Critical review on the environmental behaviors and toxicity of triclosan and its removal technologies.

As a highly effective broad-spectrum antibacterial agent, triclosan (TCS) is widely used in personal care and medical disinfection products, resulting in its widespread occurrence in aquatic and terrestrial environments, and even in the human body. Notably, the use of TCS surged during the COVID-19 outbreak, leading to increasing environmental TCS pollution pressure. From the perspective of environmental health, it is essential to systematically understand the environmental occurrence and behavior of TCS, its toxicological effects on biota and humans, and technologies to remove TCS from the environment. This review comprehensively summarizes the current knowledge regarding the sources and behavior of TCS in surface water, groundwater, and soil systems, focusing on its toxicological effects on aquatic and terrestrial organisms. Effluent from wastewater treatment plants is the primary source of TCS in aquatic systems, whereas sewage application and/or wastewater irrigation are the major sources of TCS in soil. Human exposure pathways to TCS and associated adverse outcomes were also analyzed. Skin and oral mucosal absorption, and dietary intake are important TCS exposure pathways. Reducing or completely degrading TCS in the environment is important for alleviating environmental pollution and protecting public health. Therefore, this paper reviews the removal mechanisms, including adsorption, biotic and abiotic redox reactions, and the influencing factors. In addition, the advantages and disadvantages of the different techniques are compared, and development prospects are proposed. These findings provide a basis for the management and risk assessment of TCS and are beneficial for the application of treatment technology in TCS removal.

Gender-specific effects of polystyrene nanoplastic exposure on triclosan-induced reproductive toxicity in zebrafish (Danio rerio).

Nanoplastics (NPs) and triclosan (TCS) are ubiquitous emerging environmental contaminants detected in human samples. While the reproductive toxicity of TCS alone has been studied, its combined effects with NPs remain unclear. Herein, we employed Fourier transform infrared spectroscopy and dynamic light scattering to characterize the coexposure of polystyrene nanoplastics (PS-NPs, 50 nm) with TCS. Then, adult zebrafish were exposed to TCS at environmentally relevant concentrations (0.361-48.2 µg/L), with or without PS-NPs (1.0 mg/L) for 21 days. TCS biodistribution in zebrafish tissues was investigated using ultra-performance liquid chromatography coupled with triple quadrupole mass spectrometry. Reproductive toxicity was assessed through gonadal histopathology, fertility tests, changes in steroid hormone synthesis and gene expression within the hypothalamus-pituitary-gonad-liver (HPGL) axis. Transcriptomics and proteomics were applied to explore the underlying mechanisms. The results showed that PS-NPs could adsorb TCS, thus altering the PS-NPs' physical characteristics. Our observations revealed that coexposure with PS-NPs reduced TCS levels in the ovaries, livers, and brains of female zebrafish. Conversely, in males, coexposure with PS-NPs increased TCS levels in the testes and livers, while decreasing them in the brain. We found that co-exposure mitigated TCS-induced ovary development inhibition while exacerbated TCS-induced spermatogenesis suppression, resulting in increased embryonic mortality and larval malformations. This co-exposure influenced the expression of genes linked to steroid hormone synthesis (cyp11a1, hsd17ß, cyp19a1) and attenuated the TCS-decreased estradiol (E2) in females. Conversely, testosterone levels were suppressed, and E2 levels were elevated due to the upregulation of specific genes (cyp11a1, hsd3ß, cyp19a1) in males. Finally, the integrated analysis of transcriptomics and proteomics suggested that the aqp12-dctn2 pathway was involved in PS-NPs' attenuation of TCS-induced reproductive toxicity in females, while the pck2-katnal1 pathway played a role in PS-NPs' exacerbation of TCS-induced reproductive toxicity in males. Collectively, PS-NPs altered TCS-induced reproductive toxicity by disrupting the HPGL axis, with gender-specific effects.

Triclocarban and triclosan promote breast cancer progression in vitro and in vivo via activating G protein-coupled estrogen receptor signaling pathways.

