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INTRODUCTION: Exposure to endocrine disrupting chemicals (EDCs) can result in alterations of natural hormones in the body. The aim of this review article is to highlight the knowledge about EDCs and obesity. METHODS: A scoping review of the electronic literature was performed using PubMed platform for studies on EDCs and obesity published between the years 2013-2023. A total of 10 systematic reviews and meta-analysis studies met our inclusion criteria on more prominent EDCs focusing mainly on bisphenols, including parabens, triclosan, and phthalates, and their association with obesity. DESIGN: Scoping review. RESULTS: EDCs, mostly bisphenols and phthalates, are related to health effects, while there is less information on the impact of parabens and triclosan. A series of negative physiological effects involving obesogenic, diabetogenic, carcinogenic, and inflammatory mechanisms as well as epigenetic and microbiota modulations was related to a prolonged EDCs exposure. A more profound research of particular pollutants is required to illuminate the accelerating effects of particular EDCs, mixtures or their metabolites on the mechanism of the development of obesity. CONCLUSION: Considering the characteristics of EDCs and the heterogeneity of studies, it is necessary to design specific studies of effect tracking and, in particular, education about daily preventive exposure to EDCs for the preservation of long-term public health.
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Disruptores Endocrinos , Obesidad , Ácidos Ftálicos , Humanos , Disruptores Endocrinos/efectos adversos , Obesidad/prevención & control , Ácidos Ftálicos/efectos adversos , Exposición a Riesgos Ambientales/efectos adversos , Fenoles/efectos adversos , Parabenos/efectos adversos , Contaminantes Ambientales/efectos adversos , Contaminantes Ambientales/toxicidad , Triclosán/efectos adversos , Compuestos de Bencidrilo/efectos adversos , FemeninoRESUMEN
The use of disinfectants containing benzalkonium chloride (BAC) has become increasingly widespread in response to triclosan (TCS) restrictions and the COVID-19 pandemic, leading to the increasing presence of BAC in aquatic ecosystems. However, the potential environmental health impacts of BAC on fish remain poorly explored. In this study, we show that BAC and TCS can induce the gut dysbiosis in zebrafish (Danio rerio), with substantial effects on health. Breeding pairs of adult zebrafish were exposed to environmentally relevant concentrations of BAC and TCS (0.4-40 µg/L) for 42 days. Both BAC and TCS exposure perturbed the gut microbiota, triggering the classical NF-κB signaling pathway and resulting in downstream pathological toxicity associated with inflammatory responses, histological damage, inhibited ingestion, and decreased survival. These effects were dose-dependent and sex-specific, as female zebrafish were more susceptible than male zebrafish. Furthermore, we found that BAC induced toxicity to a greater extent than the restricted TCS at environmentally relevant concentrations, which is particularly concerning. Our results suggest that environmental exposure to antimicrobial chemicals can have ecological consequences by perturbing the gut microbiota, a previously underappreciated target of such chemicals. Rigorous ecological analysis should be conducted before widely introducing replacement antimicrobial compounds into disinfecting products.
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Compuestos de Benzalconio , Microbioma Gastrointestinal , Triclosán , Pez Cebra , Animales , Compuestos de Benzalconio/farmacología , Triclosán/toxicidad , Microbioma Gastrointestinal/efectos de los fármacos , Femenino , Masculino , Exposición a Riesgos Ambientales , Antiinfecciosos/farmacología , Antiinfecciosos/toxicidadRESUMEN
Triclosan (TCS), an antimicrobial agent extensively incorporated into pharmaceuticals and personal care products, poses significant environmental risks because of its persistence and ecotoxicity. So far, a few microorganisms were suggested to degrade TCS, but the microbial degradation mechanism remains elusive. Here, a two-component angular dioxygenase (TcsAaAb) responsible for the initial TCS degradation was characterized in Sphingomonas sp. strain YL-JM2C. Whole-cell biotransformation and crude enzyme assays demonstrated that TcsAaAb catalyzed the conversion of TCS to 4-chlorocatechol and 3,5-dichlorocatechol rather than the commonly suggested product 2,4-dichlorophenol. Then two intermediates were catabolized by tcsCDEF cluster via an ortho-cleavage pathway. Critical residues (N262, F279, and F391) for substrate binding were identified via molecular docking and mutagenesis. Further, TcsAaAb showed activity toward methyl triclosan and nitrofen, suggesting its versatile potential for bioremediation. In addition, TCS-degrading genes were also present in diverse bacterial genomes in wastewater, ocean and soil, and a relatively high gene abundance was observed in marine metagenomes, revealing the transformation fate of TCS in environments and the microbial potential in pollutant removal. These findings extend the understanding of the microbe-mediated TCS degradation and contribute to the mining of TCS-degrading strains and enzymes, as well as their application in the bioremediation of contaminated environments.
