Nanomolar concentration of triclocarban increases the vulnerability of rat thymocytes to oxidative stress

Kanbara, Yasuhiro; Murakane, Kazuyoshi; Nishimura, Yumiko; Satoh, Masaya; Oyama, Yasuo

doi:10.2131/jts.38.49

Cited by 5 publications

(4 citation statements)

References 26 publications

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“…These processes were accompanied by ROS formation, LDH release, and neuronal cell death. Our results are in accordance with cytotoxic effect of triclocarban used in combination with hydrogen peroxide in rat thymocytes [ 8 ]. The results are also in line with the lethality of rat pups that were fed by lactating females exposed to triclocarban [ 6 ].…”

Section: Discussionsupporting

confidence: 89%

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

et al. 2018

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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.

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Section: Discussionsupporting

confidence: 89%

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

et al. 2018

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“…Both human cell lines (T47Dluc, H295R) showed no cell lethality when exposed up to 1.6 μM TCC. These results are in agreement with the open literature [128,129]. …”

Section: Discussionsupporting

confidence: 94%

“…Morita et al [126] showed no cell lethality after the incubation of rat thymocytes with TCC at concentrations ranging from 30 to 500 nM for 1 h. The incubation with TCC at concentrations ranging from 10 to 1 μM for 1 h did not affect the viability of rat thymocytes [128]. Another study by Kanbara et al [129] showed an increase in cell lethality when rat thymocytes were incubated with 10 μM TCC. In the present study, a cytotoxic effect to treated RTL-W1 cells was already observed at concentrations above 4 μM TCC.…”

Section: Discussionmentioning

confidence: 99%

“…Two similar studies suggested the production of reactive oxygen species in rat thymocytes after an incubation time of 1 h to 300 nM or higher concentrations of TCC [126,129]. On the contrary, Fukunaga and coworkers [128] supposed that the same cells recovered the initial loss of cellular glutathione as a biomarker of oxidative stress in the continued presence of 300 nM TCC.…”

Section: Discussionmentioning

confidence: 99%

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Effects of multiwalled carbon nanotubes and triclocarban on several eukaryotic cell lines: elucidating cytotoxicity, endocrine disruption, and reactive oxygen species generation

et al. 2014

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To date, only a few reports about studies on toxic effects of carbon nanotubes (CNT) are available, and their results are often controversial. Three different cell lines (rainbow trout liver cells (RTL-W1), human adrenocortical carcinoma cells (T47Dluc), and human adrenocarcinoma cells (H295R)) were exposed to multiwalled carbon nanotubes, the antimicrobial agent triclocarban (TCC) as well as the mixture of both substances in a concentration range of 3.13 to 50 mg CNT/L, 31.25 to 500 μg TCC/L, and 3.13 to 50 mg CNT/L + 1% TCC (percentage relative to carbon nanotubes concentration), respectively. Triclocarban is a high-production volume chemical that is widely used as an antimicrobial compound and is known for its toxicity, hydrophobicity, endocrine disruption, bioaccumulation potential, and environmental persistence. Carbon nanotubes are known to interact with hydrophobic organic compounds. Therefore, triclocarban was selected as a model substance to examine mixture toxicity in this study. The influence of multiwalled carbon nanotubes and triclocarban on various toxicological endpoints was specified: neither cytotoxicity nor endocrine disruption could be observed after exposure of the three cell lines to carbon nanotubes, but the nanomaterial caused intracellular generation of reactive oxygen species in all cell types. For TCC on the other hand, cell vitality of 80% could be observed at a concentration of 2.1 mg/L for treated RTL-W1 cells. A decrease of luciferase activity in the ER Calux assay at a triclocarban concentration of 125 μg/L and higher was observed. This effect was less pronounced when multiwalled carbon nanotubes were present in the medium. Taken together, these results demonstrate that multiwalled carbon nanotubes induce the production of reactive oxygen species in RTL-W1, T47Dluc, and H295R cells, reveal no cytotoxicity, and reduce the bioavailability and toxicity of the biocide triclocarban.

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Chronic effects of triclocarban in the amphipod Gammarus locusta : Behavioural and biochemical impairment

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Montes

Quintana

et al. 2017

Ecotoxicology and Environmental Safety

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Nanomolar concentration of triclocarban increases the vulnerability of rat thymocytes to oxidative stress

Cited by 5 publications

References 26 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

Effects of multiwalled carbon nanotubes and triclocarban on several eukaryotic cell lines: elucidating cytotoxicity, endocrine disruption, and reactive oxygen species generation

Chronic effects of triclocarban in the amphipod Gammarus locusta : Behavioural and biochemical impairment

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