Exposure Of Triclosan Research Articles

Gut microbiome as biomarker for triclosan toxicity in Labeo rohita: bioconcentration, immunotoxicity and metagenomic profiling.

Triclosan (TCS) is a lipophilic, broad spectrum antimicrobial agent commonly used in personal care products with a projected continuous escalation in aquatic environments in the post COVID 19 era. There is rich documentation in the literature on the alteration of physiological responses in fish due to TCS exposure; however, studies on gut associated bacteria of fish are still scarce. This is the first attempt to determine changes in bacterial community structure due to exposure of TCS on Labeo rohita, a commercially essential freshwater species, using 16S V3-V4 region ribosomal RNA (rRNA) next-generation sequencing (NGS). Chronic exposure of TCS at environmentally realistic concentrations viz. 1/5th (T1: 0.129 mg/L) and 1/10th (T2: 0.065 mg/L) of LC50 for 28 days resulted in the dose dependent bioconcentration of TCS in the fish gut. Prolonged exposure to TCS leads to disruption of gut bacteria evidenced by down regulation of the host immune system. Additionally, high-throughput sequencing analysis showed alternation in the abundance and diversity of microbial communities in the gut, signifying Proteobacteria and Verrucomicrobia as dominant phyla. Significant changes were also observed in the relative abundance of Chloroflexi and Gammatimonadetes phyla in TCS exposed groups. The study revealed that gut microbiome can be used as a biomarker in assessing the degree of TCS toxicity in commercially important fish species.

Exposure pattern of triclosan and tetracycline change their impacts on methanogenic digestion microbiomes

Triclosan (TCS) and tetracycline (TC) as common antibacterial agents are frequently detected in the influent of wastewater treatment plants. The TCS and TC exposure patterns may determine their impacts on wastewater treatment microbiomes, on which information remains unknown. In this study, the impacts of sequential exposure of TCS and TC on methanogenic digestion microbiomes in upflow anaerobic sludge blanket (UASB) reactors were analyzed and compared with that of the same microbiomes being simultaneously exposed to TCS and TC. Results indicated that the UASB reactor 2 (MD2) with sequential TCS-TC exposure consistently demonstrated higher chemical oxygen demand (COD) removal efficiency (94.7 %). In contrast, in the MD1 reactor, COD removal efficiency decreased from 94.4 % to 82.7 % upon simultaneous exposure to TCS and TC. Accordingly, a 1.8 times higher enrichment of total antibiotic resistance genes (ARGs) was observed in MD1 relative to MD2. Using a dissimilarity-overlap approach, the MD2 microbiome with sequential exposure was predominantly mediated by deterministic factors in their community assembly (largely contributed by abundant and intermediate biospheres), resulting in microbial interaction networks with higher average clustering coefficients and shorter average path lengths, compared to the MD1 microbiomes. Our results could support sustainable management of TCS and TC contamination in wastewater treatment plants.

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 β-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.

Chronic triclosan exposure induce impaired glucose tolerance by altering the gut microbiota

Triclosan (TCS) is an antimicrobial compound incorporated into more than 2000 consumer products. This compound is frequently detected in the human body and causes ubiquitous contamination in the environment, thereby raising concerns about its impact on human health and environmental pollution. Here, we demonstrated that 20 weeks’ exposure of TCS drove the development of glucose intolerance by inducing compositional and functional alterations in intestinal microbiota in rats. Fecal-transplantation experiments corroborated the involvement of gut microbiota in TCS-induced glucose-tolerance impairment. 16S rRNA gene-sequencing analysis of cecal contents showed that TCS disrupted the gut microbiota composition in rats and increased the ratio of Firmicutes to Bacteroidetes. Cecal metabolomic analyses detected that TCS altered host metabolic pathways that are linked to host glucose and amino acid metabolism, particularly branched-chain amino acid (BCAA) biosynthesis. BCAA measurement confirmed the increase in serum BCAAs in rats exposed to TCS. Western blot and immunostaining results further confirmed that elevated BCAAs stimulated mTOR, a nutrient-sensing complex, and following IRS-1 serine phosphorylation, resulted in insulin resistance and glucose intolerance. These results suggested that TCS may induce glucose metabolism imbalance by regulating BCAA concentration by remodeling the gut microbiota.

