Effects Of Triclosan Exposure Research Articles

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.

A systematic review and meta-analysis of the impact of triclosan exposure on human semen quality.

Triclosan is an antibacterial and antifungal compound that is frequently found in personal care and consumer products, and its its impact on male reproductive health is a growing concern. Despite existing experimental studies demonstrating its potential threats to male fertility, reports on its effects on human semen quality remains limited and inconsistent. Therefore, this study presents a systematic review and meta-analysis assessing the relationship between triclosan exposure and semen quality. This study was registered with PROSPERO (CRD42024524192) and adhered to PRISMA guidelines. The study analyzed 562 screened studies, out of which five articles including 1,312 male subjects were finally included in the study. The eligible studies were geographically diverse, with three from China, one from Belgium, and one from Poland. More so, the eligible studies were both case-control and cross-sectional. The meta-analysis revealed that triclosan exposure significantly reduced sperm concentration (Standard Mean Difference (SMD) -0.42 [95% CI: -0.75, -0.10], P = 0.01) and sperm total motility (SMD -1.30 [95% CI: -2.26, -0.34], P = 0.008). Mechanistic insights from animal and in vitro studies showed that oxidative stress may mediate the adverse effects of triclosan on semen quality. This meta-analysis is the first comprehensive evaluation of the impact of triclosan on human semen quality, highlighting its potential to impair male fertility through reductions in sperm concentration and motility. However, the high heterogeneity among the included studies underscores the need for further high-quality research to establish more definitive conclusions regarding the effects of triclosan exposure on human reproductive health.

Effects of triclosan exposure on stem cells from human exfoliated deciduous teeth (SHED) fate

Triclosan (TCS), a widely used broad-spectrum antibacterial agent and preservative, is commonly found in products and environments. Widespread human exposure to TCS has drawn increasing attention from researchers concerning its toxicological effect. However, minimal studies have focused on the impact of TCS exposure on human stem cells. Therefore, the aim of the present study was to evaluate the effects of TCS exposure on stem cells from human exfoliated deciduous teeth (SHED) and its molecular mechanisms. A series of experimental methods were conducted to assess cell viability, morphology, proliferation, differentiation, senescence, apoptosis, mitochondrial function, and oxidative stress after SHED exposure to TCS. Furthermore, transcriptome analysis was applied to investigate the response of SHED to different concentrations of TCS exposure and to explore the molecular mechanisms. We demonstrated that TCS has a dose-dependent proliferation and differentiation inhibition of SHED, while promoting cellular senescence, mitochondrial dysfunction, endoplasmic reticulum (ER) stress, and oxidative stress, as well as significantly induces apoptosis and autophagy flux inhibition at high concentrations. Interestingly, no significant morphological changes in SHED were observed after TCS exposure. Transcriptome analysis of normal and TCS-induced SHED suggested that SHED may use different strategies to counteract stress from different concentrations of TCS and showed significant differences. We discovered that TCS mediates cellular injury of SHED by enhancing the expression of PTEN, thereby inhibiting the phosphorylation levels of PI3K and AKT as well as mTOR expression. Collectively, our findings provide a new understanding of the toxic effects of TCS on human stem cell fate, which is important for determining the risk posed by TCS to human health.

Effect of triclosan exposure on ovarian hormones, trace elements and growth in female rats

Triclosan (TCS) is an antibacterial compound used mainly in personal care products. Its widespread use for decades has made it one of the most widely detected compounds in environmental matrices and in biological fluids. Although it has been shown to be an endocrine disruptor in rats and aquatic species, its safe use by humans is unclear.The aim of the present study was to evaluate the effects of exposure to TCS in female rats. To this end, 14 rats were divided into two groups and fed daily as follows: the control group with sesame oil and the TCS group at a dose of 50 mg/kg/day for 28 days. Any signs of toxicity in the rats were observed daily, and the weight and phase of the estrous cycle were recorded. At the end, the rats were decapitated, the serum and ovaries were collected. The levels of testosterone and progesterone in serum were determined by immunoassay and mass spectrometry. Estradiol (in serum) and kisspeptin-10 (in serum and ovary) were measured only by immunoassays. Trace elements were determined by inductively coupled plasma–mass spectrometry (ICP–MS).The weight gain study of the rats showed a significant decrease by exposure to TCS, while the estrous cycle was not significantly affected compared to the control. The optimized methods based on mass spectrometry showed a significant decrease in the levels of progesterone and testosterone due to exposure to TCS. In addition, elements determined by ICP–MS in rat serum showed significant changes in calcium, lithium and aluminum due to TCS treatment. Finally, the kisspeptin-10 levels did not show a negative effect due to the treatment by TCS. The results suggest that medium-term exposure to TCS did not significantly alter estrous cyclicity but caused alterations in growth, sex hormone levels and some elements in the rat serum.