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Biodegradación Ambiental , Sphingomonas , Triclosán , Aguas Residuales , Triclosán/metabolismo , Sphingomonas/metabolismo , Sphingomonas/genética , Contaminantes Químicos del Agua/metabolismo , Simulación del Acoplamiento Molecular , Dioxigenasas/metabolismo , Dioxigenasas/genética , Proteínas Bacterianas/metabolismo , Proteínas Bacterianas/genética , Antiinfecciosos Locales/metabolismo , Eliminación de Residuos Líquidos/métodosRESUMEN
Aquatic ecosystems represent a prominent reservoir of xenobiotic compounds, including triclosan (TCS), a broad-spectrum biocide extensively used in pharmaceuticals and personal care products. As a biogeochemical hotspot, the potential of aquatic sediments for the degradation of TCS remains largely unexplored. Here, we demonstrated anaerobic biotransformation of TCS in a batch microcosm established with freshwater sediment. The initial 43.4 ± 2.2 µM TCS was completely dechlorinated to diclosan, followed by subsequent conversion to 5-chloro-2-phenoxyphenol, a monochlorinated TCS (MCS) congener. Analyses of community profile and population dynamics revealed substrate-specific, temporal-growth of Dehalococcoides and Dehalogenimonas, which are organohalide-respiring bacteria (OHRB) affiliated with class Dehalococcoidia. Dehalococcoides growth was linked to the formation of diclosan but not MCS, yielding 3.6 ± 0.4 × 107 cells per µmol chloride released. A significant increase in Dehalogenimonas cells, from 1.5 ± 0.4 × 104 to 1.5 ± 0.3 × 106 mL-1, only occurred during the reductive dechlorination of diclosan to MCS. Dehalococcoidia OHRB gradually disappeared following consecutive transfers, likely due to the removal of sediment materials with strong adsorption capacity that could alleviate TCS's antimicrobial toxicity. Consequently, a solid-free, functionally stable TCS-dechlorinating consortium was not obtained. Our results provide insights into the microbial determinants controlling the environmental fate of TCS.
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Sedimentos Geológicos , Microbiota , Triclosán , Sedimentos Geológicos/microbiología , Sedimentos Geológicos/química , Triclosán/metabolismo , Halogenación , Contaminantes Químicos del Agua/metabolismo , Biodegradación Ambiental , Chloroflexi/metabolismoRESUMEN
In the context of pandemic viruses and pathogenic bacteria, triclosan (TCS), as a typical antibacterial agent, is widely used around the world. However, the health risks from TCS increase with exposure, and it is widespread in environmental and human samples. Notably, environmental transformation and human metabolism could induce potentially undesirable risks to humans, rather than simple decontamination or detoxification. This review summarizes the environmental and human exposure to TCS covering from 2004 to 2023. Particularly, health impacts from the environmental and metabolic transformation of TCS are emphasized. Environmental transformations aimed at decontamination are recognized to form carcinogenic products such as dioxins, and ultraviolet light and excessive active chlorine can promote the formation of these dioxin congeners, potentially threatening environmental and human health. Although TCS can be rapidly metabolized for detoxification, these processes can induce the formation of lipophilic ether metabolic analogs via cytochrome P450 catalysis, causing possible adverse cross-talk reactions in human metabolic disorders. Accordingly, TCS may be more harmful in environmental transformation and human metabolism. In particular, TCS can stimulate the transmission of antibiotic resistance even at trace levels, threatening public health. Considering these accruing epidemiological and toxicological studies indicating the multiple adverse health outcomes of TCS, we call on environmental toxicologists to pay more attention to the toxicity evolution of TCS during environmental transformation and human metabolism.
