Low dose cadmium poisoning results in sustained ERK phosphorylation and caspase activation

Cadmium poisoning has been known to result in a wide variety of cellular responses, including oxidative stress and kinase activation. It has been reported that ERK is activated following acute cadmium exposure, and this response is commonly seen as a classical ERK survival mechanism. Here, we analyz...

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Bibliographic Details
Published in:Biochemical and biophysical research communications 2006-11, Vol.350 (3), p.803-807
Main Authors: Martin, Patrick, Poggi, Marie Christine, Chambard, Jean Claude, Boulukos, Kim E., Pognonec, Philippe
Format: Article
Language:English
Subjects:
60 APPLIED LIFE SCIENCES
Animals
APOPTOSIS
Apoptosis - drug effects
BIOLOGICAL STRESS
CADMIUM
Cadmium Poisoning - enzymology
Cadmium Poisoning - pathology
Caspase
Caspases - metabolism
Cell death
Cells, Cultured
DAMAGE
Dose-Response Relationship, Drug
DOSES
Enzyme Activation - drug effects
ERK
Extracellular Signal-Regulated MAP Kinases - metabolism
INHIBITION
LEAD
Osteoblasts - drug effects
Osteoblasts - enzymology
Osteoblasts - pathology
PHOSPHORYLATION
Phosphorylation - drug effects
POISONING
Rats
STIMULATION
Sustained activation
TOXICITY
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Summary:Cadmium poisoning has been known to result in a wide variety of cellular responses, including oxidative stress and kinase activation. It has been reported that ERK is activated following acute cadmium exposure, and this response is commonly seen as a classical ERK survival mechanism. Here, we analyzed different cell types for their responses to low concentrations of cadmium poisoning. We found that there is an association between cell susceptibility to cadmium toxicity and ERK activation. This activation is atypical, since it consists of a sustained ERK phosphorylation, that lasts up to 6 days post stimulation. This activation is associated with the appearance of cleaved caspases 8 and 3, processed PARP, and irreversible damage. Pharmacological inhibition of ERK phosphorylation results in the ability of cells to resist cadmium poisoning. Our data indicate that low cadmium concentrations result in an unconventional ERK sustained phosphorylation, which in turn leads to death signaling.
ISSN:0006-291X
1090-2104
DOI:10.1016/j.bbrc.2006.09.126