triclosan.

Novel diaryl ether derivatives as InhA inhibitors: Design, synthesis and antimycobacterial activity.

A new series of triclosan (TCL)-mimicking diaryl ether derivatives 7-25 were synthesized and evaluated as inhibitors of enoyl acyl carrier protein reductase InhA enzyme. In addition, these derivatives were screened as inhibitors of drug-susceptible (DS), multidrug-resistant (MDR), and extensive drug-resistant (XDR) Mycobacterium tuberculosis (MTB) strains. Most compounds exihibted superior anti-TB activities and improved ClogP compared to TCL as a standard drug. The present work has led to the identification of compounds 14, 19 and 24 which possess remarkable activities against DS, MDR and XDR MTB strains with MIC values of 1.95, 3.9 and 15.63 µg/ml, respectively for compound 14, 1.95, 3.9 and 7.81 µg/ml, respectively for compound 19 and 0.98, 1.95 and 3.9 µg/ml, respectively for compound 24. Most compounds did not exhibit toxicity to HePG2 normal cell line. Compounds 14, 19 and 24, presenting the best MIC values, were further evaluated as inhibitors of InhA enzyme. They showed high binding affinities in the micromolar range with IC50 values of 1.33, 0.6, and 0.29 µM for compounds 14, 19, and 24, respectively. Furthermore, molecular docking approach was utilized to understand the difference in bioactivities between the new compounds. In particular, the results revealed strong binding interactions and high docking scores of compounds 14, 19 and 24, which could correlate with their high activities. Mainly, the molecular modelling study of compound 24 provides an excellent platform for understanding the molecular mechanism regarding InhA inhibition. Thus, compound 24 could be a lead compound for future development of new antitubercular drugs.

Involvement of sirtuins (Sirt1 and Sirt3) and aryl hydrocarbon receptor (AhR) in the effects of triclosan (TCS) on production of neurosteroids in primary mouse cortical neurons cultures.

Epidemiological studies have shown the presence of triclosan (TCS) in the brain due to its widespread use as an antibacterial ingredient. One of the confirmed mechanisms of its action is the interaction with the aryl hydrocarbon receptor (AhR). In nerve cells, sirtuins (Sirt1 and Sirt3) act as cellular sensors detecting energy availability and modulate metabolic processes. Moreover, it has been found that Sirt1 inhibits the activation of estrogen receptors, regulates the androgen receptor, and may interact with the AhR receptor. It is also known that Sirt3 stimulates the production of estradiol (E2) via the estradiol receptor ß (Erß). Therefore, the aim of the present study was to evaluate the effect of TCS alone or in combination with synthetic flavonoids on the production of neurosteroids such as progesterone (P4), testosterone (T), and E2 in primary neural cortical neurons in vitro. The contribution of Sirt1 and Sirt3 as well as AhR to these TCS-induced effects was investigated as well. The results of the experiments showed that both short and long exposure of neurons to TCS increased the expression of the Sirt1 and Sirt3 proteins in response to AhR stimulation. After an initial increase in the production of all tested neurosteroids, TCS acting for a longer time lowered their levels in the cells. This suggests that TCS activating AhR as well as Sirt1 and Sirt3 in short time intervals stimulates the levels of P4, T, and E2 in neurons, and then the amount of neurosteroids decreases despite the activation of AhR and the increase in the expression of the Sirt1 and Sirt3 proteins. The use of both the AhR agonist and antagonist prevented changes in the expression of Sirt1, Sirt3, and AhR and the production of P4, T, and E2, which confirmed that this receptor is a key in the mechanism of the TCS action.

Design and development of essential oil based nanoemulsion for topical application of triclosan for effective skin antisepsis.

The skin acts as a physical barrier to protect the body from the external physical and chemical environment. When skin is infected, the outer epidermal barrier is compromised and colonized with microbial growth. Wound infection presents an immense burden on healthcare costs and decreased the quality of life for patients. The topical application of nanoemulsions (NE) at pathological sites offers the potential advantage of direct drug delivery to the skin including the potential for follicular targeting. This may have application in the improvement of skin antisepsis. In this study, NEs of triclosan (TSN) were prepared using hot high shear homogenization followed by ultrasonication. The oil phases comprised eucalyptus oil (EO) and olive oil (OO) and pseudo-ternary phase diagrams were used to select optimum concentrations of surfactant. EO-based NEs had smaller droplet sizes and higher entrapment efficiency compared to OO-based NEs. Skin permeation was higher for EO-containing formulations, likely due to the higher solubility of TSN in EO, smaller droplet size, low viscosity, and permeation enhancement effects of EO. Significantly, TSN was retained within the skin, demonstrating the potential of NEs for targeting hair follicular delivery within the skin, which may help improve the success of topical antisepsis.