Effects of prepubertal to peripubertal exposure of triclosan on the reproductive health of the young male laboratory mice

Over the last few decades, a massive increase in environmental toxicants has played a significant role in causing hindrance in the process of sexual maturity, leading to impaired reproductive health. Several toxicants are existing in the environment because of rapid industrialization, agricultural activities, and urbanization that act as endocrine disrupting chemicals (EDCs). Triclosan (TCS; 2,4,4’-trichloro-2’-hydroxydiphenyl ether) is one of the EDCs, acts as an antimicrobial chemical, and is used widely in personal care products and several commercial preparations as preservatives. It is found to interfere with normal reproduction and sexual maturity. The present study is therefore, aimed to investigate the impact of prepubertal to peripubertal exposure of TCS (300 and 600 mg/kg BW/day from PND 22 to PND 63) to observe the age of the onset of puberty, weights of the reproductive organs, alterations in the levels of testicular cholesterol, serum testosterone, and histopathology of the testis in the young laboratory mice. TCS exposure caused a significant delay in the age of prepuce separation, an indicator of the onset of puberty. Its exposure from PND 22 to PND 63 resulted in significant reductions in the weights of the testis, epididymis, and seminal vesicle, levels of testicular cholesterol, and serum testosterone in the young mice at PND 64. Testicular histology of such mice also showed regressive changes in the seminiferous tubules, indicating the interference of TCS in the process of spermatogenesis. The findings of the present study, therefore, reveal that TCS delays the age of onset of puberty and interferes with the endocrine functions of the testis.

Biomolecular alterations in the early life stages of four food fish following acute exposure of Triclosan

We investigated the effect of acute concentrations of triclosan (TCS; 96 h exposure and 10d post exposure) on the free amino acid, primary (SDS-PAGE) and secondary (FT-IR) structure of proteins in the embryos/larvae of Cyprinus carpio, Ctenopharyngodon idella, Labeo rohita and Cirrhinus mrigala. A concentration dependent increase in free amino acids, upregulation of polypeptides (100 and 70 kDa in C. carpio, C. idella and L. rohita, 55, 45, 36 kda in C. idella and L. rohita and 22 kDa in all the fish) and a decline in percent area of all the selected peaks of the FT-IR spectra was observed after exposure and recovery period. The decline in percent area was greatest for L. rohita at peak 1080 – 1088 cm−1 (−75.99%) after exposure and at peak 2854 – 2855 cm−1 (−53.59%) after recovery. Curve fitting analysis revealed a decrease in α-helices and increase in β-sheets in all fish after exposure and recovery period. The results suggest that TCS elicits alterations in biomolecules of fish embryos.

Acute Toxicity and DNA Instability Induced by Exposure to Low Doses of Triclosan and Phthalate DEHP, and Their Combinations, in vitro.

Triclosan (TCS) is an antimicrobial agent widely used in personal care products (PCP) and the di-(2-ethyl hydroxy-phthalate) (DEHP) is a chemical compound derived from phthalic acid, used in medical devices and plastic products with polyvinyl chloride (PVCs). As result of their extensive use, TCS and DEHP have been found in the environment and previous studies demonstrated the association between their exposure and toxic effects, mostly in aquatic organisms, but there is a shortage in the literature concerning the exposure of TCS and DEHP in human cells. The aim of the present study was to assess the impact of exposure to TCS and DEHP, as well as their combinations, on biomarkers related to acute toxicity and DNA instability, in HepG2 cells, by use of cytokinesis-block micronucleus cytome (CBMNCyt) assay. For that, the cultures were exposed to TCS, DEHP and combinations at doses of 0.10, 1.0, and 10 μM for the period of 4 h and the parameters related to DNA damage (i.e., frequencies of micronuclei (MN) and nuclear buds (NBUDs), to cell division (i.e., nuclear division index (NDI) and nuclear division cytotoxic index (NDCI) and to cell death (apoptotic and necrotic cells) were scored. Clear mutagenic effects were seen in cells treated with TCS, DEHP at doses of 1.0 and 10 μM, but no combined effects were observed when the cells were exposed to the combinations of TCS + DEHP. On the other hand, the combination of the toxicants significantly increased the frequencies of apoptotic and necrotic cells, as well as induced alterations of biomarkers related to cell viability (NDI and NDCI), when compared to the groups treated only with TCS or DEHP. Taken together, the results showed that TCS and DEHP are also able to induce acute toxicity and DNA damage in human cells.