Effects of triclosan exposure on placental extravillous trophoblast motility, relevant IGF2/H19 signaling and DNA methylation-related enzymes of HTR-8/SVneo cell line

Triclosan (TCS) is an antimicrobial agent widely used in personal care products and a potential endocrine disruptor chemical (EDC). TCS can pass through the placental barrier. Any influence of EDCs on epigenetic changes of placenta and embryo may bring profound impact on later health. This study aimed to investigate the effects of TCS exposure on cell proliferation and migration, and the expression of imprinted genes IGF2/H19 and DNA methylation-related enzymes in human placental extravillous trophoblast cell line HTR-8/SVneo. After exposure to TCS levels of 0 (DMSO Control), 10−11, 10−10, 10−9, 10−8, 10−7, 10−6, 10−5, 3 × 10−5, 6 × 10−5, 10−4 M and incubated for up to 36 h, cell proliferation and migration were examined by CCK-8, EdU incorporation assay and wound healing assay; the mRNA levels of IGF2, H19, DNA methyltransferases (Dnmt3a, Dnmt3b and Dnmt1), ten-eleven translocation enzymes (Tet1, Tet2 and Tet3) and IGF2 Receptor (IGF2R) were analyzed by qRT-PCR. The protein levels of IGF2 were measured by Western blot and ELISA. The cell viability turned to decline at TCS treatment of 3 × 10−5 M and above (all p < 0.05, compared to the DMSO Control). The cell migration decreased at TCS 10−5 and 3 × 10−5 M treatment (p < 0.05), but consistently unchanged at low dose of TCS from 10−9 to 10−7 M (p > 0.05). TCS treatments below cytotoxicity doses (< 10−5 M) did not significantly alter the mRNA levels of IGF2, Dnmt1, Dnmt3a, Dnmt3b, Tet1, Tet2 and Tet3, compared to DMSO Control treatment (all p > 0.05). The transcription level of H19 was up-regulated by TCS at 3 × 10−5 M. TCS at 10−7 and 6 × 10−5 M increased the protein level of IGF2 in cell supernatant. Our data suggest that high TCS exposure may suppress HTR-8/SVneo cells viability and migration, increase H19 gene expressions and IGF2 protein secretion. The exact mechanism of TCS action in human trophoblast needs further studies.

Effect of Maternal Triclosan Exposure on Neonatal Birth Weight and Children Triclosan Exposure on Children's BMI: A Meta-Analysis.

Background: Triclosan (TCS) is an environmental chemical with endocrine disrupting effects and can enter the body through the skin or oral mucosa. Human data about the effect of TCS exposure during pregnancy on neonatal birth weight and TCS exposure during childhood on children's growth are scarce.Objectives: To investigate the association between maternal urinary TCS level and neonatal birth weight, as well as children's urinary TCS level and children's body mass index (BMI).Methods: A systematic literature search was conducted using PubMed, Cochrane Library, and Web of Science. Finally, seven epidemiological articles with 5,006 participants from September 25, 2014 to August 10, 2018 were included in the meta-analysis to identify the relationship between maternal exposure to TCS and neonatal birth weight. On the other hand, three epidemiological articles with 5,213 participants from July 22, 2014 to September 1, 2017 were included in another meta-analysis to identify the relationship between children's exposure to TCS and children's BMI. We used Stata 16.0 to test the heterogeneity among the studies and calculating the combined effect value 95% confidence interval (CI) of the selected corresponding models.Results: TCS exposure during pregnancy was not significant associated with neonatal birth weight. The results of forest plots were as follows: ES (Estimate) = 0.41 (95% CI: −11.97–12.78). Children's urinary TCS level was also irrelevant associated with children's BMI: ES = 0.03 (95% CI: −0.54–0.60).Conclusions: This meta-analysis demonstrated that there was no significant association between maternal TCS level and neonatal birth weight, also there has no relationship between children's urinary TCS level and children's BMI.

Effects of triclosan exposure on the energy budget of Ruditapes philippinarum and R. decussatus under climate change scenarios.