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Triclosán , Triclosán/metabolismo , Triclosán/toxicidad , Humanos , Exposición a Riesgos Ambientales , Contaminantes Ambientales/metabolismo , Contaminantes Ambientales/toxicidad , Antiinfecciosos Locales/metabolismo , Antiinfecciosos Locales/toxicidad , PandemiasRESUMEN
The ubiquitous presence of the disinfectant triclosan (TCS) has raised global concerns regarding its potential threat to aquatic organisms. However, the effects of TCS on lipid metabolism in fish and its underlying mechanisms remain unclear. This study investigated the effect of environmentally relevant levels of TCS on the lipid metabolism in the cyprinid fish Squalidus argentatus. Our results showed that the lipid metabolism in the cyprinid fish S. argentatus was perturbed by 28-day exposure to TCS, as evidenced by higher levels of lipid accumulation in both the liver and blood. To elucidate the mechanisms underlying toxicity, we evaluated oxidative stress, inflammatory status, and lipase activity in the liver. Our findings indicated increased ROS-specific fluorescence intensity, superoxide dismutase (SOD) activity, and malondialdehyde (MDA) content in the livers of S. argentatus exposed to TCS, suggesting oxidative damage. Additionally, TCS treatment induced the production of proinflammatory cytokines in the liver of S. argentatus exposed to TCS, which suppressed hepatic lipase activity. Intestinal tissue morphology, inflammation, and blood lipopolysaccharide (LPS) levels were also examined. Significant increases in goblet cell count and MDA levels were observed in the intestinal tract. After 28 days of TCS exposure, the serum LPS levels were significantly elevated. 16S rRNA sequencing was conducted to analyze the effects of TCS on the diversity and composition of the intestinal microbiota. Transcriptomic analysis was performed to reveal global molecular alterations following TCS exposure. In conclusion, our results indicate that TCS may disrupt the lipid metabolism in S. argentatus by (i) inducing hepatic oxidative stress and inflammation, which suppress lipoprotein lipase activity, (ii) affecting the production of beneficial metabolites and endotoxins by dysregulating gut microbiota composition, and (iii) altering the expression levels of lipid metabolism-related pathways.
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Cyprinidae , Metabolismo de los Lípidos , Triclosán , Contaminantes Químicos del Agua , Animales , Triclosán/toxicidad , Metabolismo de los Lípidos/efectos de los fármacos , Contaminantes Químicos del Agua/toxicidad , Cyprinidae/fisiología , Cyprinidae/metabolismo , Estrés Oxidativo/efectos de los fármacos , Hígado/efectos de los fármacos , Hígado/metabolismo , Microbioma Gastrointestinal/efectos de los fármacosRESUMEN
Prophages are prevalent among bacterial species, including strains carrying antibiotic resistance genes (ARGs). Prophage induction can be triggered by the SOS response to stressors, leading to cell lysis. In environments polluted by chemical stressors, ARGs and prophage co-harboring strains might pose an unknown risk of spreading ARGs through chemical pollutant-mediated prophage induction and subsequent cell lysis. In this study, we investigated the effects of common non-antibiotic water pollutants, triclosan and silver nanoparticles, on triggering prophage induction in clinical isolates carrying ARGs and the subsequent uptake of released ARGs by the naturally competent bacterium Acinetobacter baylyi. Our results demonstrate that both triclosan and silver nanoparticles, at environmentally relevant concentrations and those found in commercial products, significantly enhance prophage induction among various clinical isolates. Transmission electron microscopy imaging and plaque assays confirmed the production of infectious phage particles under non-antibiotic pollutants-mediated prophage induction. In addition, the rate of ARG transformation to A. baylyi significantly increased after the release of extracellular ARGs from prophage induction-mediated cell lysis. The mechanism of non-antibiotic pollutants-mediated prophage induction is primarily associated with excessive oxidative stress, which provokes the SOS response. Our findings offer insights into the role of non-antibiotic pollutants in promoting the dissemination of ARGs by triggering prophage induction.
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Profagos , Profagos/genética , Acinetobacter/efectos de los fármacos , Acinetobacter/genética , Farmacorresistencia Microbiana/genética , Triclosán/farmacología , Farmacorresistencia Bacteriana/genética , Antibacterianos/farmacología , Nanopartículas del Metal , Plata/farmacologíaRESUMEN
Previous studies reported that hemoprotein CYP450 catalyzed triclosan coupling is an "uncommon" metabolic pathway that may enhance toxicity, raising concerns about its environmental and health impacts. Hemoglobin, a notable hemoprotein, can catalyze endogenous phenolic amino acid tyrosine coupling reactions. Our study explored the feasibility of these coupling reactions for exogenous phenolic pollutants in plasma. Both hemoglobin and hemin were found to catalyze triclosan coupling in the presence of H2O2. This resulted in the formation of five diTCS-2â¯H, two diTCS-Cl-3â¯H, and twelve triTCS-4â¯H in phosphate buffer, with a total of nineteen triclosan coupling products monitored using LC-QTOF. In plasma, five diTCS-2â¯H, two diTCS-Cl-3â¯H, and two triTCS-4â¯H were detected in hemoglobin-catalyzed reactions. Hemin showed a weaker catalytic effect on triclosan transformation compared to hemoglobin, likely due to hemin dimerization and oxidative degradation by H2O2, which limits its catalytic efficiency. Triclosan transformation in the human plasma-like medium still occurs with high H2O2, despite the presence of antioxidant proteins that typically inhibit such transformations. In plasma, free H2O2 was depleted within 40â¯minutes when 800⯵M H2O2 was added, suggesting a rapid consumption of H2O2 in these reactions. Antioxidative species, or hemoglobin/hemin scavengers such as bovine serum albumin, may inhibit but not completely terminate the triclosan coupling reactions. Previous studies reported that diTCS-2â¯H showed higher hydrophobicity and greater endocrine-disrupting effects compared to triclosan, which further underscores the potential health risks. This study indicates that hemoglobin and heme in human plasma might significantly contribute to phenolic coupling reactions, potentially increasing health risks.
