Exp Clin Endocrinol Diabetes 2010; 118(7): 410-419
DOI: 10.1055/s-0029-1225615
Article

© J. A. Barth Verlag in Georg Thieme Verlag KG Stuttgart · New York

Antiproliferative/Cytotoxic Activity of Molecular Iodine and Iodolactones in Various Human Carcinoma Cell Lines. No Interfering with EGF-signaling, but Evidence for Apoptosis

H. Rösner1 , P. Torremante2 , W. Möller1 , R. Gärtner3
  • 1Institut für Zoologie, Universität Hohenheim-Stuttgart, Stuttgart, Germany
  • 2Praxis für Gynäkologie und Geburtshilfe, Ochsenhausen, Germany
  • 3Medizinische Klinik, Universität München, München, Germany
Further Information

Publication History

received 18.02.2009 first decision 24.04.2009

accepted 04.06.2009

Publication Date:
02 October 2009 (eFirst)

Abstract

Twelve human cancer cell lines and one non-malignant cell line were investigated with respect to a potential antiproliferative/cytotoxic activity of molecular iodine and iodolactones. Except CCL221 colon carcinoma cells, the growth of all cancer cell lines decreased if the cells were cultured in the presence of 10 μM molecular iodine (I2) for at least two days. δ-iodolactone (IL, 5 μM) was found to have a similar effect. SH-SY5Y neuroblastoma cells turned out to be most susceptible to both iodine compounds (total inhibition), followed by MCF-7 mammary carcinoma cells (60% and 77.7% inhibition in the presence of I2 respect. IL) and HS24 lung carcinoma cells (36.3% respect. 40.3% inhibition). In contrast, MCF-10 normal mammary epithelial cells were much less affected by the iodine treatment. In both, SH-SY5Y and MCF-7 cells, I2 and IL also abolished EGF-induced promotion of cell growth completely. This effect was, however, not due to an interfering with EGF-signaling, because I2 and IL did not affect the phosphorylation of EGF-receptors, EGF-induced activation of MAP-kinase (Erk1/2), or EGF-induced lamellar actin protrusion. A disruption by molecular iodine of mitochondrial transmembrane electrical potential, which was prevented by a pre-treatment of the cells with N-acetyl-cysteine, supports a mitochondria-mediated apoptotic mechanism.

References

Correspondence

Prof. Dr. H. Rösner

Institute of Zoology

Cell- and Neurobiology

University of Hohenheim-Stuttgart

Garbenstraße 30

70593 Stuttgart

Germany

Phone: +49/711/459 225 25

Fax: +49/711/459 234 50

Email: roesnerh@uni-hohenheim.de