Depletion of endogenous zinc stores induces oxidative stress and cell death in human melanoma cells.

Emil Rudolf, Miroslav Cervinka

Journal: Acta medica (Hradec Kralove) 2004;47(2):91-6

PMID: 15446356

Abstract

The role of intracellular free zinc and its chelation by TPEN (N,N,N',N'- tetrakis(2-pyridylmethyl)ethylene-diamine) was studied in Bowes human melanoma cells. The content of free Zn pools was determined by fluorescent probe Zinquin. Depletion of zinc triggered apoptosis confirmed by cell blebbing, changes in mitochondrial transmembrane potential and GSH levels, caspase-3 activation and nuclear fragmentation. Apoptosis was only partially prevented by cyclosporin A or N-acetylcystein, suggesting various independent but likely interrelated mechanisms participating in this process.

Address: Charles University in Prague, Faculty of Medicine in Hradec Králové, Department of Medical Biology and Genetics, Czech Republic. [email protected]

Link outs

Free resources

Medical:

https://medlineplus.gov/skincancer.html

Research Materials:

https://antibodies.cancer.gov/detail/CPTC-CASP3-1

MeSH Terms: Apoptosis, Chelating Agents, Ethylenediamines, Humans, Melanoma, Experimental, Membrane Potentials, Mitochondria, Oxidative Stress, Skin Neoplasms, Tumor Cells, Cultured, Zinc