Journal
BIOMETALS
Volume 30, Issue 4, Pages 623-628Publisher
SPRINGER
DOI: 10.1007/s10534-017-0023-0
Keywords
Fe(II); AMPK; Neurotoxicity; Mitochondria; ROS
Categories
Funding
- National Natural Science Foundation of China [11375213, 21390411]
- Hundred Talents Program of the Chinese Academy of Sciences and IHEP Innovation Program
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Deregulated iron homeostasis is generally believed to be implicated in neurodegenerative diseases, including Parkinson's disease. Nevertheless, it is not fully understood how iron overload can elicit neuronal cell damage. Here we examined mitochondrial reactive oxygen species (ROS) levels in human dopaminergic neuroblastoma SH-SY5Y cells upon iron exposure. A relatively high concentration of iron could significantly increase mitochondrial ROS levels in SH-SY5Y cells. Pharmacological activation of AMP-activated protein kinase (AMPK) almost completely inhibited the effect of iron on mitochondrial ROS. By contrast, AMPK inhibition aggravated the neurotoxicity of iron and enhanced the production of mitochondrial ROS. Collectively, these findings suggested that excess iron may be able to perturb mitochondrial function, and AMPK activity is important for the association of iron and mitochondria.
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