Triclosan-induced abnormal expression of miR-30b regulates fto-mediated m6A methylation level to cause lipid metabolism disorder in zebrafish

Chronic exposure of triclosan (TCS) to zebrafish triggers high incidence of fatty liver and hepatitis; however, the underlying molecular mechanisms remain unclear. Herein, we identified miR-30b as a sensitive biomarker to TCS stress, reflecting in that its decreased expression caused metabolic toxicity, abnormal development and behavior, and lipid-metabolism disorder. By microinjecting the inhibitor and mimic experiments, miR-30b was proved to regulate lipid metabolism by its main target gene fto. Over-expression of FTO resulted in fat accumulation, elevation of the TG and TC levels and up-regulation of the PPARγ and CEBPα, as well as decrease of the global m6A level in larvae. On the contrary, the knock-down of FTO using MO caused the anti-lipogenic effect, decrease of the TG and T-CHO levels, and abnormal changes of cebpɑ, acsl5, fasn, ppap2c and pparγ etc. Further fortification tests of cycloleucine and betaine evidenced that the toxic effect was strongly dependent on regulation of the m6A level. The toxicity effects in the treatments of methylated donors and receptors were consistent with the changes in physiological functions of FTO knockdown and overexpression. The effects of cycloleucine on m6A level and lipid metabolism generally consisted with those of FTO, but this was not the case for betaine, reflecting in increased m6A level and lipid accumulation in larval liver. Consequently, we posit that TCS exposure caused zebrafish lipid-metabolism disorder by decreasing miR-30b expression to regulate fto-mediated m6A methylation level. These findings contribute to our deep understanding of the underlying molecular mechanisms regarding contaminant-originating fatty liver and hepatocellular carcinoma, and also have practical significance in pollution warning and target therapy for related diseases.

Risk assessment of cardiotoxicity to zebrafish (Danio rerio) by environmental exposure to triclosan and its derivatives

Triclosan (TCS) and its two derivatives (2,4-dichlorophenol and 2,4,6-trichlorophenol) are priority pollutants that coexist in aquatic environments. Joint exposure of TCS, 2,4-dichlorophenol and 2,4,6-trichlorophenol, hereafter referred to as TCS-DT, contributes severe toxicity to aquatic organisms. There is currently a paucity of data regarding TCS-DT molecular toxicity, especially on cardiac diseases. We used zebrafish (Danio rerio) as a model organism, and evaluated the molecular-level cardiotoxicity induced by TCS-DT from embryonic to adult stages. TCS-DT exposure prominently led to phenotypic malformations, such as pericardial cysts, cardiac bleeding, increased SV-BA distance, decreased heart rate and reduced ejection fraction, as well as abnormal swimming behavior. Analyses of the GO and KEGG pathways revealed enrichment pathways related to cardiac development and screened for significantly down-regulated adrenaline signaling in cardiomyocytes. The cardiac marker genes (amhc, cmlc2, vmhc, and nkx2.5) were obtained through protein-protein interaction (PPI) networks, and expressed as down-regulation by WISH. After chronic exposure to TCS-DT from 30 to 90-dpf, both body mass and heart indexes prominently increased, showing myocardial hypertrophy, abnormal heart rate and histopathological injury. Heart tissue damage included disordered and ruptured myocardial fibers, broken and dissolved myofilaments, nuclear pyknosis, mitochondrial injury and inflammatory cell infiltration. Further, abnormal changes in a series of cardiac functions-related biomarkers, including superoxide dismutase, triglyceride, lactate dehydrogenase and creatinine kinase MB, provided evidence for cardiac pathological responses. These results highlight the molecular mechanisms involving TCS-DT induced cardiac toxicity, and provide theoretical data to guide prevention and treatment of pollutant-induced cardiac diseases.

