Advances in TCE Toxicology

Jiang, Yan; Dai, Yufei; Chen, Tao

doi:10.1016/b978-0-12-812522-9.00002-6

Cited by 3 publications

(3 citation statements)

References 118 publications

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“…1,23 However, since both TCE and TCA (the main metabolite of TCE in liver) are negative in genotoxicity tests, epigenetic modifications may be responsible for the hepatotoxicity of TCE. 1,23,24 Animal experiments have shown that chronic TCE exposure could induce hepatocellular carcinoma in mice but not in rats. 12 We have previously reported that the different patterns of DNA methylation changes induced by TCE in the liver of mice and rats might account for the species-specific hepatocarcinogenicity of TCE.…”

Section: Discussionmentioning

confidence: 76%

“…Determining the human relevance of epigenotoxic carcinogens is a major challenge due to their tissue- and species-specific effects. It has been suggested that TCE has a mutagenic mode of action for renal carcinogenesis. , However, since both TCE and TCA (the main metabolite of TCE in liver) are negative in genotoxicity tests, epigenetic modifications may be responsible for the hepatotoxicity of TCE. ,, Animal experiments have shown that chronic TCE exposure could induce hepatocellular carcinoma in mice but not in rats . We have previously reported that the different patterns of DNA methylation changes induced by TCE in the liver of mice and rats might account for the species-specific hepatocarcinogenicity of TCE. , In addition, we also showed that TCE-induced DNA methylation changes upregulated miR-182–5p, an oncogenic miRNA, in mouse liver .…”

Section: Discussionmentioning

confidence: 99%

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Effects of Trichloroethylene on the Expression of Long Intergenic Noncoding RNAs in B6C3F1 Mouse Liver

Ren

Wang

Aniagu

et al. 2020

Chem. Res. Toxicol.

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Trichloroethylene (TCE), a widely used industrial solvent, is a common environmental contaminant. We previously reported that TCE-induced changes in DNA methylation and miRNA expression contributed to the development of a liver tumor in mice. In this study, we investigated the role of long intergenic noncoding RNA (LincRNA), another type of epigenetic modification, in TCE hepatocarcinogenesis. Male B6C3F1 mice were gavaged with TCE at dose levels of 0, 100, 500, and 1000 mg/kg b.w. for 5 days. The expression changes of LincRNAs in liver samples from control and TCE-exposed mice were screened by microarray. When compared to the control group, 21 and 29 LincRNAs were upregulated and downregulated, respectively, in the liver of mice exposed to TCE at 1000 mg/kg b.w. In addition, TCE treatment increased the expression levels of LincRNA-GM8704 but decreased the expression levels of LiverLincs_chr17_4383_2 in a dose-dependent manner. We further found that the mRNAs that are highly correlated with the expression of LiverLincs_chr17_4383_2 are involved in a number of cancer-related signaling pathways including PPARs, cell cycle, and ErbB and p53 signaling pathways. Among the expression-correlated mRNAs, Cdkn1a was found to be a downstream target gene of LiverLincs_chr17_4383_2. To follow up on that, we also found that miR-182–5p might mediate the association between downregulation of LiverLincs_chr17_4383_2 and upregulation of Cdkn1a, leading to increased cell proliferation in TCE exposed liver cells. In conclusion, TCE induced extensive LincRNA expression changes in mouse liver, and the downregulation of LiverLincs_chr17_4383_2 might contribute to TCE hepatocarcinogenesis by interacting with miR-182–5p and Cdkn1a.

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Section: Discussionmentioning

confidence: 76%

Section: Discussionmentioning

confidence: 99%

Effects of Trichloroethylene on the Expression of Long Intergenic Noncoding RNAs in B6C3F1 Mouse Liver

Ren

Wang

Aniagu

et al. 2020

Chem. Res. Toxicol.

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“…Previous studies concluded that disruption of sarcolemmal Ca influx can be done during exposure to TCE in neonatal rat cardiomyocytes (19). Inhalation of TCE has also been shown to be able to be genotoxic especially those genes involved in regulation of intracellular Ca (20). These findings are consistent with the study by , who noted that TCE disrupted the expression levels of ryanodine receptor 2 (RYR2), a Ca 2+ release channel which is highly required in the normal activity of heart, in P19 mouse embryonal carcinoma cells (21).…”

Section: Discussionmentioning

confidence: 99%

Toxicological Effects of Inhalation Exposure to Trichloroethylene on Serum Immunoglobulin and Electrolyte Levels in Rats

et al. 2019

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Background: Trichloroethylene (TCE) is one of the most important environmental contaminants that can introduce both occupational and public health because of its widespread use. Objectives: This study was aimed to investigate effects of inhalation exposure to TCE on serum immunoglobulin and electrolyte levels under controlled laboratory conditions. Methods: Five equal groups (5 animals each) were randomly selected from a total of 25 adult male Sprague-Dawley rats. TCE vapor was generated by dynamic evaporation method in exposure chamber. The animals were exposed to TCE at five different concentration levels (0 ppm as control, 10, 100, 250, and 400 ppm through 8 hours inhalation during a day, for 10 consecutive days. Results: Based on results, IgG, IgM and IgA levels were significantly increased in rats following exposure to various levels of TCE ≥ 100 ppm (P < 0.05). Conversely, TCE exposure significantly caused a decrease in the levels of IgE in the case group with those values compared to control group (P < 0.05). Contrariwise, serum levels of Ca were significantly increased in rats exposed to TCE levels above 250 ppm, the high and very high exposure level (P < 0.05). At a concentration of 100 and 400 ppm, changes were noted in serum P levels (P < 0.05). A moderate positive relationship was found between serum P and the TCE concentration in sub-acute exposure (R 2 = 0.66, P < 0.05). Conclusions:In conclusion, sub-acute inhalation exposure to TCE (≥ 100 ppm) is related to the electrolyte and immunoglobulin toxicity in the form of increased Ca, P, IgA, IgG and IgM and decreased Cl, Na and IgE.

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Role of miR-182-5p overexpression in trichloroethylene-induced abnormal cell cycle functions in human HepG2 cells

Jiang

Zhou

Ren

et al. 2019

Journal of Toxicology and Environmental Health, Part A

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Advances in TCE Toxicology

Cited by 3 publications

References 118 publications

Effects of Trichloroethylene on the Expression of Long Intergenic Noncoding RNAs in B6C3F1 Mouse Liver

Effects of Trichloroethylene on the Expression of Long Intergenic Noncoding RNAs in B6C3F1 Mouse Liver

Toxicological Effects of Inhalation Exposure to Trichloroethylene on Serum Immunoglobulin and Electrolyte Levels in Rats

Role of miR-182-5p overexpression in trichloroethylene-induced abnormal cell cycle functions in human HepG2 cells

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