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Objective: To explore the neurotoxicity and mechanism of tris(2-chloroethyl) phosphate (TCEP) exposure in mice.Methods: Total 30 adult Kunming mice were randomly divided into normal control group (0 mg/kg·d), low-dose TCEP group (10 mg/kg·d), and high-dose TCEP group (100 mg/kg·d), and administered continuously by gavage for 30 days.Results: Compared with the control group, the water intake of high-dose TCEP group was declined significantly (p < 0.05), and the organ index of liver and spleen were increased significantly (p < 0.05). In addition, the escape latency of TCEP exposed mice were longer than that in the control group in water maze test (p < 0.05), while the total swimming course of high-dose TCEP group was elevated and the swimming time in target quadrant was obviously shortened compared with the control group (p < 0.05). The serum levels of total-triiodothyronine (TT3) and free triiodothyronine (FT3) were significantly higher in the high-dose TCEP group than in the control group (p<0.05). Compared with the control group, the activities of glutathione transferase (GST) and super oxide dismutase (SOD) in the high-dose TCEP group were increased, and GST in the low-dose TCEP group were decreased, while the content of malonaldehyde (MDA) in both groups was increased (p<0.05). In the CCK8 assay, the viability of PC12 cells decreased with an increase of TCEP concentration, indicating a concentration dependent neurotoxicity.Conclusion: TCEP exposure can cause neurotoxicity by increasing thyroid hormones and inducing oxidative damage in mice.

Citation

Chengqiang Wang, Zihan Chen, Yanmei Lu, Lu Wang, Yabin Zhang, Xiaonian Zhu, Jiale Song. Neurotoxicity and related mechanisms of flame retardant TCEP exposure in mice. Toxicology mechanisms and methods. 2020 Sep;30(7):490-496

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PMID: 32397869

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