Biomol Ther.  2014 Nov;22(6):503-509. 10.4062/biomolther.2014.115.

Paraquat Induces Apoptosis through Cytochrome C Release and ERK Activation

• Seo HJ
• Choi SJ
• Lee JH

• KMID: 2170591
• DOI: http://doi.org/10.4062/biomolther.2014.115

Abstract

Paraquat has been suggested to induce apoptosis by generation of reactive oxygen species (ROS). However, little is known about the mechanism of paraquat-induced apoptosis. Here, we demonstrate that extracellular signal-regulated protein kinase (ERK) is required for paraquat-induced apoptosis in NIH3T3 cells. Paraquat treatment resulted in activation of ERK, and U0126, inhibitors of the MEK/ERK signaling pathway, prevented apoptosis. Moreover, paraquat-induced apoptosis was associated with cytochrome C release, which could be prevented by treatment with the MEK inhibitors. Taken together, our findings suggest that ERK activation plays an active role in mediating paraquat-induced apoptosis of NIH3T3 cells.

Keyword

Paraquat; NIH3T3 cells; ERK1/2; Apoptosis; Cytochrome C; MAPK

MeSH Terms

Apoptosis*
Cytochromes c*
Negotiating
Paraquat*
Protein Kinases
Reactive Oxygen Species
Cytochromes c
Paraquat
Protein Kinases
Reactive Oxygen Species