| Abstrakt: |
Tris(1,3-dichloro-2-propyl) phosphate (TDCPP) was widely detected in a variety of environmental media and biota samples. C57BL/6 mice were used as an animal model to study the potential neurotoxicity mechanisms caused by TDCPP. Changes of the neural function related factors in cerebral cortex and serum metabolomics in mice were investigated after continuous exposure to TDCPP at 300 mg⋅kg-1⋅d-1 for 35 d. The results showed that, after 35 d of TDCPP exposure, the concentrations of 5-hydroxytryptamine (5-HT) and activities of acetylcholinesterase (AChE) in the cerebral cortex had no significant change (P>0.05). Significant up-regulations of the gene expression levels of the proinflammatory cytokine interleukin-6 (IL- 6), interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), inducible nitric oxide synthase ( iNOS) and glial cell line-derived neurotrophic factor (GDNF) were observed ( P<0.05) in exposed mice. However, the gene expression level of neurotrophic factor-3 (Ntf3) was significantly down-regulated (P<0.05). Meanwhile, TDCPP exposure interfered with the metabolic process of amino acid metabolism, glycometabolism and lipid metabolism, leading to changes in the levels of biomarkers such as isoleucine, glutamate, glycine and β-glucose, which were associated with a variety of neurological diseases. The results showed that the neurotoxic effects of TDCPP were related to changes in the transcriptional levels of neuroinflammation and neuronal damage-related factors as well as the metabolic signal disorder caused by metabolic imbalance. [ABSTRACT FROM AUTHOR] |
