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Autophagy plays a protective role in Mn-induced toxicity in PC12 cells

Qian Zhou1, Xiaolong Fu1, Xueting Wang1

  • 1Joint International Research Laboratory of Ethnomedicine, and Key Laboratory of Basic Pharmacology of Ministry of Education, Zunyi Medical College, Guizhou, China.

Toxicology
|December 10, 2017
PubMed

Insights

Manganese (Mn) exposure causes neurotoxicity, but autophagy plays a protective role. Enhancing autophagy reduces Mn-induced cell death, while inhibiting it worsens toxicity, highlighting autophagy

Area of Science:

  • Neuroscience
  • Toxicology
  • Cell Biology

Background:

  • Environmental and occupational manganese (Mn) exposure is linked to neurodegenerative disorders.
  • Oxidative stress and mitochondrial dysfunction are key mechanisms in Mn neurotoxicity.
  • Autophagy, the process of removing damaged mitochondria, is a potential protective mechanism against neurotoxicity.

Purpose of the Study:

  • To investigate the effect of Mn exposure on cellular autophagy.
  • To determine if modulating autophagic flux impacts sensitivity to Mn-induced cytotoxicity.
  • To elucidate the role of autophagy in manganese neurotoxicity.

Main Methods:

  • PC12 cells were exposed to Mn to model toxicity.
  • Autophagic flux was assessed by monitoring LC3-II and p62 protein levels.
  • Cell viability was evaluated after treatment with Mn, autophagy inhibitors (chloroquine), autophagy inducers (rapamycin), and antioxidants (NAC, resveratrol).
  • Mitochondrial function (oxygen consumption, ROS generation, GSH levels) was measured.

Main Results:

  • Mn exposure increased LC3-II and p62 levels, indicating impaired autophagic flux.
  • Inhibiting autophagy with chloroquine exacerbated Mn-induced cytotoxicity.
  • Inducing autophagy with rapamycin significantly reduced Mn-induced cell death.
  • Antioxidants NAC and resveratrol improved cell survival by maintaining mitochondrial function, not primarily by modulating autophagy.

Conclusions:

  • Autophagy plays a significant protective role against manganese-induced cytotoxicity.
  • Modulating autophagic flux, particularly through induction, can mitigate Mn neurotoxicity.
  • Antioxidants protect against Mn toxicity mainly by preserving mitochondrial function.
Keywords:
AutophagyLC3-IIManganeseMitochondriap62

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