Exposure of Triclosan in Porcine Oocyte Leads to Superoxide Production and Mitochondrial-Mediated Apoptosis During In Vitro Maturation.

While triclosan (TCS) exerts detrimental effects on female reproduction, the effect of TCS-derived toxins on porcine oocytes during in vitro maturation (IVM) is unclear. This study investigated the effects of TCS on mitochondrion-derived reactive oxygen species (ROS) production and apoptosis pathways during porcine oocyte maturation. Porcine oocytes were treated with TCS (1, 10, and 100 μM) and triphenylphosphonium chloride (Mito-TEMPO; 0.1 μM), and matured cumulus oocyte complexes (COCs) were stained with orcein, dichlorofluorescein diacetate (DCF-DA), and Mito-SOX. Proteins and mRNA levels of factors related to cumulus expansion and mitochondrion-mediated apoptosis and antioxidant enzymes were analyzed by western blotting and reverse-transcription polymerase chain reaction (RT-PCR), respectively. Meiotic maturation and cumulus cell expansion significantly decreased for COCs after TCS treatment along with an increase in mitochondrial superoxide levels at 44 h of IVM. Further, mitochondrion-related antioxidant enzymes and apoptosis markers were significantly elevated in porcine COCs following TCS-mediated oxidative damage. The protective effect of Mito-TEMPO as a specific superoxide scavenger from TCS toxin improved the maturation capacity of porcine COCs. Mito-TEMPO downregulated the mitochondrial apoptosis of TCS-exposed porcine COCs by reducing superoxide level. In conclusion, our data demonstrate that TCS mediates toxicity during porcine oocyte maturation through superoxide production and mitochondrion-mediated apoptosis.

Maternal exposure of triclosan causes fetal development restriction and female reproductive alterations in rat offspring

Maternal exposure of triclosan causes fetal development restriction and female reproductive alterations in rat offspring

Triclosan alters adult zebrafish behavior and targets acetylcholinesterase activity and expression

Triclosan is widely used in consumer products as an antimicrobial agent. Epidemiological studies have reported the association of triclosan with adverse birth outcomes. The toxic effects of triclosan on the developing stages of zebrafish are reported, however, its role as behavioral modifier is limited. In the present study, adult zebrafish were exposed to triclosan (0.3 and 0.6 mg/L) for 48 h and the exploratory behavior was analyzed using ZebraTrack. Triclosan exposed group showed significantly reduced locomotion concomitant with increased freezing duration. They also showed erratic movements suggesting that triclosan induced anxiety-like behavior in adult zebrafish. Next, we tested the hypothesis that the anxiety-like behavior is linked to altered acetylcholinesterase activity. We found that the triclosan exposure decreased acetylcholinesterase activity in the brain and skeletal muscle but acetylcholinesterase (ache) gene was significantly down-regulated only in the skeletal muscle of the adult zebrafish exposed to triclosan. In addition, we also observed a down-regulation of myelin basic protein (mbp) gene in the skeletal muscle of adult zebrafish treated with triclosan. Thus, our data indicates that even short exposure of triclosan is potent enough to induce behavioral anomalies in adult zebrafish that appear to involve acetylcholinesterase and other structural proteins especially in the skeletal muscle.

Docking-based inverse virtual screening strategy for identification of novel protein targets for triclosan

