Objective To observe the neurotoxic effects and mechanism of TCPP ( tris ( 2-chloroisopropyl)phosphate) exposure on mice. Methods Thirty adult KM mice were randomly divided into normal control (0 mg / ( kg·d)), low- (10 mg / (kg·d)) and high-dose TCPP groups (100 mg / (kg·d)), and were given oral gavage exposure once aday for consecutive 30 days. The body mass of mice was recorded. Morris water maze was used to examine the ability oflearning and memory ability in mice. The serum levels of total-triiodothyronine (TT3), total-tetraiodothyronine (TT4), freetetraimethionine ( FT4) and free triiodothyronine ( FT3) were detected with electro-chemiluminescence. The levels ofglutathione transferase (GST), superoxide dismutase ( SOD), catalase ( CAT), and malonaldehyde ( MDA) in braintissues were detected by chemical colorimetry. Results Compared with the control group, the water intake of the high-doseTCPP group was significantly reduced ( P < 0. 05), and the argan coefficients of the liver and spleen were significantlyincreased ( P < 0. 05). In addition, the escape latency of TCPP exposure mice was longer than that of control group in thewater maze test ( P < 0. 05). Furthermore, the total swimming course of the high-dose TCPP group was increased ( P <0. 05) and swimming time in the target quadrant was significantly reduced compared with the control group ( P < 0. 05). Inthe high-dose TCPP group, the serum levels of TT3 and FT3 were increased ( P < 0. 05), the activities of GST and SODwere decreased, and the content of MDA was increased ( P < 0. 05) compared with the control group. In the low-doseTCPP group, the activity of GST was decreased and the content of MDA was increased ( P < 0. 05) compared with thecontrol group. Conclusions TCPP exposure is neurotoxic by increasing thyroid hormones and inducing oxidative damage inmice.