Triclocarban (TCC) and triclosan (TCS) have been detected ubiquitously in human body and evoked increasing concerns. This study aimed to reveal the induction risks of TCC and TCS on triple negative breast cancer through non-genomic GPER-mediated signaling pathways. Molecular simulation indicated that TCC exhibited higher GPER binding affinity than TCS theoretically. Calcium mobilization assay displayed that TCC/TCS activated GPER signaling pathway with the lowest observed effective concentrations (LOEC) of 10 nM/100 nM. TCC and TCS also upregulated MMP-2/9, EGFR, MAPK3 but downregulated MAPK8 via GPER-mediated signaling pathway. Proliferation assay showed that TCC/TCS induced 4 T1 breast cancer cells proliferation with the LOEC of 100 nM/1000 nM. Wound-healing and transwell assays showed that TCC/TCS promoted 4 T1 cells migration in a concentration-dependent manner with the LOEC of 10 nM. The effects of TCC on breast cancer cells proliferation and migration were stronger than TCS and both were regulated by GPER. TCC/TCS induced migratory effects were more significantly than proliferative effect. Mechanism study showed that TCC/TCS downregulated the expression of epithelial marker (E-cadherin) but upregulated mesenchymal markers (snail and N-cadherin), which was reversed by GPER inhibitor G15. These biomarkers results indicated that TCC/TCS-induced 4 T1 cells migration was a classic epithelial to mesenchymal transition mechanism regulated by GPER signaling pathway. Orthotopic tumor model verified that TCC promoted breast cancer in-situ tumor growth and distal tissue metastasis via GPER-mediated signaling pathway at human-exposure level of 10 mg/kg/d. TCC-induced tissue metastasis of breast cancer was more significantly than in-situ tumor growth. Overall, we demonstrated for the first time that TCC/TCS could activate the GPER signaling pathways to induce breast cancer progression.

Comparative impact of pristine and aged microplastics with triclosan on lipid metabolism in larval zebrafish: Unveiling the regulatory role of miR-217.

The prevalence of microplastics (MPs), especially aged particles, interacting with contaminants like triclosan (TCS), raises concerns about their toxicological effects on aquatic life. This study focused on the impact of aged polyamide (APA) MPs and TCS on zebrafish lipid metabolism. APA MPs, with rougher surfaces and lower hydrophobicity, exhibited reduced TCS adsorption than unaged polyamide (PA) MPs. Co-exposure to PA/APA MPs and TCS resulted in higher TCS accumulation in zebrafish larvae, notably more with PA than APA. Larvae exposed to PA + TCS exhibited greater oxidative stress, disrupted lipid metabolism, and altered insulin pathway genes than those exposed to TCS. However, these negative effects were lessened in the APA + TCS group. Through miRNA-seq and miR-217 microinjection, it was revealed that PA + TCS co-exposure upregulated miR-217, linked to lipid metabolic disorders in zebrafish. Moreover, molecular docking showed stable interactions formed between PA, TCS, and the insulin signaling protein Pik3r2. This study demonstrated that PA and TCS co-exposure significantly inhibited the insulin signaling in zebrafish, triggering lipid metabolism dysregulation mediated by miR-217 upregulation, while APA and TCS co-exposure alleviated these disruptions. This research underscored the ecological and toxicological risks of aged MPs and pollutants in aquatic environments, providing crucial insights into the wider implications of MPs pollution.

Exposure to endocrine disrupting chemicals (bisphenols, parabens, and triclosan) and their associations with preterm birth in humans.

Preterm birth in humans (PTB), defined as birth prior to 37 weeks of gestation, is one of the most important causes of neonatal morbidity and mortality and is associated with adverse health outcomes later in life. Attributed to many different etiological factors, estimated 15.1 million or 11.1% of births each year are preterm, which is more than 1 per 10 livebirths globally. Environmental pollution is a well-established risk factor that could influence the pathogenesis of PTB. Increasing evidence has shown an association between maternal exposure to endocrine disrupting chemicals (EDCs) and PTB. This scoping review aims to summarize current research on the association between EDC exposure and PTB in humans. Database PubMed was used to identify articles discussing the effect of selected EDCs, namely bisphenol A, bisphenol S, bisphenol F, parabens, and triclosan, found in plastics, cosmetics and other personal care products, on PTB occurrence. Regardless of some inconsistences in the findings across studies, the reviewed studies suggest a potential association between involuntary exposure to reviewed EDCs and the risk of PTB. However, further studies are needed to delineate exact correlations and mechanisms through which EDC exposure causes PTB so that efficient preventative measures could be implemented. Until then, health care providers should inform women about possible EDC exposure thus empowering them to make healthy choices and at the same time decrease the EDC negative effects.

Reproductive endocrine disruption effect and mechanism in male zebrafish after life cycle exposure to environmental relevant triclosan.