Triclosan (TCS) is chemically designated as 5-chloro-2-(2,4-dichlorophenoxy) phenol and is considered as endocrine-disrupting chemical (EDC). The various diseases found due to exposure of TCS, have been linked with modulation of the human enoyl-acyl carrier protein-reductase (hER). However, the new protein targets for TCS other than hER, which are responsible for various diseases, are still unknown. In the present study, a bioinformatics approach was used to identify new possible targets for TCS. A text mining study was initially performed to understand the association of TCS in various biochemical processes. Discovery studio software 4.1 was used to carry out inverse virtual screening for 226 numbers of pathway proteins by docking study using CHARMm based docking tool, and twenty proteins were screened. CDOCKER energy values lower than −12.65 kcal/mol was considered for the screening of selected proteins. Three new proteins; Receptor-interacting protein 1 (RIP1), Apoptosis signal-regulating kinase 1 (ASK1) and B-cell lymphoma 2 (Bcl-2) from Apoptosis Signaling Pathway revealed best CDOCKER energy with triclosan which was −26.88, −23.34 and −22.96 kcal/mol respectively. The interaction of TCS with RIP1 and ASK1 were mostly hydrophobic; however, hydrogen bond type interaction was found in TCS/Bcl2 complex. Therefore, docking-based inverse virtual screening study suggests that TCS has other targets rather than hER, which can modulate various biochemical processes. The docking protocol was validated through evaluation of root-mean-square deviation (RMSD), key interaction score system (KISS) and the relationship between the docking energy and toxicity data available in ToxCast database. Low RMSD value (0.55 ˚A) and high KISS score (0.66) along with higher correlation (R2 = 0.9798) between docking affinity and toxicity indicated that docking protocol can be used to optimize the binding energetics.

Optimization of experimental conditions and measurement of oxygen consumption rate (OCR) in zebrafish embryos exposed to organophosphate flame retardants (OPFRs)

The measurement of oxygen consumption rate (OCR) provides a comprehensive understanding of mitochondrial metabolism. However, no study has been conducted to investigate the mitochondrial dysfunction caused by organophosphate flame retardants (OPFRs). The objectives of this study were to optimize the experimental conditions to measure OCR in zebrafish embryos using the Seahorse XFe 24 Extracellular Flux Analyzer, and to investigate the changes of OCR in zebrafish embryos exposed to OPFRs. We first optimized the experimental conditions such as the number of embryos, concentrations of inhibitors, and time points. We determined the factors, i.e., three embryos, 12.5 μM of oligomycin, 8 μM of carbonyl cyanaide 4-(trifluoromethoxy) phenylhydrazone (FCCP), and 24 hpf (hours post-fertilization) time point, for obtaining the typical pattern of OCR in dechorinated zebrafish embryos. After confirming the determinants upon exposure of triclosan, the inhibition of OCR was measured in zebrafish embryos exposed to two major OPFRs, triphenyl phosphate (TPHP) and tris (1,3-dichloro-2-propyl) phosphate (TDCIPP). We found that significant inhibition of OCR was observed in basal respiration for TPHP, and in basal and maximal respiration for TDCIPP exposure, respectively. We suggest the optimum conditions of the Seahorse XFe 24 analyzer to better evaluate OCR in zebrafish embryos, and demonstrate the potential of TPHP and TDCIPP to cause the disruption of energy metabolism associated with mitochondrial dysfunction.

Maternal exposure of triclosan cause intrauterine development restriction, delay in puberty installation and deregulation of testicular function in rat offspring

This study aimed to evaluate the effects of maternal exposure to triclosan (TCS), during gestation and lactation on physical development, puberty installation and testicular function of male offspring in puberty and sexual maturity. Sixteen pregnant Wistar rats were used and divided into four experimental groups: GI- they received corn oil daily by gavage; GII- they received 75 mg kg -1 day -1 of TCS; GIII- they received 150 mg kg -1 day -1 of TCS and GIV- they received 300 mg kg -1 day -1 of TCS during pregnancy and lactation. The mean weight of the treated rat’s offspring was lower in comparison to GI group. In the exposed offspring. A delay in puberty installation was observed following the exposure to triclosan. Regarding to the stages of the seminiferous epithelium in puberty, it was noticed an increase of the I-VI stages in GIV group, compared with to GI. In sexual maturity, it was observed an increase of VII-VIII, IX-XIII in contrast to a reduction of XIV stage in treated animals, comparing to GI. There was no difference in the number of Sertoli cells. We conclude that the maternal exposure to TCS during gestation and lactation causes restriction of the intrauterine development, delay in the puberty installation and deregulation in the seminiferous epithelium cycle.

