Journal
BIOMETALS
Volume 22, Issue 5, Pages 855-862Publisher
SPRINGER
DOI: 10.1007/s10534-009-9214-7
Keywords
Iron; Reactive oxygen species; Signal transduction; Apoptosis
Categories
Funding
- NIH [DK056160, DK064750, ES014638, T90 DK070078, T32 ES007155]
- Milton Fund (Harvard University)
- FAPESP (Brazil)
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Reactive oxygen species (ROS) display cytotoxicity that can be exacerbated by iron. Paradoxically, HeLa cells treated with the ROS-generators menadione and 2,3-dimethoxy-1,4-naphthoquinone display increased free labile iron. HeLa cells exposed to ROS undergo apoptosis but iron chelation limits the extent of cell death suggesting the rise in intracellular iron plays a signaling role in this pathway. This idea is supported by the fact that iron chelation also alters the pattern of ROS-induced phosphorylation of stress-activated protein kinases SAPK/JNK and p38 MAPK. Thus, ROS-induced increases in cellular free iron contribute to signaling events triggered during oxidative stress response.
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