Triclosan/triclocarban levels in maternal and umbilical blood samples and their association with fetal malformation

Wei, Ling; Qiao, Pengyun; Shi, Ying; Ruan, Yan; Yin, Jie; Wu, Qingqing; Shao, Bing

doi:10.1016/j.cca.2016.12.024

Cited by 75 publications

(44 citation statements)

References 20 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…In a recent ranking of potentially dangerous organic pollutants, antimicrobial compound, such as triclocarban, was positioned in the middle of the ranking, but with a higher ranking than bisphenol A (BPA), which has been recognized as a developmental risk factor. Triclocarban accumulates in human tissues, including the maternal and umbilical cord sera where it reaches the values of 2.75 and 0.82 μg/l, respectively [ 3 ]. This antimicrobial agent has been detected in urine and cord blood of mother/child pairs from Brooklyn, New York, as well as in two distinct brain regions of the human brain, i.e., the hypothalamus and white-matter tissue [ 4 , 5 ].…”

Section: Introductionmentioning

confidence: 99%

Triclocarban Disrupts the Epigenetic Status of Neuronal Cells and Induces AHR/CAR-Mediated Apoptosis

et al. 2018

View full text Add to dashboard Cite

Triclocarban is a phenyl ether that has recently been classified as a contaminant of emerging concern. Evidence shows that triclocarban is present in human tissues, but little is known about the impact of triclocarban on the nervous system, particularly at early developmental stages. This study demonstrated that triclocarban that was used at environmentally relevant concentrations induced apoptosis in mouse embryonic neurons, inhibited sumoylation, and changed the epigenetic status, as evidenced by impaired activities of HDAC, sirtuins, and DNMT, global DNA hypomethylation, and alterations of methylation levels of bax, bcl2, Ahr, and Car genes. The use of selective antagonists and specific siRNAs, which was followed by the co-localization of aryl hydrocarbon receptor (AHR) and constitutive androstane receptor (CAR) in mouse neurons, points to the involvement of AHR and CAR in triclocarban-induced neurotoxicity. A 24-h treatment with triclocarban enhanced protein levels of the receptors which was paralleled by Car hypomethylation and Ahr hypermethylation. Car hypomethylation is in line with global DNA hypomethylation and explains the increased mRNA and protein levels of CAR in response to triclocarban. Ahr hypermethylation could reflect reduced Ahr mRNA expression and corresponds to lowered protein levels after 3- and 6-h exposures to triclocarban that is likely related to proteasomal degradation of activated AHR. We hypothesize that the triclocarban-induced apoptosis in mouse neurons and the disruption of epigenetic status involve both AHR- and CAR-mediated effects, which may substantiate a fetal basis of the adult onset of neurological diseases; however, the expression of the receptors is regulated in different ways.

show abstract

Section: Introductionmentioning

confidence: 99%

Triclocarban Disrupts the Epigenetic Status of Neuronal Cells and Induces AHR/CAR-Mediated Apoptosis

et al. 2018

View full text Add to dashboard Cite

show abstract

“…However, numerous recent epidemiological studies report detrimental TCS effects on human health, including problems with thyroid function (Wang et al, 2017), reproduction (Hua et al, 2017), and immune function and development (Wei et al, 2017;reviewed in Weatherly & Gosse, 2017). Additional recent epidemiological studies have revealed increased risks due to TCS exposure of gestational diabetes (Ouyang et al, 2018), abnormalities of sperm morphology (Jurewicz et al, 2018) and lowered cognitive test scores in children (Jackson-Browne et al, 2018).…”

Section: Introductionmentioning

confidence: 99%

Antimicrobial agent triclosan suppresses mast cell signaling via phospholipase D inhibition