Triclosan-induced liver injury in zebrafish (Danio rerio) via regulating MAPK/p53 signaling pathway

Long-term exposure of triclosan (TCS), an important antimicrobial agent, can lead to deleterious effects on liver growth and development. However, the related mechanisms on TCS-induced hepatocyte injury remain unclear. Herein, we found that after long-time TCS exposure to adult zebrafish (Danio rerio) from 6 hpf (hours post-fertilization) to 90 dpf (days post-fertilization), the body weight and hepatic weight were significantly increased in concomitant with a large amount of lipid droplet accumulation in liver. Also, TCS exposure resulted in occurrence of oxidative stress by increasing the concentrations of malondialdehyde and reducing the activity of superoxide dismutase both in zebrafish larvae (120 hpf) and adult liver. By H&E staining, we observed a series of abnormal phenomena such as severely hepatocellular atrophy and necrosis, as well as prominently increased hepatic plate gap in TCS-exposure treatment groups. Through AO staining, TCS induced obvious apoptosis in larval heart and liver; through TUNEL assay, a concentration-dependent apoptosis was found to mainly occur in adult liver and its surrounding tissues. The mRNA and protein expression of anti-apoptotic protein Bcl-2 decreased, while that of pro-apoptosis protein Bax significantly increased, identifying that liver injury was closely related to hepatocyte apoptosis. The significant up-regulation of MAPK and p53 at both mRNA and protein levels proved that TCS-induced hepatocyte apoptosis was closely related to activating the MAPK/p53 signaling pathway. These results strongly suggest that long-term TCS-exposure may pose a great injury to zebrafish liver development by means of activating MAPK/p53 apoptotic signaling pathway, also lay theoretical foundation for further assessing TCS-induced ecological healthy risk.

Triclosan in Treated Wastewater from a City Wastewater Treatment Plant and its Environmental Risk Assessment

Triclosan (TCS) is a potential endocrine-disrupting compound (EDC), which produces an adverse impact on aquatic life and human beings. Wastewater discharge is considered as the primary source of triclosan in water bodies. The study is aimed to investigate the occurrence and environmental risk of triclosan released by municipal wastewater treatment plants (WWTP). An analytical protocol was developed and validated to determine the presence of TCS in the samples through offline solid-phase extraction (SPE) and liquid chromatography - electron spray ionization (ESI)—quadrupole mass spectrum (LC/ESI/MS). The limit of detection and quantification of protocol was estimated as 2.8 ng/L and 6.25 ng/L, respectively. The season-wise influent and effluent samples from two WWTP in Chennai, India, were monitored. The TCS concentrations in samples were found in the range of 443 to 1757 ng/L. The Risk Quotient (RQ) method was performed to evaluate the environmental (ecotoxicological and human health) risk associated with the exposure of TCS-containing wastewater. The results of the study revealed that primary producer (algae) was highly vulnerable to exposure of TCS in the aquatic environment. The estimated daily intake of TCS was much lower than the reference dosage, and this indicates that TCS did not produce any considerable risk to human health. Also, it suggested that additional treatment was required for complete removal of triclosan residues.

Triclosan toxicity alters behavioral and hematological parameters and vital antioxidant and neurological enzymes in Pangasianodon hypophthalmus (Sauvage, 1878)

Triclosan and its metabolites are detected in a diverse aquatic environment and are major concerns for various aquatic organisms. The present study investigated the impact of acute and sub-lethal exposure of triclosan on behaviour, activities of acetylcholinesterase and selected antioxidant enzymes, haematological and serum gas-electrolyte parameters of Pangasianodon hypophthalmus. The 96 h LC50 of triclosan for P. hypophthalmus was estimated as 1458 μg L−1. Further, sub-lethal triclosan exposure to 1/15th (97 μg L-1), 1/10th (145 μg L-1) and 1/5th (291 μg L-1) of 96 h LC50 concentration for a period of 45 days lead to decrease in total erythrocyte count, haemoglobin content and packed cell volume of blood while total leukocyte count increased significantly (p < 0.05) as compared to control. A concentration-dependent increase in the serum chloride and decrease in partial pressure of oxygen in blood serum was noted on 45th day. An increased activity of catalase and superoxide dismutase in gill and liver tissues and inhibition of acetylcholinesterase activity in brain was observed on 15th, 30th and 45th day of exposure which was dependent on both - concentration of triclosan and duration of exposure. A significant high activity of glutathione-S-transferase in gill and liver tissue was observed in triclosan exposed groups in comparison to control during the experimental period. The study shows that long-term sub-lethal exposure of triclosan to fish can lead to several physiological alterations such as enzymatic scavenging of oxygen radicals and the normal neurological functions mediated by the enzyme acetylcholinesterase. With increasing anthropogenic activity, the study provides a convincing evidence for the necessity of a regulated use and safer disposal of triclosan to the environment.