Triclosan (TCS) is a wide-spectrum antibacterial agent that is found in various water environments. It has been reported to have estrogenic effects. However, the impact of TCS exposure on the reproductive system of zebrafish (Danio rerio) throughout their life cycle is not well understood. In this study, zebrafish fertilized eggs were exposed to 0, 10, and 50 µg/L TCS for 120 days. The study investigated the effects of TCS exposure on brain and testis coefficients, the expression of genes related to the hypothalamus-pituitary-gonadal (HPG) axis, hormone levels, vitellogenin (VTG) content, histopathological sections, and performed RNA sequencing of male zebrafish. The results revealed that life cycle TCS exposure had significant effects on zebrafish reproductive parameters. It increased the testis coefficient, while decreasing the brain coefficient. TCS exposure also led to a decrease in mature spermatozoa and altered the expression of genes related to the HPG axis. Furthermore, TCS disrupted the balance of sex hormone levels and increased VTG content of male zebrafish. Transcriptome sequencing analysis indicated that TCS affected reproductive endocrine related pathways, including PPAR signaling pathway, cell cycle, GnRH signaling pathway, steroid biosynthesis, cytokine-cytokine receptor interaction, and steroid hormone biosynthesis. Protein-protein interaction (PPI) network analysis confirmed the enrichment of hub genes in these pathways, including bub1bb, ccnb1, cdc20, cdk1, mcm2, mcm5, mcm6, plk1, and ttk in the brain, as well as fabp1b.1, fabp2, fabp6, ccr7, cxcl11.8, hsd11b2, and hsd3b1 in the testis. This study sheds light on the reproductive endocrine-disrupting mechanisms of life cycle exposure to TCS.

Triclosan, an antimicrobial drug, induced reproductive impairment in the freshwater fish, Anabas testudineus (Bloch, 1792).

Triclosan (TCS), an antimicrobial drug, is known to occupy different compartments in aquatic ecosystems. The present study focused to evaluate the reproductive toxicity of triclosan, at environmentally relevant (0.009 and 9 µg L-1) and sublethal (176.7 µg L-1) concentrations for 90 days in the pre-spawning phase of the fish, Anabas testudineus. The reproductive biomarkers, namely, gonadal steroidogenic enzymes, expression of aromatic genes, levels of serum gonadotropins, sex hormones, and histology of gonads were analyzed. The weight of the animal, brain weights along with gonadosomatic index decreased while mucus deposition increased significantly at all concentrations of triclosan as the primary defensive mechanism to prevent the entry of toxicants. Triclosan disrupted gonadal steroidogenesis as evidenced by a reduction in the activities of gonadal steroidogenic enzymes. The expressions of cyp19a1a and cyp19a1b genes were up-regulated in the brain of both sexes and testis, while down-regulated in the ovary indicating estrogenic effects of the compound. The endocrine-disrupting effects of triclosan were confirmed. The current results suggest that chronic exposure to triclosan altered reproductive endpoints thereby impairing normal reproductive functions in fish.

Dynamic alterations in physiological and biochemical indicators of Cirrhinus mrigala hatchlings: A sublethal exposure of triclosan.

Triclosan (TCS), a biocide used in various day-to-day products, has been associated with several toxic effects in aquatic organisms. In the present study, biochemical and hematological alterations were evaluated after 14 d (sublethal) exposure of tap water (control), acetone (solvent control), 5, 10, 20, and 50 µg/L (environmentally relevant concentrations) TCS to the embryos/hatchlings of Cirrhinus mrigala, a major freshwater carp distributed in tropic and sub-tropical areas of Asia. A concentration-dependent increase in the content of urea and protein carbonyl, while a decrease in the total protein, glucose, cholesterol, triglycerides, uric acid, and bilirubin was observed after the exposure. Hematological analysis revealed a decrease in the total erythrocyte count, hemoglobin, and partial pressure of oxygen, while there was an increase in the total leucocyte count, carbon dioxide, and partial pressure of carbon dioxide and serum electrolytes. Comet assay demonstrates a concentration-dependent increase in tail length, tail moment, olive tail moment, and percent tail DNA. An amino acid analyzer showed a TCS-dose-dependent increase in various amino acids. Sodium dodecyl sulphate polyacrylamide gel electrophoresis analysis revealed different proteins ranging from 6.5 to 200 kDa, demonstrating TCS-induced upregulation. Fourier transform infrared spectra analysis exhibited a decline in peak area percents with an increase in the concentration of TCS in water. Curve fitting of amide I (1,700-1600 cm-1) showed a decline in α-helix and turns and an increase in ß-sheets. Nuclear magnetic resonance study also revealed concentration-dependent alterations in the metabolites after 14 d exposure. TCS caused alterations in the biomolecules and heamatological parameters of fish, raising the possibility that small amounts of TCS may change the species richness in natural aquatic habitats. In addition, consuming TCS-contaminated fish may have detrimental effects on human health. Consequently, there is a need for the proper utilisation and disposal of this hazardous compound in legitimate quantities.

