Intestinal damage, neurotoxicity and biochemical responses caused by tris (2-chloroethyl) phosphate and tricresyl phosphate on earthworm

Yang, Yang; Xiao, Yao; Chang, Yeqian; Cui, Yibin; Klobučar, Göran; Li, Mei

doi:10.1016/j.ecoenv.2018.04.012

Cited by 96 publications

(20 citation statements)

References 60 publications

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“…By means of the comet assay, the present study explicates that TCEP in a concentration-dependent manner introduced strand breaks in DNA. Broken DNA in the matrix of microgel was found similar to that reported with higher doses (1-10 mg/kg) of OPFR-exposed earthworm coelomocytes and HepG2 cells exposed to TCP (400 µM) [28,33]. The quantum of DNA damage specifies towards the impairment of DNA repair machinery to rectify the damage.…”

Section: Discussionsupporting

confidence: 79%

Tris(2-chloroethyl) Phosphate (TCEP) Elicits Hepatotoxicity by Activating Human Cancer Pathway Genes in HepG2 Cells

Alsalem

Saquib

Siddiqui

et al. 2020

Toxics

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Tris(2-chloroethyl) phosphate (TCEP) is one of the organophosphorus flame retardants (OPFRs) used in consumer commodities and have been detected in human body fluids. Research on TCEP-induced transcriptomic alterations and toxicological consequences in liver cells is still lacking. Herein, human hepatocellular (HepG2) cells were treated with 100, 200, and 400 μM TCEP for 3 days to quantify hepatotoxicity by MTT, NRU, and comet assays. Apoptosis, mitochondrial membrane potential (ΔΨm), oxidative stress, and Ca2+ influx were measured by flow cytometry. A qPCR array was employed for transcriptomic analysis. MTT and NRU data showed 70.92% and 75.57% reduction in cell survival at 400 μM. In addition, 20-fold greater DNA damage was recorded at 400 μM. Cell cycle data showed 65.96% subG1 apoptotic peak in 400 μM treated cells. An elevated level of oxidative stress, esterase, Ca2+ influx, and ΔΨm dysfunction were recorded in TCEP-treated cells. Out of 84 genes, the qPCR array showed upregulation of 17 genes and downregulation of 10 key genes belonging to human cancer pathways. Our study endorses the fact that TCEP possesses hepatotoxic potential at higher concentrations and prolonged exposure. Hence, TCEP may act as a cancer-inducing entity by provoking the gene network of human cancer pathways.

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Section: Discussionsupporting

confidence: 79%

Tris(2-chloroethyl) Phosphate (TCEP) Elicits Hepatotoxicity by Activating Human Cancer Pathway Genes in HepG2 Cells

Alsalem

Saquib

Siddiqui

et al. 2020

Toxics

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“…They found that both TCEP and TCPP at the concentrations from 1 µM to 1 mM did not cause statistically significant changes in this parameter neither without an external enzymatic metabolizing system nor in the presence of S9-mix. On the other hand, recently, Yang et al 21 confirmed genotoxic potential of different concentrations of TCEP on intestinal cells of Eisenia fetida earthworm.…”

Section: Discussionmentioning

confidence: 98%

DNA damage and methylation induced by organophosphate flame retardants: Tris(2-chloroethyl) phosphate and tris(1-chloro-2-propyl) phosphate in human peripheral blood mononuclear cells

et al. 2019

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Phosphorus flame retardants are a group of chemicals that are used to slow or prevent the spread of fire. These compounds have been detected in different environments including human organism. In the present study, we have investigated DNA-damaging potential and effect on DNA methylation of tris(2-chloroethyl) phosphate (TCEP) and tris(1-chloro-2-propyl) phosphate (TCPP) in human peripheral blood mononuclear cells (PBMCs). In order to determine DNA damage and repair, the alkaline and neutral versions of the comet assay were used. The level of DNA methylation was determined with specific antibodies against methylated DNA. PBMCs were exposed to TCEP and TCPP at the concentrations in the range of 1–1000 µM for 24 h. We have observed that TCEP and TCPP induced DNA damage—DNA breaks and alkali-labile sites. All DNA damages were effectively repaired during 120-min repair incubation. The results have also shown that TCEP and TCPP decreased the level of DNA methylation in PBMCs. In the case of TCEP, this effect was observed at a very low concentration of 1 µM.

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“…20 Yang et al have reported that, trin-butyl phosphate (TnBP) and TCP might show acute toxic effect to earthworm (Eisenia fetida). 21,22 Therefore, it is necessary to study the neurotoxic effects of alkyl and aromatic OPFRs. Based on these, TnBP and TCP were selected as test substances.…”

Section: Introductionmentioning

confidence: 99%

“…Limited studies have described the toxicity and particularly acute neurotoxicity of alkyl and aromatic substituted OPFRs which are usually considered to be degradable in the environment 20 . Yang et al have reported that, tri‐n‐butyl phosphate (TnBP) and TCP might show acute toxic effect to earthworm ( Eisenia fetida ) 21,22 . Therefore, it is necessary to study the neurotoxic effects of alkyl and aromatic OPFRs.…”

Section: Introductionmentioning

confidence: 99%

Comparative assessment of neurotoxicity impacts induced by alkyl tri‐n‐butyl phosphate and aromatic tricresyl phosphate in PC12 cells

Chang

Cui

Jiang

et al. 2020

Environmental Toxicology

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Organophosphate flame retardants (OPFRs) have become a growing concern due to their potential environmental and health risk. However, limited studies have described the toxicity, particularly neurotoxicity of alkyl and aromatic OPFRs. This study investigated the neurotoxicity of alkyl tri‐n‐butyl phosphate (TnBP) and aromatic tricresyl phosphate (TCP) to rat adrenal pheochromocytoma (PC12) cells for 24 h. Viability detection showed dose‐response toxicity effect of TCP and TnBP to PC12 cells. The half‐maximal inhibitory concentration of 24 h (24 h‐IC50) of TCP and TnBP were 2415.61 and 338.09 μM, respectively. Both TnBP and TCP significantly changed the acetylcholinesterase (AChE) activity, and TnBP is more likely to cause neurotoxicity to PC12 cells compared to TCP. Also, The results of LDH and caspase‐3 activity detection as well as Hoechst staining suggested that cell apoptosis induced by TCP and TnBP may be the primary pathway. These findings provide a toxicity data of aromatic and alkyl‐substituted OPFRs to PC12 cells, and a new insight into the toxicity of OPFRs on health risk assessment.

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Intestinal damage, neurotoxicity and biochemical responses caused by tris (2-chloroethyl) phosphate and tricresyl phosphate on earthworm

Cited by 96 publications

References 60 publications

Tris(2-chloroethyl) Phosphate (TCEP) Elicits Hepatotoxicity by Activating Human Cancer Pathway Genes in HepG2 Cells

Tris(2-chloroethyl) Phosphate (TCEP) Elicits Hepatotoxicity by Activating Human Cancer Pathway Genes in HepG2 Cells

DNA damage and methylation induced by organophosphate flame retardants: Tris(2-chloroethyl) phosphate and tris(1-chloro-2-propyl) phosphate in human peripheral blood mononuclear cells

Comparative assessment of neurotoxicity impacts induced by alkyl tri‐n‐butyl phosphate and aromatic tricresyl phosphate in PC12 cells

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