Multiple bio-analytical methods to reveal possible molecular mechanisms of developmental toxicity in zebrafish embryos/larvae exposed to tris(2-butoxyethyl) phosphate

Han, Zhihua; Wang, Qiangwei; Fu, Jie; Chen, Hongshan; Zhao, Ye; Zhou, Bingsheng; Gong, Zhiyuan; Wei, Si; Li, Jun; Liu, Hongling; Zhang, Xiaowei; Liu, Chunsheng; H, Yu

doi:10.1016/j.aquatox.2014.03.013

Cited by 50 publications

(12 citation statements)

References 36 publications

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“…This could explain why this compound, unlike all PhACs and most of the EDCs detected, was found in all living compartments already in the control reach. TBEP can alter embryonic development and protein expression when present in high concentrations (150 μg L -1 to 100 mg L -1 ; Han et al, 2014), but effects on biota within concentration ranges comparable to ours have not been reported to our knowledge.…”

Section: Trophic Magnification Of Tbepcontrasting

confidence: 54%

Bioaccumulation and trophic magnification of pharmaceuticals and endocrine disruptors in a Mediterranean river food web

Ruhí

Acuña

Barceló

et al. 2016

Science of The Total Environment

150

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Section: Trophic Magnification Of Tbepcontrasting

confidence: 54%

Bioaccumulation and trophic magnification of pharmaceuticals and endocrine disruptors in a Mediterranean river food web

Ruhí

Acuña

Barceló

et al. 2016

Science of The Total Environment

150

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“…For example, Saitoh et al () reported that giving diet containing 3.0% TBEP to Wistar rats could increase gamma‐glutamyl transferase activity and amylase contents in serum while decrease body weight and serum cholinesterase activity. In another study, it was observed that 10.7 mg/L TBEP could reduce survival rate of zebrafish larvae by half at 120 h post fertilization, which consequence was similar to 7.0 mg/ l tris‐(1, 3‐dichloro‐2‐propyl) phosphate (TDCPP) exposure according to the previous published reports (Liu et al, ; Han et al, ). Crump et al () observed that 10 μM/mL or higher concentration of TDCPP notably declined the viability of both avian hepatocytes and neuronal cells.…”

Section: Discussionsupporting

confidence: 64%

“…Egloff et al () observed that 241.5 μg/g triethyl phosphate (TEP) could modulate the expression of genes associated with lipid metabolism and the thyroid hormone pathway as well as decrease the plasma thyroxine levels of chicken embryos. Han et al () reported that 800 μg/L TBEP could significantly affect the expression levels of vitellogenin ( vtg ) 2, 4, and 5 in 120 hpf zebrafish larvae. In the current study, visible declines were observed in the transcriptional levels of P450scc, P450‐17α , and 17β‐HSD after the treatment with 100 μg/mL TBEP for 24 h, suggesting that high concentration of TBEP could cause endocrine disorder in TM3 cells and as a result inhibited T production (Fig.…”

Section: Discussionmentioning

confidence: 99%

Effects of TBEP on the induction of oxidative stress and endocrine disruption in Tm3 Leydig cells

Jin

Chen

2015

Environ. Toxicol.

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The flame retardant tris (2-butoxyethyl) phosphate (TBEP) is a frequently detected contaminant in the environment. In the cultured TM3 cells (originated from ATCC), effects of TBEP on the induction of oxidative stress and endocrine disruption were evaluated. It was observed that exposure to 100 μg/mL TBEP for 24 h significantly reduced the viability of TM3 cells. The mRNA levels of genes related to oxidative stress including Sod, Gpx1, Cat, and Gsta1 were changed in a dose-dependent and/or time-dependent manner after exposure to 30 and 100 μg/mL TBEP for 6, 12, or 24 h. Moreover, notable decrease in glutathione (GSH) contents and increases in oxidized glutathione (GSSG) contents as well as the antioxidant enzyme activities like superoxide dismutase, catalase, glutathione peroxidase, and glutathione S-transferase were found in the group treated with 100 μg/mL TBEP for 24 h, indicating that TBEP induced oxidative stress in TM3 Leydig cells. In addition, the expression of genes related to testosterone (T) synthesis including cytochrome P450 cholesterol side-chain cleavage enzyme (P450scc), cytochrome P450 17α-hydroxysteroid dehydrogenase (P450-17α), and 17β-hydroxysteroid dehydrogenase (17β-HSD) and T levels in medium were remarkably declined by the treatment of 100 μg/mL TBEP for 24 h. And TBEP could inhibit the expression of P450-17α and 17β-HSD and T levels up-regulated by hCG in TM3 cells. Taken together, these findings indicated that TBEP can induce oxidative stress and alter steroidogenesis in TM3 cells. © 2015 Wiley Periodicals, Inc. Environ Toxicol 31: 1276-1286, 2016.

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“…37 The lowest observed effect concentration (LOEC, 50 μM) of TBEP to cause general toxicity in the developing zebrafish was significantly higher than the reported environmental concentration. 38 Giraudo et al also found that the mortality of 50% of individuals (LC 50 ) due to TBEP in a 48 h acute toxicity testing in D. magna reached 147 mg L −1 (369 μM). 39 Our previous study also showed that TBP and TBEP exposure (24 h) below 100 μM seems to have no remarkable proliferation-inhibiting effect on HepG2, human lung cancer (A549) and human colon cancer (Caco-2) cells.…”

Section: Discussionmentioning

confidence: 94%

Tributylphosphate (TBP) and tris (2-butoxyethyl) phosphate (TBEP) induced apoptosis and cell cycle arrest in HepG2 cells

Ren

Shang

et al. 2017

Toxicol. Res.

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The purpose of this study was to investigate the cytotoxic effects of tributylphosphate (TBP) and tris (2-butoxyethyl) phosphate (TBEP) and to explore the underlying molecular mechanism focusing on oxidative stress, apoptosis, and cell cycle arrest. The results showed that TBP and TBEP could inhibit cell proliferation, induce cellular reactive oxidative stress, and suppress the mitochondrial membrane potential in HepG2 cells. TBP and TBEP could induce both mitochondrial and p53 mediated apoptosis through different mitogen-activated protein kinase (MAPK) signal pathways. TBP activated the c-Jun N-terminal kinase (JNK) and extracellular regulated protein kinase (ERK1/2) pathways, while TBEP activated the JNK pathway. Furthermore, TBP and TBEP caused a concentration-dependent decrease of cyclin D1 expression and an increase of cyclin-dependent kinase (CDK) inhibitor proteins such as p21 and p27, resulting in significant cell cycle arrest in the G0/G1 phase. Taken together, the toxicity of TBP and TBEP on the HepG2 cells was associated with apoptosis and cell cycle arrest induced by oxidative stress.

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Multiple bio-analytical methods to reveal possible molecular mechanisms of developmental toxicity in zebrafish embryos/larvae exposed to tris(2-butoxyethyl) phosphate

Cited by 50 publications

References 36 publications

Bioaccumulation and trophic magnification of pharmaceuticals and endocrine disruptors in a Mediterranean river food web

Bioaccumulation and trophic magnification of pharmaceuticals and endocrine disruptors in a Mediterranean river food web

Effects of TBEP on the induction of oxidative stress and endocrine disruption in Tm3 Leydig cells

Tributylphosphate (TBP) and tris (2-butoxyethyl) phosphate (TBEP) induced apoptosis and cell cycle arrest in HepG2 cells

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