Induction of differentiation and apoptosis by sodium selenite in human colonic carcinoma cells (HT29)

M S Stewart; R L Davis; L P Walsh; B C Pence

doi:10.1016/s0304-3835(97)00212-7

Induction of differentiation and apoptosis by sodium selenite in human colonic carcinoma cells (HT29)

Cancer Lett. 1997 Jul 15;117(1):35-40. doi: 10.1016/s0304-3835(97)00212-7.

Authors

M S Stewart¹, R L Davis, L P Walsh, B C Pence

Affiliation

¹ Department of Pathology, Texas Tech University Health Sciences Center, Lubbock 79430, USA.

PMID: 9233829
DOI: 10.1016/s0304-3835(97)00212-7

Abstract

To explore the mechanism(s) by which selenium (Se) exerts its cancer chemopreventive activity, we studied the effect of selenite (0-100 microM) on cell growth, viability, differentiation, detachment, DNA fragmentation and apoptosis in human colonic carcinoma cells (HT29). Selenite (>5 microM) decreased cell growth, increased cell detachment and decreased intracellular levels of reduced glutathione (GSH), whereas >10 microM selenite induced cell differentiation and apoptosis. The chemopreventive effects of selenite may be related in part to the generation of reactive oxygen species (ROS) resulting from the reaction between selenite and GSH.

Publication types

Research Support, Non-U.S. Gov't

MeSH terms

Apoptosis / drug effects*
Cell Adhesion / drug effects
Cell Differentiation / drug effects*
Glutathione / metabolism
HT29 Cells
Humans
Oxidation-Reduction
Sodium Selenite / pharmacology*

Substances

Glutathione
Sodium Selenite