Toxic effects of triclosan on hepatic and intestinal lipid accumulation in zebrafish via regulation of m6A-RNA methylation.

Triclosan (TCS), recognized as an endocrine disruptor, has raised significant concerns due to its widespread use and potential health risks. To explore the impact of TCS on lipid metabolism, both larval and adult zebrafish were subjected to acute and chronic exposure to TCS. Through analyzes of biochemical and physiological markers, as well as Oil Red O (ORO) and hematoxylin and eosin (H&E) staining, our investigation revealed that TCS exposure induced hepatic and intestinal lipid accumulation in larval and adult zebrafish, leading to structural damage and inflammatory responses in these tissues. The strong affinity of TCS with PPARγ and subsequent pathway activation indicate that PPARγ pathway plays a crucial role in TCS-induced lipid buildup. Furthermore, we observed a decrease in m6A-RNA methylation levels in the TCS-treated group, which attributed to the increased activity of the demethylase FTO and concurrent suppression of the methyltransferase METTL3 gene expression by TCS. The alteration in methylation dynamics is identified as a potential underlying mechanism behind TCS-induced lipid accumulation. To address this concern, we explored the impact of folic acid-a methyl donor for m6A-RNA methylation-on lipid accumulation in zebrafish. Remarkably, folic acid administration partially alleviated lipid accumulation by restoring m6A-RNA methylation. This restoration, in turn, contributed to a reduction in inflammatory damage observed in both the liver and intestines. Additionally, folic acid partially mitigates the up-regulation of PPARγ and related genes induced by TCS. These findings carry substantial implications for understanding the adverse effects of environmental pollutants such as TCS. They also emphasize the promising potential of folic acid as a therapeutic intervention to alleviate disturbances in lipid metabolism induced by environmental pollutants.

Uptake, tissue distribution, and biotransformation pattern of triclosan in tilapia exposed to environmentally-relevant concentrations.

Although triclosan has been ubiquitously detected in aquatic environment and is known to have various adverse effects to fish, details on its uptake, bioconcentration, and elimination in fish tissues are still limited. This study investigated the uptake and elimination toxicokinetics, bioconcentration, and biotransformation potential of triclosan in Nile tilapia (Oreochromis niloticus) exposed to environmentally-relevant concentrations under semi-static regimes for 7 days. For toxicokinetics, triclosan reached a plateau concentration within 5-days of exposure, and decreased to stable concentration within 5 days of elimination. Approximately 50 % of triclosan was excreted by fish through feces, and up to 29 % of triclosan was excreted through the biliary excretion. For fish exposed to 200 ng·L-1, 2000 ng·L-1, and 20,000 ng·L-1, the bioconcentration factors (log BCFs) of triclosan in fish tissues obeyed similar order: bile ≈ intestine > gonad ≈ stomach > liver > kidney ≈ gill > skin ≈ plasma > brain > muscle. The log BCFs of triclosan in fish tissues are approximately maintained constants, no matter what triclosan concentrations in exposure water. Seven biotransformation products of triclosan, involved in both phase I and phase II metabolism, were identified in this study, which were produced through hydroxylation, bond cleavages, dichlorination, and sulfation pathways. Metabolite of triclosan-O-sulfate was detected in all tissues of tilapia, and more toxic product of 2,4-dichlorophenol was also found in intestine, gonad, and bile of tilapia. Meanwhile, two metabolites of 2,4-dichlorophenol-O-sulfate and monohydroxy-triclosan-O-sulfate were firstly discovered in the skin, liver, gill, intestine, gonad, and bile of tilapia in this study. These findings highlight the importance of considering triclosan biotransformation products in ecological assessment. They also provide a scientific basis for health risk evaluation of triclosan to humans, who are associated with dietary exposure through ingesting fish.

