A DEHP plasticizer alters synaptic proteins via peroxidation

作者：Wang, Shaohui; Zhang, Pengyan; Liu, Ruifang; Li, Yuan; Liu, Chao; Liao, Xiaomei^*

来源：Toxicology Research, 2017, 6(1): 89-97.

DOI：10.1039/c6tx00361c

• GLYCOGEN-SYNTHASE KINASE-3
• OXIDATIVE STRESS
• VITAMIN-E
• DI(2-ETHYLHEXYL) PHTHALATE
• ALZHEIMERS-DISEASE
• TAU-PROTEIN
• HUMAN-CELLS
• EXPOSURE
• MODEL
• PHOSPHORYLATION

Di-(2-ethylhexyl) phthalate (DEHP) is a widely used commercial plasticizer. DEHP exposure has a negative impact on brain development and cognition, but the mechanisms responsible for DEHP-induced neurotoxicity are not well understood. Here we showed that DEHP exposure increased maleic dialdehyde and reactive oxygen species contents and decreased endogenous superoxide dismutase activity in a mouse neuroblastoma cell line (N2a cell line). DEHP exposure not only induced reduction of neurite outgrowth, but also led to microtubule-associated protein tau hyperphosphorylation and dissociation from microtubules. Furthermore, DEHP exposure decreased the levels of synapsin-1 and postsynaptic density protein 95 (PSD95), which play critical roles in synaptic function. Antioxidant vitamin E pretreatment prevented DEHP-induced abnormalities in the cells. These results indicate that DEHP exposure could induce abnormal action of proteins including tau, synapsin-1 and PSD95, which play critical roles in the synaptic structure and function, and that these alterations might be mediated by peroxidative damage.

• 出版日期2017-1-1
• 单位华中师范大学