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).
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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.