We built a simulation model based on Dynamic Energy Budget theory (DEB) to assess the growth and reproductive potential of the native European clam Ruditapes decussatus and the introduced Manila clam Ruditapes philippinarum under current temperature and pH conditions in a Portuguese estuary and under those forecasted for the end of the 21st c. The climate change scenario RCP8.5 predicts temperature increase of 3°C and a pH decrease of 0.4units. The model was run under additional conditions of exposure to the emerging contaminant triclosan (TCS) and in the absence of this compound. The parameters of the DEB model were calibrated with the results of laboratory experiments complemented with data from the literature available for these two important commercial shellfish resources. For each species and experimental condition (eight combinations), we used data from the experiments to produce estimates for the key parameters controlling food intake flux, assimilation flux, somatic maintenance flux and energy at the initial simulation time. The results showed that the growth and reproductive potential of both species would be compromised under future climate conditions, but the effect of TCS exposure had a higher impact on the energy budget than forecasted temperature and pH variations. The egg production of R. philippinarum was projected to suffer a more marked reduction with exposure to TCS, regardless of the climatic factor, while the native R. decussatus appeared more resilient to environmental causes of stress. The results suggest a likely decrease in the rates of expansion of the introduced R. philippinarum in European waters, and negative effects on fisheries and aquaculture production of exposure to emerging contaminants (e.g., TCS) and climate change.

Effects of Triclosan Exposure on the Gut Microbiome in Zebrafish

Background/Aim Triclosan (TCS) is a widely used antibacterial agent in personal care products and ubiquitous in environment. As gut microbiota is known important for health, it is unclear whether TCS exposure may affect gut microbiota . This study aimed to examine the effects of early life long-term exposure to TCS and concurrent short-term exposure on gut microbiota in zebrafish. Methods Zebrafish fertilized eggs were cultured in TCS concentrations of 0 (Dimethyl Sulphoxide, DMSO control), 0.03, 0.3, 3, 30, 100, and 300 ng/mL from 0 to 120 days post fertilization (dpf) to examine its early life exposure effect. At 120 dpf, intestine samples were collected for analysis of gut microbiota based on the V3-V4 hypervariable regions of the 16S ribosomal RNA gene. We also exposed adult zebrafishes to TCS for 7 days to examine its short-term effect on gut microbiota of adult zebrafish. Results In exposure to TCS for 0-120 pdf , compared with those in DMSO control group, gut microbiota of zebrafish at TCS 300 ng/mL had 54.5 lower mean number of operational taxonomic units (OTUs) (mean ± SE, 71.29 ± 11.22 vs. 125.75 ± 2.39, p = 0.003), 41.40 lower Chao index (p = 0.03), and 34.10 lower ace index (p = 0.006), with lower relative abundance in Proteobacteria, Planctomycetes and Cyanobacteria and CKC4, but higher abundance in Bacteroidetes, at phylum level, and lower relative abundance in Acinetobacter, Cyanobacteria_norank, Hyphomicrobium, Methylobacterium, Sphingomonas, but higher abundance in CKC4_norank, Aeromonas, Staphylococcus, Prevotella and Bacteroides, at genus level. The short-term 7-day TCS exposure was not associated with the alpha or beta diversity of gut microbiota in adult zebrafish. Conclusions Early life exposure to high TCS concentration may lower diversity and richness of gut microbiota, and altered its composition in zebrafish. Such effect was not observed for short-term TCS exposure in adult zebrafish.

Effect of Triclosan Exposure on Developmental Competence in Parthenogenetic Porcine Embryo during Preimplantation.

Triclosan (TCS) is included in various healthcare products because of its antimicrobial activity; therefore, many humans are exposed to TCS daily. While detrimental effects of TCS exposure have been reported in various species and cell types, the effects of TCS exposure on early embryonic development are largely unknown. The aim of this study was to determine if TCS exerts toxic effects during early embryonic development using porcine parthenogenetic embryos in vitro. Porcine parthenogenetic embryos were cultured in in vitro culture medium with 50 or 100 µM TCS for 6 days. Developmental parameters including cleavage and blastocyst formation rates, developmental kinetics, and the number of blastomeres were assessed. To determine the toxic effects of TCS, apoptosis, oxidative stress, and mitochondrial dysfunction were assessed. TCS exposure resulted in a significant decrease in 2-cell rate and blastocyst formation rate, as well as number of blastomeres, but not in the cleavage rate. TCS also increased the number of apoptotic blastomeres and the production of reactive oxygen species. Finally, TCS treatment resulted in a diffuse distribution of mitochondria and decreased the mitochondrial membrane potential. Our results showed that TCS exposure impaired porcine early embryonic development by inducing DNA damage, oxidative stress, and mitochondrial dysfunction.