Triclosan treatment decreased the antitumor effect of sorafenib on hepatocellular carcinoma cells.

BackgroundTriclosan is a widely applied antimicrobial agent which affects the endocrine system and homeostasis; it may also promote the cirrhosis and hepatocellular carcinoma (HCC) growth in a mice model. The exact roles of triclosan in regulating human hepatocellular carcinoma development and treatment remain unknown.MethodsMHCC97-H, a highly aggressive HCC cell line, was treated with indicated concentration of triclosan or sorafenib. The expression of drug-resistance genes was examined by qPCR. The clearance or metabolism of sorafenib was determined by liquid chromatograph-mass spectrometer/mass spectrometer (LC-MS/MS). MTT assay was used to examine the MHCC97-H cell proliferation. Nude mice were used to exam the anti-tumor effect of sorafenib on subcutaneous and intrahepatic growth of MHCC97-H cells.ResultsIn the present study, triclosan could induce the expression of drug-resistance genes in MHCC97-H cells (a highly aggressive HCC cell line), accelerate the clearance of sorafenib, and attenuate the anti-proliferation effect of this molecular targeted agent in MHCC97-H cells. Triclosan decreased the antitumor effect of sorafenib on subcutaneous and intrahepatic growth of MHCC97-H in nude mice.ConclusionBy discovering the fact that triclosan treatment enhances sorafenib resistance in HCC cells, this work suggests exposure of triclosan is detrimental to HCC patients during chemotherapy.

Response mechanisms to joint exposure of triclosan and its chlorinated derivatives on zebrafish (Danio rerio) behavior

Triclosan (TCS), 2,4,6-trichlorophenol (2,4,6-TCP) and 2,4-dichlorophenol (2,4-DCP) frequently co-exist in real-world aquatic environments; the latter two contaminants contributing to TCS photolytic products or chlorinated derivatives. There is a paucity of information regarding their joint toxicity to aquatic organisms leading us to study their effects on the swimming behavior of zebrafish (Danio rerio). Herein, we reported that 0.28 mg/L TDT exposure (mixtures of TCS, 2,4,6-TCP and 2,4-DCP) enhanced 24-hpf embryonic spontaneous movement frequency, 96-hpf larval activity; however, the 0.56 and 1.12 mg/L TDT treatments decreased all of these behavioral endpoints. All adult behavioral tests demonstrated that chronic TDT exposure (0.14 mg/L) led to hyperactivity and restlessness in adult zebrafish. A 0.14 mg/L TD DATE /@ "M/d/yyyy" 11/21/2017T treatment led to anxiety-like behavior in a bottom dwelling test and excessive panic and low hedging capacity in a conditioned place preference test. Social interaction test demonstrated that zebrafish preferred quiet and isolated space in response to TDT stress. Zebrafish memory was significantly decreased in a T-maze experiment. Whole mount in situ hybridization of pax2a and bcl2l11 genes revealed that their differential expression in the brain and skeleton were related to the corresponding phenotypic behavioral abnormality. A series of biomarker and estrogen receptor assays demonstrated that TDT acute exposure caused abnormal energy metabolism and neurological diseases. AO staining revealed that TDT exposure produced vascular ablation in the head, as well as the occurrence of massive apoptosis in the brain. TEM observation showed pyknosis of nucleus following TDT exposure. These results allow assessment of mechanisms for zebrafish abnormal behavior in response to TDT exposure, and are useful for early intervention and gene therapy of contaminant-induced diseases.