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Hemina , Hemoglobinas , Peróxido de Hidrógeno , Oxidación-Reducción , Triclosán , Triclosán/toxicidad , Hemoglobinas/química , Humanos , Peróxido de Hidrógeno/química , Catálisis , Contaminantes Ambientales , FenolesRESUMEN
In recent years, exposure to triclosan (TCS) has been linked to an increase in psychiatric disorders. Nonetheless, the precise mechanisms of this occurrence remain elusive. Therefore, this study developed a long-life TCS-exposed rat model, an SH-SY5Y cell model, and an atomoxetine hydrochloride (ATX) treatment model to explore and validate the neurobehavioral mechanisms of TCS from multiple perspectives. In the long-life TCS-exposed model, pregnant rats received either 0â¯mg/kg (control) or 50â¯mg/kg TCS by oral gavage throughout pregnancy, lactation, and weaning of their offspring (up to 8 weeks old). In the ATX treatment model, weanling rats received daily injections of either 0â¯mg/kg (control) or 3â¯mg/kg ATX via intraperitoneal injection until they reached 8 weeks old. Unlike the TCS model, ATX exposure only occurred after the pups were weaned. The results indicated that long-life TCS exposure led to attention-deficit hyperactivity disorder (ADHD)-like behaviors in male offspring rats accompanied by dopamine-related mRNA and protein expression imbalances in the prefrontal cortex (PFC). Moreover, in vitro experiments also confirmed these findings. Mechanistically, TCS reduced dopamine (DA) synthesis, release, and transmission, and increased reuptake in PFC, thereby reducing synaptic gap DA levels and causing dopaminergic deficits. Additional experiments revealed that increased DA concentration in PFC by ATX effectively alleviated TCS-induced ADHD-like behavior in male offspring rats. These findings suggest that long-life TCS exposure causes ADHD-like behavior in male offspring rats through dopaminergic deficits. Furthermore, ATX treatment not only reduce symptoms in the rats, but also reveals valuable insights into the neurotoxic mechanisms induced by TCS.
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Trastorno por Déficit de Atención con Hiperactividad , Dopamina , Corteza Prefrontal , Efectos Tardíos de la Exposición Prenatal , Triclosán , Animales , Triclosán/toxicidad , Corteza Prefrontal/efectos de los fármacos , Corteza Prefrontal/metabolismo , Trastorno por Déficit de Atención con Hiperactividad/inducido químicamente , Femenino , Ratas , Embarazo , Masculino , Efectos Tardíos de la Exposición Prenatal/inducido químicamente , Dopamina/metabolismo , Ratas Sprague-Dawley , Conducta Animal/efectos de los fármacos , Clorhidrato de Atomoxetina , HumanosRESUMEN
The thyroid gland, a vital component of the endocrine system, plays a pivotal role in regulating metabolic processes, growth, and development. To better characterize thyroid system disrupting chemicals (TSDC), we followed the next-generation risk assessment approach, which further considers the mechanistic profile of xenobiotics. We combined targeted in vitro testing with untargeted metabolomics. Four known TSDC, propyl-thiouracil (PTU), sodium perchlorate, triclosan, and 5-pregnen-3ß-ol-20-one-16αcarbonitrile (PCN) were investigated using rat in vitro models, including primary hepatocytes, PCCL3 cells, thyroid microsomes, and three-dimensional thyroid follicles. We confirmed each compound's mode of action, PTU inhibited thyroperoxidase activity and thyroid hormones secretion in thyroid cells model, sodium perchlorate induced a NIS-mediated iodide uptake decrease as triclosan to a lesser extent, and PCN activated expression and activity of hepatic enzymes (CYPs and UGTs) involved in thyroid hormones metabolism. In parallel, we characterized intracellular metabolites of interest. We identified disrupted basal metabolic pathways, but also metabolites directly linked to the compound's mode of action as tyrosine derivates for sodium perchlorate and triclosan, bile acids involved in beta-oxidation, and precursors of cytochrome P450 synthesis for PCN. This pilot study has provided metabolomic fingerprinting of dedicated TSDC exposures, which could be used to screen and differentiate specific modes of action.
