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Shaohui Wang1, Pengyan Zhang1, Ruifang Liu1

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Di-(2-ethylhexyl) phthalate (DEHP) exposure harms brain cells by increasing oxidative stress and damaging key proteins like tau, synapsin-1, and PSD95. Vitamin E can protect against these harmful neurotoxic effects.

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Area of Science:

  • Neuroscience
  • Toxicology
  • Cell Biology

Background:

  • Di-(2-ethylhexyl) phthalate (DEHP) is a common plasticizer with known negative impacts on brain development.
  • The precise mechanisms underlying DEHP-induced neurotoxicity remain unclear.
  • Understanding these mechanisms is crucial for mitigating potential health risks.

Purpose of the Study:

  • To investigate the cellular and molecular mechanisms of DEHP-induced neurotoxicity.
  • To examine the effects of DEHP on oxidative stress markers and neuronal proteins.
  • To evaluate the protective role of antioxidant vitamin E against DEHP's adverse effects.

Main Methods:

  • Utilized a mouse neuroblastoma (N2a) cell line exposed to DEHP.
  • Assessed levels of maleic dialdehyde (MDA), reactive oxygen species (ROS), and superoxide dismutase (SOD) activity.
  • Analyzed neurite outgrowth, tau protein phosphorylation, microtubule association, and levels of synapsin-1 and PSD95.
  • Investigated the effects of vitamin E pretreatment.

Main Results:

  • DEHP exposure significantly increased MDA and ROS levels, while decreasing SOD activity in N2a cells.
  • DEHP reduced neurite outgrowth and induced hyperphosphorylation of tau protein, leading to its dissociation from microtubules.
  • Levels of synapsin-1 and postsynaptic density protein 95 (PSD95) were decreased following DEHP exposure.
  • Vitamin E pretreatment effectively prevented the DEHP-induced cellular and molecular abnormalities.

Conclusions:

  • DEHP exposure induces neurotoxicity in N2a cells, likely mediated by peroxidative damage.
  • DEHP disrupts critical neuronal proteins involved in synaptic structure and function, including tau, synapsin-1, and PSD95.
  • Antioxidant intervention with vitamin E shows potential in mitigating DEHP-induced neurotoxic effects.