【Animal Modeling】-Observation of neurotoxicological effects of flame retardant TCPP exposure in mice and related mechanisms

  Objective: To investigate the neurotoxicological effects of flame retardant TCPP exposure in mice and related mechanisms

  Methods: Thirty adult KM mice were randomly divided into normal control group (0 mg / ( kg d)) and low-dose (TCPP) group (10 mg / ( kg d))

  and the high-dose TCPP group (100 mg / ( kg·d)) were continuously administered orally administered for 30 d. After the exposure, the body weight and general condition of the mice were observed. The water maze test was used to detect the learning and memory ability of the mice. Chemiluminescence immunoassay was used. Determination of total triiodothyronine (TT3), free triiodothyronine (FT3), total tetraiodothyronine (TT4) and free tetraiodothyronine (FT4) in mouse serum ) levels Glutathione transferase (GST) and superoxide dismutase (SOD), malondialdehyde (MDA) and catalase (CAT) levels in mouse brain tissue were determined by colorimetry

  Results: Compared with the control group, the water intake of the TCPP high-dose group decreased significantly (P<0.05), and the liver and spleen index increased significantly (P<0.05). The TCPP-exposed group escaped the water maze test. The incubation period was longer than that in the normal group ( P< 0.05) The total swimming distance of the mice in the high-dose group was significantly increased ( P< 0.05) and the residence time in the target quadrant was also significantly shortened ( P< 0.05) High-dose TCPP exposure Compared with control group mice, TT3 and FT3 were significantly increased ( P<0.05) Compared with control group mice, GST and SOD were significantly decreased in high-dose TCPP exposure group, and MDA was significantly increased ( P<0.05) Compared with the control group, the mice in the low-dose TCPP exposure group only had a decrease in GST and an increase in MDA ( P<0.05)

  Conclusion: TCPP exposure has obvious neurotoxic effects, which can cause the loss of learning and memory ability in mice. The toxicity mechanism may be related to the oxidative damage of brain tissue and the increase of thyroid hormones.