Association between triclosan levels and white blood cell counts in US adults from NHANES, 2011–2012

Triclosan is a broad-spectrum antimicrobial agent used in a multitude of healthcare and consumer products. Epidemiological studies link triclosan exposure to several adverse health outcomes including alterations in thyroid function and an increased risk for allergies and asthma suggesting an immunomodulatory role for the endocrine disrupting synthetic chemical. The effects of triclosan on the human immune system, particularly on the levels and function of white blood cells, have yet to be fully characterized. Using cross-sectional data from the NHANES 2011–2012 survey, we examined the relationship between triclosan exposure levels and white blood cell counts in adults 18–65 years of age. Results from multivariable linear regression analysis show lack of a statistically signficant association between urinary triclosan levels and white blood cell counts (β = −0.0007, p = 0.90, 95% CI = −0.012, 0.010). Findings may demonstrate an absence of association or may indicate that triclosan exposure levels were too low to have a significant detectable impact on white blood cell counts. Considering that prior animal and epidemiological studies have established links between triclosan exposure and alterations in immune system parameters and susceptibility to allergic diseases, the effects of triclosan exposure on the immune system should continue to be evaluated.

Effects of triclosan on antioxidant- and apoptosis-related genes expression in the gill and ovary of zebrafish.

Triclosan (TCS) is a broad-spectrum antibacterial and anti-fungal agent used in a broad variety of personal care products (PCPs) throughout the world. However, the molecular mechanism of TCS’s effects on the gill and ovary of fish is not clear. In this study, the effects of TCS exposure on expression of antioxidant- and apoptosis-related genes were investigated in the gill and ovary of zebrafish (Danio rerio). Zebrafish were exposed to 0, 17, 34, or 68 µg/l TCS for 42 days. Antioxidant-related genes (SOD, GPx1a, CAT, sMT-B, and MT-2) in the gill were significantly downregulated in the 34 (except GPx1a) and 68 µg/l TCS groups, and these genes (except MT-2) in the ovary were significantly downregulated in the 68 µg/l TCS group. Apoptosis-related gene (Bax and p53) expression level in the gill were significantly downregulated in the 68 µg/l TCS group, while the ratios of BCL-2 to Bax and MDM2 gene were significantly upregulated. The Bax gene in the ovary was significantly upregulated in the 34 and 68 µg/l TCS groups, while the ratio of BCL-2 to Bax was significantly downregulated. Moreover, the p53 gene in the ovary in the 34 µg/l TCS group was significantly upregulated. In addition, the MDA contents in the gill in the 34 and 68 μg/l TCS treated groups and in the ovary in 68 μg/l group were significantly increased. The results showed that the higher dose of TCS might cause oxidative damage in the gills and ovaries and accelerate ROS-dependent ovary apoptosis in zebrafish.

Full life-cycle toxicity assessment on triclosan using rotifer Brachionus calyciflorus

Triclosan (TCS) is an antimicrobial and is an aquatic contaminant. Little is known on aquatic toxicity of TCS. Rotifers are common members of freshwater zooplankton. In this study, Brachionus calyciflorus was chosen as a test organism to assess the acute and complete life cycle toxicity of TCS in this study. The acute toxicity results showed that the 24-h median lethal concentration (LC50) of TCS was 345±0.11μg/L (95% confidence limits of 212–564µg/L). Reproductive bioassays demonstrated that TCS could inhibit the population growth rate at the concentration higher than 1.0μg/L. Resting egg production encompasses the full life-cycle of rotifer, and thus its hatching rate were explored to assess the toxicity of TCS towards rotifer population at TCS concentrations ranging from 0.1 to 200µg/L at two different growth periods. When resting eggs were exposed to TCS during the formation period, 0.1 and 1.0µg/L of TCS increased the hatching rate from 0.402 to 0.502, and 0.475, respectively. Exposure to 100 and 200µg/L of TCS reduced the hatching rate to 0.309 and 0.275, respectively. When the resting eggs were formed in the control medium and hatched in medium with TCS, their hatching rates were not significantly influenced by TCS, except that 200µg/L of TCS decreased the hatching rate from 0.402 to 0.34 significantly. The effects of TCS exposure on the hatching rate during the formation period were greater than those during the resting egg hatching period.