Thimerosal-induced apoptosis in human SCM1 gastric cancer cells: Activation of p38 MAP kinase and caspase-3 pathways without involvement of [Ca2+]i elevation

Shiuh Inn Liu, Chorng Chih Huang, Chun Jen Huang, Being Whey Wang, Po Min Chang, Yi Chien Fang, Wei Chuan Chen, Jue Long Wang, Yih Chau Lu, Sau Tung Chu, Chiang Ting Chou, Chung Ren Jan*

*Corresponding author for this work

Research output: Contribution to journalJournal Article peer-review

30 Scopus citations

Abstract

Thimerosal is a mercury-containing preservative in some vaccines. The effect of thimerosal on human gastric cancer cells is unknown. This study shows that in cultured human gastric cancer cells (SCM1), thimerosal reduced cell viability in a concentration- and time-dependent manner. Thimerosal caused apoptosis as assessed by propidium iodide-stained cells and caspase-3 activation. Although immunoblotting data revealed that thimerosal could activate the phosphorylation of extracellular signal-regulated kinase, c-Jun NH2-terminal protein kinase, and p38 mitogen-activated protein kinase (p38 MAPK), only SB203580 (a p38 MAPK inhibitor) partially prevented cells from apoptosis. Thimerosal also induced [Ca2+]i increases via Ca2+ influx from the extracellular space. However, pretreatment with (bis(o-aminophenoxy)ethane-N,N,N′, N′-tetraacetate)/AM, a Ca2+ chelator, to prevent thimerosal-induced [Ca2+]i increases did not protect cells from death. The results suggest that in SCM1 cells, thimerosal caused Ca2+-independent apoptosis via phosphorylating p38 MAPK resulting in caspase-3 activation.

Original languageEnglish
Pages (from-to)109-117
Number of pages9
JournalToxicological Sciences
Volume100
Issue number1
DOIs
StatePublished - 11 2007
Externally publishedYes

Keywords

  • Apoptosis
  • Caspase-3
  • Gastric cancer cells
  • MAPKs
  • Thimerosal

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