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Disruptores Endocrinos , Metabolómica , Propiltiouracilo , Glándula Tiroides , Triclosán , Animales , Glándula Tiroides/efectos de los fármacos , Glándula Tiroides/metabolismo , Disruptores Endocrinos/toxicidad , Propiltiouracilo/toxicidad , Propiltiouracilo/farmacología , Triclosán/toxicidad , Hepatocitos/efectos de los fármacos , Hepatocitos/metabolismo , Hormonas Tiroideas/metabolismo , Percloratos/toxicidad , Células Cultivadas , Masculino , Ratas , Línea Celular , Microsomas/metabolismo , Microsomas/efectos de los fármacos , Ratas Sprague-DawleyRESUMEN
Microplastics (MPLs) are contaminants of emerging concern (CECs) ubiquitous in aquatic environments, which can be bioaccumulated along the food chain. In this study, the accumulation of polyethylene (PE), polystyrene (PS) and polyethylene terephthalate (PET) microplastics (MPLs) of sizes below 63 µm was assessed in Mediterranean mussels (Mytilus galloprovincialis spp). Moreover, the potential of mussels to uptake and bioaccumulate other organic contaminants, such as triclosan (TCS) and per- and polyfluoroalkyl substances (PFASs), was evaluated with and without the presence of MPLs. Then, the modulation of MPLs in the human bioaccessibility of co-contaminants was assessed by in vitro assays that simulated the human digestion process. Exposure experiments were carried out in 15 L marine microcosms. The bioaccumulation and bioaccessibility of PE, PS, PET, and co-contaminants were assessed by means of liquid chromatography -size exclusion chromatography-coupled to high-resolution mass spectrometry (LC(SEC)-HRMS). Our outcomes confirm that MPL bioaccumulation in filter-feeding organisms is a function of MPL chemical composition and particle sizes. Finally, despite the lower accumulation and bioaccumulation of PFASs in the presence of MPLs, the bioaccessibility assays revealed that PFASs bioaccessibility was favoured in the presence of MPLs. Since part of the bioaccumulated PFASs are adsorbed onto MPL surfaces by hydrophobic and electrostatic interactions, these interactions easily change with the pH during digestion, and the PFASs bioaccessibility increases.
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Bioacumulación , Microplásticos , Mytilus , Contaminantes Químicos del Agua , Animales , Microplásticos/metabolismo , Contaminantes Químicos del Agua/metabolismo , Contaminantes Químicos del Agua/análisis , Mytilus/metabolismo , Polietileno/química , Polietileno/metabolismo , Poliestirenos/química , Tereftalatos Polietilenos/química , Tereftalatos Polietilenos/metabolismo , Humanos , Bivalvos/metabolismo , Triclosán/metabolismo , Cadena Alimentaria , Monitoreo del AmbienteRESUMEN
Endocrine-disrupting chemicals (EDCs) are pervasive in the environment, prompting significant public concern regarding human exposure to these pollutants. In this study, we analyzed the levels of various endocrine-disrupting compounds, including parabens (PBs), benzophenones (BzPs), triclocarban (TCC) and triclosan (TCS), across 565 urine samples collected from residents of South China. All 11 target chemicals were detected at relatively high frequencies (41-100%), with the most prevalent ones being 3,4-dihydroxybenzoic acid (5.39 ng/mL), methyl-paraben (5.12 ng/mL), ethyl-paraben (3.11 ng/mL) and triclosan (0.978 ng/mL). PBs emerged as the most predominant group with a median concentration of 32.2 ng/mL, followed by TCs (sum of TCC and TCS, 0.998 ng/mL) and BzPs (0.211 ng/mL). Notably, urinary concentrations of PBs in adults were significantly higher (p < 0.01) compared to children, while BzPs and TCs were elevated in children (p < 0.001). The increased presence of BzPs and TCs in children is a cause for concern, given their heightened sensitivity and vulnerability to chemicals. Significant correlations were found between urinary target compounds and demographic factors, including gender, age and body mass index. Specifically, females, younger adults (18 ≤ age ≤ 35) and individuals with under/normal weight (16 ≤ BMI ≤ 23.9) were found to have higher exposure levels to EDCs, as indicated by the median values of their estimated daily intakes. Despite these higher levels still being lower than the acceptable daily intake thresholds, the health risks stemming from simultaneous exposure to these EDCs must not be overlooked.