The effect of triclosan on intergeneric horizontal transmission of plasmid-mediated tigecycline resistance gene tet(X4) from Citrobacter freundii isolated from grass carp gut.

The transmission of antibiotic resistance genes (ARGs) in pathogenic bacteria affects culture animal health, endangers food safety, and thus gravely threatens public health. However, information about the effect of disinfectants - triclosan (TCS) on ARGs dissemination of bacterial pathogens in aquatic animals is still limited. One Citrobacter freundii (C. freundii) strain harboring tet(X4)-resistant plasmid was isolated from farmed grass carp guts, and subsequently conjugative transfer frequency from C. freundii to Escherichia coli C600 (E. coli C600) was analyzed under different mating time, temperature, and ratio. The effect of different concentrations of TCS (0.02, 0.2, 2, 20, 200 and 2000 µg/L) on the conjugative transfer was detected. The optimum conditions for conjugative transfer were at 37 °C for 8h with mating ratio of 2:1 or 1:1 (C. freundii: E. coli C600). The conjugative transfer frequency was significantly promoted under TCS treatment and reached the maximum value under 2.00 µg/L TCS with 18.39 times that of the control group. Reactive oxygen species (ROS), superoxide dismutase (SOD) and catalase (CAT) activities, cell membrane permeability of C. freundii and E. coli C600 were obviously increased under TCS stress. Scanning electron microscope showed that the cell membrane surface of the conjugative strains was wrinkled and pitted, even broken at 2.00 µg/L TCS, while lysed or even ruptured at 200.00 µg/L TCS. In addition, TCS up-regulated expression levels of oxidative stress genes (katE, hemF, bcp, hemA, katG, ahpF, and ahpC) and cell membrane-related genes (fimC, bamE and ompA) of donor and recipient bacteria. Gene Ontology (GO) enrichment demonstrated significant changes in categories relevant to pilus, porin activity, transmembrane transporter activity, transferase activity, hydrolase activity, material transport and metabolism. Taken together, a tet(X4)-resistant plasmid could horizontal transmission among different pathogens, while TCS can promote the propagation of the resistant plasmid.

The pharmaceutical triclosan induced oxidative stress and physiological disorder in marine organism and nanoparticles as a potential mitigating tool.

Environmental research plays a crucial role in formulating novel approaches to pollution management and preservation of biodiversity. This study aims to assess the potential harm of pharmaceutical triclosan (TCS) to non-target aquatic organism, the mussel Mytilus galloprovincialis. Furthermore, our study investigates the potential effectiveness of TiO2 and ZnO nanomaterials (TiO2 NPs and ZnO NPs) in degrading TCS. To ascertain the morphology, structure, and stability of the nanomaterials, several chemical techniques were employed. To evaluate the impact of TCS, TiO2 NPs, and ZnO NPs, both physiological (filtration rate (FR) and respiration rate (RR)), antioxidant enzymes (superoxide dismutase (SOD), catalase (CAT), glutathione-S-transferase (GST)) activities and malondialdehyde (MDA) contents were measured in M. galloprovincialis gills and digestive gland. The mussel's responses varied depending on the contaminant, concentration, and organ, underscoring the significance of compiling these factors in ecotoxicity tests. The main toxic mechanisms of TCS and ZnO NPs at a concentration of 100 µg/L were likely to be a decrease in FR and RR, an increase in oxidative stress, and increased lipid peroxidation. Our findings indicate that a mixture of TCS and NPs has an antagonist effect on the gills and digestive gland. This effect is particularly notable in the case of TCS2 = 100 µg/L combined with TiO2 NP2 = 100 µg/L, which warrants further investigation to determine the underlying mechanism. Additionally, our results suggest that TiO2 NPs are more effective than ZnO NPs at degrading TCS, which may have practical implications for pharmaceutical control in marine ecosystems and in water purification plants. In summary, our study provides valuable information on the impact of pharmaceuticals on non-target organisms and sheds light on potential solutions for their removal from aqueous environments.

Current state of knowledge of triclosan (TCS)-dependent reactive oxygen species (ROS) production.

