N-Acetyl Cysteine Protects against Methamphetamine-Induced Dopaminergic Neurodegeneration via Modulation of Redox Status and Autophagy in Dopaminergic Cells

@inproceedings{Shivalingappa2012NAcetylCP,
  title={N-Acetyl Cysteine Protects against Methamphetamine-Induced Dopaminergic Neurodegeneration via Modulation of Redox Status and Autophagy in Dopaminergic Cells},
  author={Prashanth Chandramani Shivalingappa and Huajun Jin and Vellareddy Anantharam and Anumantha G Kanthasamy and Arthi Kanthasamy},
  booktitle={Parkinson's disease},
  year={2012}
}
Methamphetamine- (MA-) induced neurotoxicity is associated with mitochondrial dysfunction and enhanced oxidative stress. Our previous study demonstrated that MA induces autophagy in a dopaminergic neuronal cell model (N27 cells). The cellular mechanisms underlying MA-induced autophagy and apoptosis remain poorly characterized. In the present study we sought to investigate the importance of GSH redox status in MA-induced neurotoxicity using a thiol antioxidant, N-acetylcysteine (NAC… CONTINUE READING

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Together , these results suggest that NAC exhibits significant protective effects against MA - induced dopaminergic cell death , presumably via modulation of the GSH level and autophagy .
Collectively , our data provide mechanistic insights into the role of cellular GSH redox status in MA - induced autophagy and apoptotic cell death , and additional studies are needed to determine the therapeutic effectiveness of cellular redox modifiers in attenuating dopaminergic neurodegeneration in vivo .
Together , these results suggest that NAC exhibits significant protective effects against MA - induced dopaminergic cell death , presumably via modulation of the GSH level and autophagy .
Collectively , our data provide mechanistic insights into the role of cellular GSH redox status in MA - induced autophagy and apoptotic cell death , and additional studies are needed to determine the therapeutic effectiveness of cellular redox modifiers in attenuating dopaminergic neurodegeneration in vivo .
Collectively , our data provide mechanistic insights into the role of cellular GSH redox status in MA - induced autophagy and apoptotic cell death , and additional studies are needed to determine the therapeutic effectiveness of cellular redox modifiers in attenuating dopaminergic neurodegeneration in vivo .
Together , these results suggest that NAC exhibits significant protective effects against MA - induced dopaminergic cell death , presumably via modulation of the GSH level and autophagy .
Collectively , our data provide mechanistic insights into the role of cellular GSH redox status in MA - induced autophagy and apoptotic cell death , and additional studies are needed to determine the therapeutic effectiveness of cellular redox modifiers in attenuating dopaminergic neurodegeneration in vivo .
The cellular mechanisms underlying MA - induced autophagy and apoptosis remain poorly characterized .
Collectively , our data provide mechanistic insights into the role of cellular GSH redox status in MA - induced autophagy and apoptotic cell death , and additional studies are needed to determine the therapeutic effectiveness of cellular redox modifiers in attenuating dopaminergic neurodegeneration in vivo .
The cellular mechanisms underlying MA - induced autophagy and apoptosis remain poorly characterized .
Collectively , our data provide mechanistic insights into the role of cellular GSH redox status in MA - induced autophagy and apoptotic cell death , and additional studies are needed to determine the therapeutic effectiveness of cellular redox modifiers in attenuating dopaminergic neurodegeneration in vivo .
Collectively , our data provide mechanistic insights into the role of cellular GSH redox status in MA - induced autophagy and apoptotic cell death , and additional studies are needed to determine the therapeutic effectiveness of cellular redox modifiers in attenuating dopaminergic neurodegeneration in vivo .
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