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Benzofenonas , Carbanilidas , Disruptores Endocrinos , Exposición a Riesgos Ambientales , Contaminantes Ambientales , Parabenos , Triclosán , Humanos , Carbanilidas/orina , Parabenos/análisis , Triclosán/orina , Niño , China , Benzofenonas/orina , Adulto , Femenino , Masculino , Disruptores Endocrinos/orina , Contaminantes Ambientales/orina , Exposición a Riesgos Ambientales/estadística & datos numéricos , Exposición a Riesgos Ambientales/análisis , Adulto Joven , Adolescente , Persona de Mediana Edad , PreescolarRESUMEN
The emerging contaminant triclosan (TCS) is widely distributed both in surface water and in wastewater and poses a threat to aquatic organisms and human health due to its resistance to degradation. The dioxygenase enzyme TcsAB has been speculated to perform the initial degradation of TCS, but its precise catalytic mechanism remains unclear. In this study, the function of TcsAB was elucidated using multiple biochemical and molecular biology methods. Escherichia coli BL21(DE3) heterologously expressing tcsAB from Sphingomonas sp. RD1 converted TCS to 2,4-dichlorophenol. TcsAB belongs to the group IA family of two-component Rieske nonheme iron ring-hydroxylating dioxygenases. The highest amino acid identity of TcsA and the large subunits of other dioxygenases in the same family was only 35.50%, indicating that TcsAB is a novel dioxygenase. Mutagenesis of residues near the substrate binding pocket decreased the TCS-degrading activity and narrowed the substrate spectrum, except for the TcsAF343A mutant. A meta-analysis of 1492 samples from wastewater treatment systems worldwide revealed that tcsA genes are widely distributed. This study is the first to report that the TCS-specific dioxygenase TcsAB is responsible for the initial degradation of TCS. Studying the microbial degradation mechanism of TCS is crucial for removing this pollutant from the environment.
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Dioxigenasas , Triclosán , Triclosán/metabolismo , Dioxigenasas/metabolismo , Dioxigenasas/genética , Biodegradación Ambiental , Escherichia coli , Sphingomonas/enzimología , Sphingomonas/metabolismo , Contaminantes Químicos del Agua/metabolismoRESUMEN
The toxicity of triclosan (TCS) to various aquatic organisms has been demonstrated at environmental concentrations. However, the effects and mechanisms of TCS on toxic cyanobacteria remains largely unexplored. This study investigated the physiological and molecular variations in two representative toxic Microcystis species (M. aeruginosa and M. viridis) under exposure to TCS for 12 d. Our findings demonstrated that the median effective concentration (EC50) of TCS for both Microcystis species were close to the levels detected in the environment (M. aeruginosa: 9.62 µg L-1; M. viridis: 27.56 µg L-1). An increased level of reactive oxygen species (ROS) was observed in Microcystis, resulting in oxidative damage when exposed to TCS at concentrations ranging from 10 µg L-1 to 50 µg L-1. The photosynthetic activity of Microcystis had a certain degree of recovery capability at low concentrations of TCS. Compared to M. aeruginosa, the higher recovery capability of the photosynthetic system in M. viridis would be mainly attributed to the increased ability for PSII repair and phycobilisome synthesis. Additionally, the synthesis of microcystins in the two species and the release rate in M. viridis significantly increased under 10-50 µg L-1 TCS. At the molecular level, exposure to TCS at EC50 for 12 d induced the dysregulation of genes associated with photosynthesis and antioxidant system. The upregulation of genes associated with microcystin synthesis and nitrogen metabolism further increased the potential risk of microcystin release. Our results revealed the aquatic toxicity and secondary ecological risks of TCS at environmental concentrations, and provided theoretical data with practical reference value for TCS monitoring.
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Microcistinas , Microcystis , Fotosíntesis , Especies Reactivas de Oxígeno , Transcriptoma , Triclosán , Contaminantes Químicos del Agua , Microcystis/efectos de los fármacos , Microcystis/genética , Microcystis/metabolismo , Triclosán/toxicidad , Fotosíntesis/efectos de los fármacos , Transcriptoma/efectos de los fármacos , Contaminantes Químicos del Agua/toxicidad , Especies Reactivas de Oxígeno/metabolismo , Microcistinas/toxicidad , Estrés Oxidativo/efectos de los fármacosRESUMEN
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.