Triclosan (TCS) is widely used in a number of industrial and personal care products. This molecule can induce reactive oxygen species (ROS) production in various cell types, which results in diverse types of cell responses. Therefore, the aim of the present study was to summarize the current state of knowledge of TCS-dependent ROS production and the influence of TCS on antioxidant enzymes and pathways. To date, the TCS mechanism of action has been widely investigated in non-mammalian organisms that may be exposed to contaminated water and soil, but there are also in vivo and in vitro studies on plants, algae, mammalians, and humans. This literature review has revealed that mammalian organisms are more resistant to TCS than non-mammalian organisms and, to obtain a toxic effect, the effective TCS dose must be significantly higher. The TCS-dependent increase in the ROS level causes damage to DNA, protein, and lipids, which together with general oxidative stress leads to cell apoptosis or necrosis and, in the case of cancer cells, faster oncogenesis and even initiation of oncogenic transformation in normal human cells. The review presents the direct and indirect TCS action through different receptor pathways.

Co-exposure to polystyrene nanoplastics and triclosan induces synergistic cytotoxicity in human KGN granulosa cells by promoting reactive oxygen species accumulation.

In recent years, nanoplastics (NPs) and triclosan (TCS, a pharmaceutical and personal care product) have emerged as environmental pollution issues, and their combined presence has raised widespread concern regarding potential risks to organisms. However, the combined toxicity and mechanisms of NPs and TCS remain unclear. In this study, we investigated the toxic effects of polystyrene NPs and TCS and their mechanisms on KGN cells, a human ovarian granulosa cell line. We exposed KGN cells to NPs (150 µg/mL) and TCS (15 µM) alone or together for 24 hours. Co-exposure significantly reduced cell viability. Compared with exposure to NPs or TCS alone, co-exposure increased reactive oxygen species (ROS) production. Interestingly, co-exposure to NPs and TCS produced synergistic effects. We examined the activity of superoxide dismutase (SOD) and catalase (CAT), two antioxidant enzymes; it was significantly decreased after co-exposure. We also noted an increase in the lipid oxidation product malondialdehyde (MDA) after co-exposure. Furthermore, co-exposure to NPs and TCS had a more detrimental effect on mitochondrial function than the individual treatments. Co-exposure activated the NRF2-KEAP1-HO-1 antioxidant stress pathway. Surprisingly, the expression of SESTRIN2, an antioxidant protein, was inhibited by co-exposure treatments. Co-exposure to NPs and TCS significantly increased the autophagy-related proteins LC3B-II and LC3B-Ⅰ and decreased P62. Moreover, co-exposure enhanced CASPASE-3 expression and inhibited the BCL-2/BAX ratio. In summary, our study revealed the synergistic toxic effects of NPs and TCS in vitro exposure. Our findings provide insight into the toxic mechanisms associated with co-exposure to NPs and TCS to KGN cells by inducing oxidative stress, activations of the NRF2-KEAP1-HO-1 pathway, autophagy, and apoptosis.

Acute/chronic triclosan exposure induces downregulation of m6A-RNA methylation modification via mettl3 suppression and elicits developmental and immune toxicity to zebrafish.

Triclosan (TCS), a prevalent contaminant in aquatic ecosystems, has been identified as a potential threat to both aquatic biota and human health. Despite its widespread presence, research into the immunotoxic effects of TCS on aquatic organisms is limited, and the underlying mechanisms driving these effects remain largely unexplored. Herein, we investigated the developmental and immune toxicities of environmentally relevant concentrations of TCS in zebrafish, characterized by morphological anomalies, histopathological impairments, and fluctuations in cytological differentiation and biomarkers following both acute (from 6 to 72/120 hpf) and chronic exposure periods (from 30 to 100 dpf). Specifically, acute exposure to TCS resulted in a significant increase in innate immune cells, contrasted by a marked decrease in T cells. Furthermore, we observed that TCS exposure elicited oxidative stress and a reduction in global m6A levels, alongside abnormal expressions within the m6A modification enzyme system in zebrafish larvae. Molecular docking studies suggested that mettl3 might be a target molecule for TCS interaction. Intriguingly, the knock-down of mettl3 mirrored the effects of TCS exposure, adversely impacting the growth and development of zebrafish, as well as the differentiation of innate immune cells. These results provide insights into the molecular basis of TCS-induced immunotoxicity through m6A-RNA epigenetic modification and aid in assessing its ecological risks, informing strategies for disease prevention linked to environmental contaminants.

Triclosan induces liver injury in long-life exposed mice via activation of TLR4/NF-κB/NLRP3 pathway.

