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mTOR Modulates Methamphetamine-Induced Toxicity through Cell Clearing Systems.

Gloria Lazzeri1, Francesca Biagioni2, Federica Fulceri3

  • 1Department of Translational Research and New Technologies in Medicine and Surgery, Human Anatomy, University of Pisa, Via Roma 55, Pisa 56126, Italy.

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|January 17, 2019
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Summary
This summary is machine-generated.

Methamphetamine toxicity involves the autophagoproteasome (APP), a combined cell clearing pathway. Inhibiting mTOR reduces METH-induced cell death by decreasing APP levels, offering a potential therapeutic strategy.

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Area of Science:

  • Cell Biology
  • Neuroscience
  • Toxicology

Background:

  • Methamphetamine (METH) abuse causes widespread public health issues.
  • METH exposure induces oxidative stress, leading to cellular damage like lipid peroxidation and protein misfolding.
  • Cellular waste removal pathways, ubiquitin-proteasome (UP) and autophagy (ATG), are implicated in METH toxicity.

Purpose of the Study:

  • To investigate the role of the autophagoproteasome (APP), a newly identified convergence of UP and ATG, in METH toxicity.
  • To analyze how modulating the mTOR pathway affects APP formation and METH-induced cellular damage.

Main Methods:

  • Coimmunoprecipitation to detect interactions between UP and ATG markers (LC3, P20S, p62, alpha-synuclein).
  • Western blotting, light and confocal microscopy, and transmission electron microscopy to quantify APP and assess cellular damage.
  • Administration of METH alone and with mTOR modulators in various doses and time intervals.

Main Results:

  • Coimmunoprecipitation confirmed the binding of LC3 and P20S, forming APPs that also recruited p62 and alpha-synuclein.
  • METH-induced toxicity levels correlated positively with the observed APP levels.
  • mTOR inhibition protected against METH-induced cell death, while mTOR activation exacerbated it, correlating with APP levels.

Conclusions:

  • The autophagoproteasome (APP) is a key pathway involved in methamphetamine toxicity.
  • Modulating the mTOR pathway significantly impacts APP formation and METH-induced cell death.
  • Targeting APP formation via mTOR modulation presents a potential therapeutic avenue for mitigating METH toxicity and other oxidative damages.