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Astrocitos , Progesterona , Sirtuina 1 , Sirtuina 3 , Triclosán , Animales , Astrocitos/metabolismo , Astrocitos/efectos de los fármacos , Triclosán/farmacología , Ratones , Células Cultivadas , Progesterona/metabolismo , Sirtuina 1/metabolismo , Sirtuina 1/genética , Sirtuina 3/metabolismo , Sirtuina 3/genética , PPAR gamma/metabolismo , PPAR gamma/genética , Estradiol/farmacología , Estradiol/metabolismo , Testosterona/metabolismo , Esteroide 17-alfa-Hidroxilasa/metabolismo , Esteroide 17-alfa-Hidroxilasa/genética , Disruptores Endocrinos/farmacología , Compuestos de Bifenilo/farmacología , Rosiglitazona/farmacologíaRESUMEN
Low activation performance is a critical issue limiting the practical application of low-cost biochar in the advanced oxidation. Given the high potential of transition metals in the persulfate activation process and abundant oxygen-containing groups of hydrochar, hydrochar derived from cobalt (Co)-modified iron (Fe)-enriched sludge was synthesized and its performance and activation mechanism for the degradation of triclosan were investigated. Co modification significantly altered the morphology of hydrochar, and the increased Co-Fe mass ratios transformed hydrochar from granular to rose-shaped lamellar and then to helical sheet structures. Specific surface area, defect degree, and oxygen-containing groups of hydrochar increased with increasing cobalt-iron mass ratios. The highest removal of triclosan was up to 98% in the hydrochar/peroxymonosulfate (PMS) system under a wide range of pHs (3-10) and still remained higher than 90% after four cycles. Both Radical (mainly hydroxyl radical) and nonradical pathways (singlet oxygen and electron transfer) were evidenced to play roles in the triclosan removal. Fe3+ promoted the regeneration of Co2+ and realized the efficient circulation of Co3+/Co2+. A ternary system consisting of electron donor (triclosan)-electron mediator (hydrochar)-electron acceptor (PMS) provided channels for electron transfer. No measurable Co and Fe were released during the reaction, and the toxicity of degradation intermediates was lower than that of triclosan. Beside triclosan, rhodamine B, bisphenol A, sulfamethoxazole, and phenol were also almost degraded completely in this oxidation system. This study provides a promising way for the enhancement of catalytic activity of carbonaceous material.
Asunto(s)
Cobalto , Hierro , Triclosán , Contaminantes Químicos del Agua , Triclosán/química , Cobalto/química , Hierro/química , Contaminantes Químicos del Agua/química , Carbón Orgánico/química , Oxidación-Reducción , Eliminación de Residuos Líquidos/métodos , PeróxidosRESUMEN
BACKGROUND: Triclosan (TCS), as an endocrine disrupter, has been found to affect male fertility. However, the potential molecular mechanism is still unknown. We aimed to investigate whether the toxic effects of TCS on spermatocyte cells was mediated by the regulation of microRNA-20a-5â¯P on PTEN. METHODS: GC-2 and TM4 cells were treated with TCS (0.5-80⯵M) for 24 or 48â¯hours. Effect of TCS on proliferation of GC-2 and TM4 cells was detected using a cell counting kit-8 (CCK8) assay. Expression of miR-17 family and autophagy genes were detected. The interaction between miR-20a-5â¯P and PTEN was determined by a dual-luciferase reporter assay. RESULTS: TCS decreased cell proliferation of GC-2 and TM4 cells. Expression of autophagy-related genes and miR-17 family was altered by TCS. PTEN expression was significantly increased, whereas the expression of miR-20a-5â¯P was significantly decreased in GC-2 and TM4 cells. As predicted in relevant databases, there is a binding site of miR-20a-5â¯P in PTEN. The expression of PTEN was significantly down-regulated by the miR-20a-5â¯P mimic. CONCLUSION: As a downstream target of miR-20a-5â¯P, PTEN functioned in the autophagy process of which TCS inhibited the proliferation of spermatocyte cells. Our results provided new ideas for revealing the molecular mechanism and protective strategy on male infertility.