Preimplantation triclosan exposure alters uterine receptivity through affecting tight junction protein†.

Triclosan is a broad-spectrum antibacterial agent and widely exists in environmental media and organisms. Triclosan exposure has been reported to have adverse effects on reproduction including embryo implantation disorder. During the embryo implantation window, it is vital that the endometrium develops into a receptive state under the influence of ovarian hormones. However, the effect of triclosan on embryo implantation and endometrial receptivity remains unclear. In the current study, we found a decreased embryo implantation rate, serum estrogen, and progesterone levels in mice exposed to triclosan from gestation days 0.5 to 5.5. Through RNA sequencing (RNA-seq), we identified nearly 800 differentially expressed genes, which were enriched in various pathways, including uterus development, inflammatory response, and immune system processes. Among those enriched pathways, the tight junction pathway is essential for the establishment of the receptive state of the endometrium. Then, genes involved in the tight junction pathway, including Cldn7, Cldn10, and Crb3, were validated by quantitative real-time polymerase chain reaction and the results were consistent with those from RNA-seq. Through immunofluorescence staining and western blotting, we confirmed that the tight junction protein levels of CLDN7 and CRB3 were increased. All these findings suggest that preimplantation triclosan exposure reduces the rate of embryo implantation through upregulating the expression of the tight junction genes and affecting the receptivity of the endometrium. Our data could be used to determine the sensitive time frame for triclosan exposure and offer a new strategy to prevent implantation failure.

Biochemical and structural basis for Moraxella catarrhalis enoyl-acyl carrier protein reductase (FabI) inhibition by triclosan and estradiol.

The enoyl-acyl carrier protein reductase (ENR) is an established drug target and catalyzes the last reduction step of the fatty acid elongation cycle. Here, we report the crystal structures of FabI from Moraxella catarrhalis (McFabI) in the apo form, binary complex with NAD+ and ternary complex with NAD + -triclosan (TCL) determined at 2.36, 2.12 and 2.22 Å resolutions, respectively. The comparative study of these three structures revealed three different conformational states for the substrate-binding loop (SBL), including an unstructured intermediate, a structured intermediate and a closed conformation in the apo, binary and ternary complex forms, respectively; indicating the flexibility of SBL during the ligand binding. Virtual screening has suggested that estradiol cypionate may be a potential inhibitor of McFabI. Subsequently, estradiol (EST), the natural form of estradiol cypionate, was assessed for its FabI-binding and -inhibition properties. In vitro studies demonstrated that TCL and EST bind to McFabI with high affinity (KD = 0.038 ± 0.004 and 5 ± 0.06 µM respectively) and inhibit its activity (Ki = 62.93 ± 3.95 nM and 25.97 ± 1.93 µM respectively) and suppress the growth of M. catarrhalis. These findings reveal that TCL and EST inhibit the McFabI activity and thereby affect cell growth. This study suggests that estradiol may be exploited as a novel scaffold for the designing and development of more potential FabI inhibitors.

Melaleuca alternifolia essential oil soap: a potential alternative for hand hygiene.

This study aimed to compare the antimicrobial action of three soaps for hand hygiene (HH): 2.0% Tea Tree Oil (TTO); 0.5% triclosan; 2.0% chlorhexidine, and to explore the perception of healthcare professionals about TTO. Two-step study: a quantitative, to determine the logarithmic reduction of Escherichia coli K12 colony-forming units before and after HH of 15 volunteers and quali-quantitative, through interviews with 23 health professionals. All the three products demonstrated antimicrobial action (a log10 reduction factor of 4.18 for TTO, 4.31 for triclosan, 3.89 for chlorhexidine, and 3.17 for reference soap). Professionals remarked the pleasant aroma and non-dryness of skin when using soap containing TTO.

Triclosan induces apoptosis in Burkitt lymphoma-derived BJAB cells through caspase and JNK/MAPK pathways.