Shim

Caron

Weatherly

et al. 2019

J of Applied Toxicology

View full text Add to dashboard Cite

Humans are exposed to the antimicrobial agent triclosan (TCS) through use of TCS‐containing products. Exposed tissues contain mast cells, which are involved in numerous biological functions and diseases by secreting various chemical mediators through a process termed degranulation. We previously demonstrated that TCS inhibits both Ca2+ influx into antigen‐stimulated mast cells and subsequent degranulation. To determine the mechanism linking the TCS cytosolic Ca2+ depression to inhibited degranulation, we investigated the effects of TCS on crucial signaling enzymes activated downstream of the Ca2+ rise: protein kinase C (PKC; activated by Ca2+ and reactive oxygen species [ROS]) and phospholipase D (PLD). We found that TCS strongly inhibits PLD activity within 15 minutes post‐antigen, a key mechanism of TCS mast cell inhibition. In addition, experiments using fluorescent constructs and confocal microscopy indicate that TCS delays antigen‐induced translocations of PKCβII, PKCδ and PKC substrate myristoylated alanine‐rich C‐kinase. Surprisingly, TCS does not inhibit PKC activity or overall ability to translocate, and TCS actually increases PKC activity by 45 minutes post‐antigen; these results are explained by the timing of both TCS inhibition of cytosolic Ca2+ (~15+ minutes post‐antigen) and TCS stimulation of ROS (~45 minutes post‐antigen). These findings demonstrate that it is incorrect to assume that all Ca2+‐dependent processes will be synchronously inhibited when cytosolic Ca2+ is inhibited by a toxicant or drug. The results offer molecular predictions of the effects of TCS on other mammalian cell types, which share these crucial signal transduction elements and provide biochemical information that may underlie recent epidemiological findings implicating TCS in human health problems.

show abstract

“… 8–10 Widespread exposures to TCS have been observed in many countries. 11–14 Public concerns over the ubiquitous exposure to TCS and other EEDCs have increased. 12–15 Evidence from animal and in vitro studies suggested a variety of hormonal activities of TCS, including oestrogenic, androgenic and antiandrogenic activities, and disturbance of thyroid hormone activities, 16–19 all of which are related to PCOS-like syndrome.…”

Section: Introductionmentioning

confidence: 99%

Environmental exposure to triclosan and polycystic ovary syndrome: a cross-sectional study in China

Zhu

Liu

et al. 2018

BMJ Open

View full text Add to dashboard Cite

ObjectivesPolycystic ovary syndrome (PCOS) is the most common endocrinopathy of women at reproductive age. Although the aetiology of PCOS remains unclear, potential effects of environmental endocrine-disrupting compounds on the development of PCOS have drawn increasing attention. The aim of the current study was to examine the association between triclosan (TCS) and PCOS, and explore possible mechanisms on how TCS may contribute to the development of clinical manifestations of PCOS.DesignCross-sectional study.SettingThis study was conducted in one tertiary-level hospital located in Zhejiang, China.ParticipantsA total of 674 infertile women at 18–45 years of age were recruited in 2014–2015. Participants with (n=84) and without (n=212) PCOS with urinary TCS concentration available were included in the analyses.MethodsUrinary TCS concentration was measured using a high-performance liquid chromatography–electrospray ionisation tandem mass spectrometry. Logistic regression model was used to examine the association between TCS and PCOS. Fractional polynomial regression models were built to fit the potential non-linear relationship between TCS concentrations and luteinising hormone (LH) and LH/follicle stimulate hormone (FSH).ResultsThe PCOS group had significantly higher level of TCS concentration than the non-PCOS group (the median of TCS (IQR), μg/g creatinine: 1.49 (0.68–3.80) vs 1.06 (0.52–3.02), p=0.0407). Compared with the lowest tertile, the highest tertile of TCS concentration was associated with an increased odd of PCOS (OR 2.12, 95% CI 1.12 to 3.99). After adjusting for potential confounders, the significant association remained (OR 1.99, 95% CI 1.05 to 3.79). Positive relationships were found between TCS levels and LH and LH/FSH ratio in non-PCOS participants.ConclusionsTCS exposure at a relatively low level is associated with PCOS in Chinese women. Further epidemiological studies are needed to confirm our finding, which may have important public health implications.

show abstract

Triclosan/triclocarban levels in maternal and umbilical blood samples and their association with fetal malformation

Cited by 75 publications

References 20 publications

Triclocarban Disrupts the Epigenetic Status of Neuronal Cells and Induces AHR/CAR-Mediated Apoptosis

Triclocarban Disrupts the Epigenetic Status of Neuronal Cells and Induces AHR/CAR-Mediated Apoptosis

Antimicrobial agent triclosan suppresses mast cell signaling via phospholipase D inhibition

Environmental exposure to triclosan and polycystic ovary syndrome: a cross-sectional study in China

Contact Info

Product

Resources

About