Asunto(s)
Autofagia , Proliferación Celular , MicroARNs , Fosfohidrolasa PTEN , Espermatocitos , Triclosán , MicroARNs/genética , MicroARNs/metabolismo , Masculino , Fosfohidrolasa PTEN/genética , Fosfohidrolasa PTEN/metabolismo , Autofagia/efectos de los fármacos , Proliferación Celular/efectos de los fármacos , Línea Celular , Triclosán/toxicidad , Humanos , Espermatocitos/efectos de los fármacos , Disruptores Endocrinos/toxicidad , AnimalesRESUMEN
Microplastics (MPs) are commonly found with hydrophobic contaminants in the water column and pose a serious threat to aquatic organisms. The effects of polystyrene microplastics of different particle sizes on the accumulation of triclosan in the gut of Xenopus tropicalis, its toxic effects, and the transmission of resistance genes were evaluated. The results showed that co-exposure to polystyrene (PS-MPs) adsorbed with triclosan (TCS) caused the accumulation of triclosan in the intestine with the following accumulation capacity: TCS + 5 µm PS group > TCS group > TCS + 20 µm PS group > TCS + 0.1 µm PS group. All experimental groups showed increased intestinal inflammation and antioxidant enzyme activity after 28 days of exposure to PS-MPs and TCS of different particle sizes. The TCS + 20 µm PS group exhibited the highest upregulated expression of pro-inflammatory factors (IL-10, IL-1ß). The TCS + 20 µm group showed the highest increase in enzyme activity compared to the control group. PS-MPs and TCS, either alone or together, altered the composition of the intestinal microbial community. In addition, the presence of more antibiotic resistance genes than triclosan resistance genes significantly increased the expression of tetracycline resistance and sulfonamide resistance genes, which may be associated with the development of intestinal inflammation and oxidative stress. This study refines the aquatic ecotoxicity assessment of TCS adsorbed by MPs and provides informative information for the management and control of microplastics and non-antibiotic bacterial inhibitors.
Asunto(s)
Microplásticos , Tamaño de la Partícula , Poliestirenos , Triclosán , Contaminantes Químicos del Agua , Xenopus , Animales , Triclosán/toxicidad , Poliestirenos/toxicidad , Contaminantes Químicos del Agua/toxicidad , Microplásticos/toxicidad , Intestinos/efectos de los fármacos , Adsorción , Expresión Génica/efectos de los fármacosRESUMEN
Triclosan (TCS), an antibacterial biocide, pervades water and sediment matrices globally, posing a threat to aquatic life. In densely populated cities like Mumbai, rivers and coastal bodies demand baseline TCS data for ecotoxicological assessment due to the excessive use of personal care products comprising TCS. This pioneering study compares spatiotemporal TCS variations and risks in freshwater and marine ecosystems employing multivariate analysis of physicochemical parameters. Over five months (January to May 2022), Mithi River exhibited higher TCS concentrations (water: 1.68 µg/L, sediment: 3.19 µg/kg) than Versova Creek (water: 0.49 µg/L, sediment: 0.69 µg/kg). Principal component analysis revealed positive correlations between TCS and physicochemical parameters. High-risk quotients (>1) underscore TCS threats in both water bodies. This study furnishes crucial baseline data, emphasizing the need for effective treatment plans for TCS in effluent waters released into the adjacent aquatic systems.
Asunto(s)
Ecosistema , Monitoreo del Ambiente , Estuarios , Ríos , Triclosán , Contaminantes Químicos del Agua , Triclosán/análisis , Contaminantes Químicos del Agua/análisis , Medición de Riesgo , Ríos/química , Ecotoxicología , Sedimentos Geológicos/químicaRESUMEN
Triclosan (TCS), triclocarban (TCC), and chlorophenols (CPs) are broad-spectrum antibacterials widely used in dermatological and oral hygiene products, which could induce severe liver and intestine injuries. Hence, it is essential to establish a rapid and sensitive method to monitor TCS, TCC, and CPs in various organisms. In this work, fluorine-functionalized covalent organic framework (COF-F) was prepared by using 4,4',4''-(1,3,5-triazine-2,4,6-triyl)tri-aniline and 2,3,5,6-tetrafluoroterephthalaldehyde as two building units and employed as a solid phase microextraction (SPME) probe for the extraction of TCS, TCC and CPs. The COF-F possessed excellent hydrophobicity, a large specific surface area (1354.3 m2 g-1) and high uniform porosity (3.2 nm), which facilitated high selectivity and adsorption properties towards TCS, TCC, and CPs. Therefore, the as-prepared COF-F-SPME in combination with electrospray ionization mass spectrometry has been developed to provide fast and ultrasensitive detection of TCS, TCC, and CPs in biological samples. The established method demonstrated satisfactory linear ranges (0.01-100.00 µg L-1) and low limits of detection (0.003-0.040 µg L-1) for TCS, TCC and CPs. The developed method could be successfully applied to detect TCS, TCC and CPs in the liver and kidney tissues of mice, demonstrating the potential for the detection of chlorinated aromatic pollutants in the biological samples.