Abstract:
:Methamphetamine (MA), an amphetamine-type psychostimulant, is associated with dopaminergic toxicity and has a high abuse potential. Numerous in vivo and in vitro studies have suggested that impaired mitochondria are critical in dopaminergic toxicity induced by MA. Mitochondria are important energy-producing organelles with dynamic nature. Evidence indicated that exposure to MA can disturb mitochondrial energetic metabolism by inhibiting the Krebs cycle and electron transport chain. Alterations in mitochondrial dynamic processes, including mitochondrial biogenesis, mitophagy, and fusion/fission, have recently been shown to contribute to dopaminergic toxicity induced by MA. Furthermore, it was demonstrated that MA-induced mitochondrial impairment enhances susceptibility to oxidative stress, pro-apoptosis, and neuroinflammation in a positive feedback loop. Protein kinase Cδ has emerged as a potential mediator between mitochondrial impairment and oxidative stress, pro-apoptosis, or neuroinflammation in MA neurotoxicity. Understanding the role and underlying mechanism of mitochondrial impairment could provide a molecular target to prevent or alleviate dopaminergic toxicity induced by MA.
journal_name
Neurochem Resjournal_title
Neurochemical researchauthors
Shin EJ,Tran HQ,Nguyen PT,Jeong JH,Nah SY,Jang CG,Nabeshima T,Kim HCdoi
10.1007/s11064-017-2318-5subject
Has Abstractpub_date
2018-01-01 00:00:00pages
66-78issue
1eissn
0364-3190issn
1573-6903pii
10.1007/s11064-017-2318-5journal_volume
43pub_type
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