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Updated: May 21, 2025

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ROS Regulate Rotenone-induced SH-SY5Y Dopamine Neuron Death Through Ferroptosis-mediated Autophagy and Apoptosis.

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Rotenone induces Parkinson

Keywords:
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Area of Science:

  • Neuroscience
  • Cell Biology
  • Toxicology

Background:

  • Rotenone is a widely used insecticide for creating Parkinson's disease (PD) models.
  • The precise mechanisms underlying rotenone-induced neuronal cell death are not fully understood.
  • Investigating rotenone's effects is crucial for understanding PD pathogenesis.

Purpose of the Study:

  • To elucidate the mechanisms of rotenone-induced cell death in dopamine neurons.
  • To investigate the roles of oxidative stress, ferroptosis, autophagy, and apoptosis in rotenone neurotoxicity.
  • To explore potential therapeutic targets for rotenone-induced Parkinson's-like pathology.

Main Methods:

  • SH-SY5Y dopamine neuron cell model treated with rotenone.
  • Assessment of cell viability, PD-like pathological changes (TH, α-synuclein).
  • Measurement of reactive oxygen species (ROS), ferroptosis markers (GPX4, xCT, COX2, NCOA4), autophagy markers (mTOR, Beclin-1, ATG5, LC3, p62), and apoptosis markers (Bcl-2, MMP, BAX, Caspase-3).
  • Treatment with N-acetylcysteine (NAC), ferrostatin-1 (Fer-1), deferoxamine (DFO), and ML385 to investigate mechanistic pathways.

Main Results:

  • Rotenone suppressed neuron viability and induced PD-like changes, increasing ROS and oxidative stress.
  • Rotenone triggered ferroptosis, inhibited autophagy flux, and initiated apoptosis.
  • Inhibitors of ROS and ferroptosis (NAC, Fer-1, DFO) ameliorated rotenone-induced autophagy and apoptosis.
  • Nrf2 inhibition exacerbated rotenone-induced ferroptosis.

Conclusions:

  • Reactive oxygen species (ROS) mediate rotenone-induced Parkinson's-like pathology by regulating ferroptosis, autophagy, and apoptosis.
  • Inhibition of ferroptosis effectively blocks rotenone-induced autophagy and apoptosis.
  • ROS-driven neuronal death in rotenone models is dependent on ferroptosis, highlighting ferroptosis as a key therapeutic target.