Calcium Signaling Is Involved in Cadmium-Induced Neuronal Apoptosis via Induction of Reactive Oxygen Species and Activation of MAPK/mTOR Network
2011

Calcium Signaling and Cadmium-Induced Neuronal Apoptosis

publication 10 minutes Evidence: moderate

Author Information

Author(s): Xu Baoshan, Chen Sujuan, Luo Yan, Chen Zi, Liu Lei, Zhou Hongyu, Chen Wenxing, Shen Tao, Han Xiuzhen, Chen Long, Huang Shile

Primary Institution: Louisiana State University Health Sciences Center

Hypothesis

Cadmium (Cd) induces neuronal apoptosis through calcium signaling and activation of MAPK/mTOR pathways.

Conclusion

Cadmium elevates intracellular calcium levels, which induces reactive oxygen species and activates MAPK and mTOR pathways, leading to neuronal apoptosis.

Supporting Evidence

  • Cadmium exposure leads to increased intracellular calcium levels in neuronal cells.
  • Calcium chelators prevented cadmium-induced cell death.
  • Cadmium activates MAPK and mTOR pathways through calcium signaling.
  • Reactive oxygen species are induced by cadmium and contribute to neuronal apoptosis.
  • Calmodulin antagonists reduced cadmium's effects on neuronal cells.

Takeaway

Cadmium is a toxic metal that can cause brain cell death by messing with calcium levels in cells, which leads to harmful reactions.

Methodology

The study used PC12, SH-SY5Y cells, and primary murine neurons to investigate the effects of cadmium on calcium signaling and apoptosis through various assays including calcium detection and Western blotting.

Limitations

The study primarily focused on in vitro models, which may not fully replicate in vivo conditions.

Statistical Information

P-Value

p<0.05

Statistical Significance

p<0.05

Digital Object Identifier (DOI)

10.1371/journal.pone.0019052

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