Burkitt's lymphoma (BL) is the fastest growing human tumor. Current treatment consists of a multiagent regimen of cytotoxic drugs with serious side effjects including tumor lysis, cardiotoxicity, hepatic impairment, neuropathy, myelosuppression, increased susceptibility to malignancy, and death. Furthermore, therapeutic interventions in areas of BL prevalence are not as feasible as in high-income countries. Therefore, there exists an urgent need to identify new therapies with a safer profile and improved accessibility. Triclosan (TCS), an antimicrobial used in personal care products and surgical scrubs, has gained considerable interest as an antitumor agent due to its interference with fatty acid synthesis. Here, we investigate the antitumor properties and associated molecular mechanisms of TCS in BL-derived BJAB cells. Dose-dependent cell death was observed following treatment with 10-100 µM TCS for 24 h, which was associated with membrane phospholipid scrambling, compromised permeability, and cell shrinkage. TCS-induced cell death was accompanied by elevated intracellular calcium, perturbed redox balance, chromatin condensation, and DNA fragmentation. TCS upregulated Bad expression and downregulated that of Bcl2. Moreover, caspase and JNK MAPK signaling were required for the full apoptotic activity of TCS. In conclusion, this report identifies TCS as an antitumor agent and provides new insights into the molecular mechanisms governing TCS-induced apoptosis in BL cells.

Triclosan leads to dysregulation of the metabolic regulator FGF21 exacerbating high fat diet-induced nonalcoholic fatty liver disease.

Triclosan (TCS), employed as an antiseptic and disinfectant, comes into direct contact with humans through a plethora of consumer products and its rising environmental release. We have demonstrated that TCS promotes liver tumorigenesis in mice, yet the biological and molecular mechanisms by which TCS exerts its toxicity, especially in early stages of liver disease, are largely unexplored. When mice were fed a high-fat diet (HFD), we found that fatty liver and dyslipidemia are prominent early signs of liver abnormality induced by TCS. The presumably protective HFD-induced hepatic expression of the metabolic regulator fibroblast growth factor 21 (FGF21) was blunted by TCS. TCS-altered Fgf21 expression aligned with aberrant expression of genes encoding metabolic enzymes manifested as profound systemic metabolic changes that disturb homeostasis of amino acids, fatty acids, and glucose. Using a type 1 diabetic animal model, TCS potentiates and accelerates the development of steatohepatitis and fibrosis, accompanied by increased levels of hepatic lipid droplets and oxidative stress. Analysis of fecal samples revealed that HFD-fed mice exhibited a reduction in fecal species richness, and that TCS further diminished microbial diversity and shifted the bacterial community toward lower Bacteriodetes and higher Firmicutes, resembling changes in microbiota composition in nonalcoholic steatohepatitis (NASH) patients. Using reverse-genetic approaches, we demonstrate that, along with HFD, TCS induces hepatic steatosis and steatohepatitis jointly regulated by the transcription factor ATF4 and the nuclear receptor PPARα, which participate in the transcriptional regulation of the Fgf21 gene. This study provides evidence linking nutritional imbalance and exposure to TCS with the progression of NASH.

Triclosan: antimicrobial mechanisms, antibiotics interactions, clinical applications, and human health.

The large-scale applications of Triclosan in industrial and household products have created many health and environmental concerns. Despite the fears of its drug-resistance and other issues, Triclosan is still an effective drug against many infectious organisms. Knowing the cross-interactions of Triclosan with different antibiotics, bacteria, and humans can provide much-needed information for the risk assessment of this drug. We review the current understanding of the antimicrobial mechanisms of Triclosan, how microbes become resistant to Triclosan, and the synergistic and antagonistic effects of Triclosan with different antibiotics. Current literature on the clinical applications of Triclosan and its effect on fetus/child development are also summarized.

Detection of the effects of triclosan (TCS) on the metabolism of VOCs in HepG2 cells by SPI-TOFMS.

Volatile organic compounds (VOCs) emitted by organisms and cell metabolism have demonstrated great physiological and pathological values. At present, there is a great interest in the study of volatile metabolome to determine whether VOCs can serve as potential diagnostic biomarkers. In view of the sensitivity of VOCs to physiological changes, the aim of this study was to investigate alterations in VOC profiles in the in vitro headspace of HepG2 cells after exposure to triclosan (TCS). Since the in vivo biological effects of TCS are clearly defined, several TCS-related VOCs may potentially be traced back to common cellular processes. In this study, HepG2 cells were cultured in TCS-containing medium for 2 h, and the emitted VOCs in the headspace of the culture flask were detected using a single photon ionization time-of-flight mass spectrometry instrument. The control group and the TCS-treated group could be well separated by differential VOC profiles, which were related to the physiological states of the HepG2 cells. Compared to the control group, eleven and ten specific VOCs were identified in the 20 µm and 50 µm TCS-treated groups, respectively. Among them, five specific VOCs (m/z 62, 64, 70, 121 and 146) were commonly observed in these two TCS-treated groups. These results indicate that TCS can cause changes in cellular metabolic VOCs, and different concentrations of TCS lead to different VOCs profiles. Based on the findings of the study, the detection of VOCs in cell metabolism can be used as an auxiliary tool to explore the mechanism of drug action, and also as an exploratory method to determine whether drugs play a role in disease treatment.