Triclosan (TCS) is a widely used synthetic, with broad-spectrum antibacterial properties found in both pharmaceuticals and personal care products. More specifically, it is hepatotoxic in rodents and exhibits differential effects in mice and humans. However, the mechanisms underlying TCS-induced liver toxicity have not been elucidated. This study examined the role of the toll-like receptor 4 (TLR4)/ nuclear factor kappa B (NF-κB)/ nod-like receptor protein 3 (NLRP3) pathway in TCS-exposed liver toxicity by established a long-life TCS-exposed mice liver injury model. The 24 C57BL/6 pregnant mice exposed to TCS (0, 50 and 100 mg/kg) every day during the gestation and nursing period. After weaning, the male mice were left to continue administrate with TCS until 8 weeks of age. Then, mice in each group were sacrificed for investigation. Long-life exposure to TCS resulted in a reduction of body weight in growth mice. TCS exposure caused the increase of serum ALT, AST and ALP. The situation of inflammatory cell infiltration, macrophage recruitment and collagen fiber deposition in TCS-exposed mice liver tissues were performed by histological analysis including hematoxylin-eosin, Masson, Sirius red, and immunohistochemistry staining. Protein expression levels in TLR4/NF-κB/NLRP3 pathway was measured through Western blot, and the NLRP3 inflammasome activation was measured using real-time quantitative PCR (RT-qPCR). The results showed that exposure to TCS elevated TLR4, myeloid differentiation factor 88 (Myd88), TNF receptor associated factor 6 (TRAF6), enhanced NF-κB activation, and affected NLRP3 inflammasome activation in mice liver. Collectively, these findings indicate that long-life exposure to TCS-induced mice by upregulating the TLR4-Myd88-TRAF6 pathway, activating the NF-κB signaling cascade, initiating the NLRP3 inflammasome pathway, and ultimately leading to liver injury, including inflammation, hepatocyte pyroptosis and hepatofibrosis. Henceforth, the TLR4/NF-κB/NLRP3 pathway may now provide a theoretical basis and valuable therapeutic targets for overcoming TCS-induced liver toxicity.

The pleiotropic role of Salinicoccus bacteria in enhancing ROS homeostasis and detoxification metabolism in soybean and oat to cope with pollution of triclosan.

Triclosan has been extensively used as a preservative in cosmetics and personal care products. However, its accumulation represents a real environmental threat. Thus, its phytotoxic impact needs more consideration. Our study was conducted to highlight the phytotoxic effect of triclosan on the growth, ROS homeostasis, and detoxification metabolism of two different plant species i.e., legumes (Glycine max) and grass (Avena sativa). Moreover, we investigated the potentiality of plant growth-promoting bacteria (ST-PGPB) in mitigating the phytotoxic effect of triclosan. Triclosan induced biomass (fresh and dry weights) reduction in both plants, but to a higher extent in oats. This decline was associated with a noticeable increment in the oxidative damage (e.g., MDA and H2O2) and detoxification metabolites such as metallothionein (MTC), phytochelatins (PCs), and glutathione-S-transferase (GST). This elevation was associated with a remarkable reduction in both enzymatic and non-enzymatic antioxidants. On the other hand, the bioactive strain of ST-PGPB, Salinicoccus sp. JzA1 significantly alleviated the harmful effect of triclosan on both soybean and oat plants by enhancing their biomass, photosynthesis, as well as levels of minerals (K, Ca, P, Mn, and Zn). In parallel, a striking quenching in oxidative damage and an obvious improvement in non-enzymatic (polyphenols, tocopherols, flavonoids) and enzymatic antioxidants were observed. Furthermore, Salinicoccus sp. JzA1 augmented the detoxification metabolism by enhancing the levels of phytochelatins, metallothionein, and glutathione-S-transferase (GST) activity in a species-specific manner which is more apparent in soybean rather than in oat plants. To this end, stress mitigating impact of Salinicoccus sp. JzA1 provides a basis to improve the resilience of crop species under cosmetics and personal care products toxicity.

Biochemical and physiological alterations caused by Diuron and Triclosan in mussels (Mytilus galloprovincialis).

