LINE-1 gene hypomethylation and p16 gene hypermethylation in HepG2 cells induced by low-dose and long-term triclosan exposure: The role of hydroxyl group

Zeng, Lanting; Ma, Huimin; Pan, Shangxia; You, Jing; Zhang, Gan; Yu, Zhiqing; Sheng, Guoying; Fu, Jiamo

doi:10.1016/j.tiv.2016.03.002

Cited by 16 publications

(9 citation statements)

References 44 publications

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“…Shima reported that hydroxyl and carbonyl functional groups in the n-hexane-insoluble fraction of diesel exhaust particles may have been responsible for the inflammatory response in a rat alveolar epithelial cell line (SV40T2) 29 . In our previous paper, we reported that hydroxyl groups had an important role in the liver tumor-promoting effect of triclosan 20 . Therefore, hydroxyl functional groups in the WSF of PM2.5 may have played an important role in IL-6 release in this study.…”

Section: Il-6 and Organic Compoundsmentioning

confidence: 95%

“…Hypomethylation of the iNOS gene promoter has been reported to have a significant down-regulating effect on PM2.5 35 . We assessed this relationship in vitro using pyrosequencing to analyze iNOS promoter gene methylation 20 . The results showed that iNOS exhibited DNA hypomethylation (80.26 ± 38.08 %; Table 3) and but no significantly correlated with IL-6 release (r = 0.311, p = 0.057, Pearson correlation analysis).…”

Section: Mechanisms Of Il-6 Induction Via Exposure To the Wsf Of Pm25mentioning

confidence: 99%

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Inflammation Response of Water-Soluble Fractions in Atmospheric Fine Particulates: A Seasonal Observation in 10 Large Chinese Cities

Wan

et al. 2019

Environ. Sci. Technol.

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Spatiotemporal trends in pro-inflammatory (interleukin (IL)-6 and IL-8) release after exposure to the water-soluble fractions (WSFs) of PM2.5 sampled in 10 large Chinese cities over 1 year were investigated. Chemical components (water-soluble ions, metal(loid) elements, water-soluble organic carbon (WSOC), humic-like substances (HULIS), and endotoxins) in PM2.5 samples were measured, and the molecular structure of WSOC was also analyzed by nuclear magnetic resonance. Changes in DNA methylation and gene expression of candidate genes were also evaluated to explore the potential mechanisms. PM2.5 from southern cities induced lower pro-inflammatory responses than those from northern cities. Seasonal differences in toxicity were noted among the cities. IL-6 was significantly correlated with HULIS (as the main fraction of WSOC with oxygenated carbohydrate structures characteristic), Pb and endotoxin. Furthermore, DNA methylation and gene expression changes in RASSF2, and CYP1B1 were related to pro-inflammatory secretion. Certain components of PM2.5, rather than PM2.5 mass itself, determine the pro-inflammatory release. In particular, HULIS, which originated from primary biomass burning and residual coal combustion, and secondary organic aerosols, appear to be the key component in PM2.5 to induce human health risk.

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Section: Il-6 and Organic Compoundsmentioning

confidence: 95%

Section: Mechanisms Of Il-6 Induction Via Exposure To the Wsf Of Pm25mentioning

confidence: 99%

Inflammation Response of Water-Soluble Fractions in Atmospheric Fine Particulates: A Seasonal Observation in 10 Large Chinese Cities

Wan

et al. 2019

Environ. Sci. Technol.

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“…In human liver carcinoma cells (HepG2), long term administration of low nanomolar TCS and mTCS induced changes in gene expression via effects on methylation status (Zeng et al 2016). Interestingly, mTCS and TCS seemed to exert opposite effects on methylation of p16 tumor suppressor gene, an effectnot seen in higher micromolar TCS concentrations (Zeng et al 2016). Triclosan-methyl also undergoes hydrophobic interactions with human serum albumin (HSA), leading to spontaneous binding and conformation changes to HSA (Lv et al 2013).…”

Section: Triclosan Breakdown Productsmentioning

confidence: 99%

Triclosan exposure, transformation, and human health effects

Weatherly

Gosse

2017

Journal of Toxicology and Environmental Health, Part B

428

236

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Triclosan (TCS) is an antimicrobial used so ubiquitously that 75% of the U.S.A. population is likely exposed to this compound via consumer goods and personal care products. In September 2016, TCS was banned from soap products following the risk assessment by the U.S.A. Food and Drug Administration (FDA). However, TCS still remains, at high concentrations, in other personal care products such as toothpaste, mouthwash, hand sanitizer, and surgical soaps. Triclosan is readily absorbed into human skin and oral mucosa and found in various human tissues and fluids. The aim of this review was to describe TCS exposure routes and levels as well as metabolism and transformation processes. The burgeoning literature on human health effects associated with TCS exposure, such as reproductive problems was also summarized.

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“…Low‐level TCS increased p 16 gene methylation along with reduced expression. The hypermethylation of tumor‐suppressor genes can significantly contribute to their functional inactivity, leading to the initiation and progression of carcinogenesis (Soberanes et al, 2012; Zeng et al, 2016). These experimental data suggest that TCS plays crucial roles for the altered epigenetics, which lead to hepatotoxicity and developmental abnormalities.…”

Section: Epigenetic Changes Link Ecs To Adverse Health Outcomesmentioning

confidence: 99%

“…Low-level TCS increased p 16 gene methylation along with reduced expression. The hypermethylation of tumor-suppressor genes can significantly contribute to their functional inactivity, leading to the initiation and progression of carcinogenesis (Soberanes et al, 2012;Zeng et al, 2016).…”

Section: Airborne Pmsmentioning

confidence: 99%

Linking emerging contaminants exposure to adverse health effects: Crosstalk between epigenome and environment

Alam

Shapla

Shen

et al. 2020

J of Applied Toxicology

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Environmental epigenetic findings shed new light on the roles of epigenetic regulations in environmental exposure‐induced toxicities or disease susceptibilities. Currently, environmental emerging contaminants (ECs) are in focus for further investigation due to the evidence of human exposure in addition to their environmental occurrences. However, the adverse effects of these environmental ECs on health through epigenetic mechanisms are still poorly addressed in many aspects. This review discusses the epigenetic mechanisms (DNA methylation, histone modifications, and microRNA expressions) linking ECs exposure to health outcomes. We emphasized on the recent literature describing how ECs can dysregulate epigenetic mechanisms and lead to downstream health outcomes. These up‐to‐date research outputs could provide novel insights into the toxicological mechanisms of ECs. However, the field still faces a demand for further studies on the broad spectrum of health effects, synergistic/antagonistic effects, transgenerational epigenetic effects, and epidemiologic and demographic data of ECs.

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LINE-1 gene hypomethylation and p16 gene hypermethylation in HepG2 cells induced by low-dose and long-term triclosan exposure: The role of hydroxyl group

Cited by 16 publications

References 44 publications

Inflammation Response of Water-Soluble Fractions in Atmospheric Fine Particulates: A Seasonal Observation in 10 Large Chinese Cities

Inflammation Response of Water-Soluble Fractions in Atmospheric Fine Particulates: A Seasonal Observation in 10 Large Chinese Cities

Triclosan exposure, transformation, and human health effects

Linking emerging contaminants exposure to adverse health effects: Crosstalk between epigenome and environment

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