The rise in the utilization of pesticides within industrial and agricultural practices has been linked to the occurrence of these substances in aquatic environments. The objective of this work was to evaluate the uptake and adverse impacts of Diuron (Di) and Triclosan (TCS) on the mussel species Mytilus galloprovincialis. To accomplish this, the accumulation and toxicity of these pesticides were gauged following a brief period of exposure spanning 14 days, during which the mussels were subjected to two concentrations (50 and 100 µg/L) of each substance that are ecologically relevant. Chemical analysis of Di and TCS within gills and digestive gland showed that these pesticides could be accumulated in mussel's tissues. In addition, Di and TCS are preferably accumulated in digestive gland. Measured biomarkers included physiological parameters (filtration FC and respiration RC capacity), antioxidant enzyme activities (superoxide dismutase and catalase), oxidative damage indicator (Malondialdheyde concentration) and neurotoxicity level (acetylcholinesterase activity) were evaluated in gills and digestive glands. Both pesticides were capable of altering the physiology of this species by reducing the FC and RC in concentration and chemical dependent manner. Both pesticides induced also an oxidative imbalance causing oxidative stress. The high considered concentration exceeded the antioxidant defense capacity of the mussel and lead to membrane lipid peroxidation that resulted in cell damage. Finally, the two pesticides tested were capable of interacting with the neuromuscular barrier leading to neurotoxicity in mussel's tissues by inhibiting acetylcholinesterase. The ecotoxicological effect depended on the concentration and the chemical nature of the contaminant. Obtained results revealed also that the Di may exert toxic effects on M. galloprovincialis even at relatively low concentrations compared to TCS. In conclusion, this study presents innovative insights into the possible risks posed by Diuron (Di) and Triclosan (TCS) to the marine ecosystem. Moreover, it contributes essential data to the toxicological database necessary for developing proactive environmental protection measures.

Ecotoxicological and human health risk assessment of triclosan antibacterial agent from municipal wastewater treatment plants.

In this study, the occurrence and environmental risks related to triclosan (TCS) in the two wastewater treatment plants (WWTPs) were investigated in Isfahan, Iran. Influent and effluent samples were collected and analyzed by dispersive liquid-liquid microextraction (DLLME)-GC-MS method with derivatization. Moreover, the risk of TCS exposure was conducted for aquatic organisms (algae, crustaceans, and fishes) and humans (males and females). TCS mean concentrations in influent and effluent of WWTPs were in the range of 3.70-52.99 and 0.83-1.09 µg/L, respectively. There were also no differences in the quantity of TCS and physicochemical parameters among the two WWTPs. The mean risk quotient (RQ) for TCS was higher than 1 (in algae) with dilution factors (DFs) equal to 1 in WWTP1. Moreover, the RQ value was higher than 1 for humans based on the reference dose of MDH (RFDMDH) in WWTP1. Furthermore, TCS concentration in wastewater effluent was the influential factor in varying the risk of TCS exposure. The results of the present study showed the risk of TCS exposure from the discharge of effluent of WWTP1 was higher than WWTP2. Moreover, the results of this study may be suitable for promoting WWTP processes to completely remove micropollutants.

Effects of chronic triclosan exposure on nephrotoxicity and gut microbiota dysbiosis in adult mice.

Triclosan (TCS), a broad-spectrum, lipophilic, and antibacterial agent, has been commonly used in cosmetics, medical devices, and household products. The toxicity of TCS has recently become a research hotspot. Emerging evidence has shown that TCS can easily migrate to humans and animals and cause adverse effects on various target organs. However, the effects of TCS exposure on nephrotoxicity and underlying mechanisms remain unknown. The aim of the present study was to explore TCS-induced nephrotoxicity. Therefore, we establish a mouse model based on adult male mice to explore the effects of 10-week TCS exposure (50 mg/kg) on kidney. After mice were sacrificed, their blood, feces, and renal tissues were harvested for further analysis. We found that TCS treatment dramatically caused kidney structural damage, and increased blood urea nitrogen (BUN) and creatinine (Cr) expression levels, which indicated renal dysfunction. In addition, TCS exposure increased the malondialdehyde (MDA) and decreased superoxide dismutase (SOD) and total cholesterol (TCHO) expression levels, which indicated oxidative stress and lipid metabolism changes. The RNA sequencing (RNA-seq) of kidney tissue identified 221 differentially expressed genes (DEGs) enriched in 50 pathways, including drug metabolism-other enzymes, oxidative phosphorylation, glutathione metabolism, and inflammatory mediator regulation of TRP channels signaling pathways. The full-length 16S rRNA gene sequencing results showed that TCS exposure altered the community of gut microbiota, which was closely related to renal function damage. The above findings provide new insights into the mechanism of TCS-induced nephrotoxicity.