Colorectal Cancer
Copyright ©The Author(s) 2005. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Jul 14, 2005; 11(26): 3990-3997
Published online Jul 14, 2005. doi: 10.3748/wjg.v11.i26.3990
Hydrogen sulfide protects colon cancer cells from chemopreventative agent β-phenylethyl isothiocyanate induced apoptosis
Peter Rose, Philip K Moore, Shen Han Ming, Ong Choon Nam, Jeffrey S Armstrong, Matt Whiteman
Peter Rose, Jeffrey S Armstrong, Matt Whiteman, Department of Biochemistry, National University of Singapore, 8 Medical Drive, 117597, Singapore
Philip K Moore, Department of Pharmacology, National University of Singapore, 18 Medical Drive, 117597 Singapore
Shen Han Ming, Ong Choon Nam, Department of Community, Occupational and Family Medicine, National University of Singapore, 16 Medical Drive, 117597, Singapore
Author contributions: All authors contributed equally to the work.
Correspondence to: Dr. Peter Rose, Department of Biochemistry, National University of Singapore, 8 Medical Drive, 117597, Singapore. bchpcr@nus.edu.sg
Telephone: +65-6874-4996
Received: August 25, 2004
Revised: September 10, 2004
Accepted: September 15, 2004
Published online: July 14, 2005
Abstract

AIM: Hydrogen sulfide (H2S) is a prominent gaseous constituent of the gastrointestinal (GI) tract with known cytotoxic properties. Endogenous concentrations of H2S are reported to range between 0.2-3.4 mmol/L in the GI tract of mice and humans. Considering such high levels we speculate that, at non-toxic concentrations, H2S may interact with chemical agents and alter the response of colonic epithelium cells to such compounds. The GI tract is a major site for the absorption of phytochemical constituents such as isothiocyanates, flavonoids, and carotenoids, with each group having a role in the prevention of human diseases such as colon cancer. The chemopreventative properties of the phytochemical agent β-phenyethyl isothiocyanate (PEITC) are well recognized. However, little is currently known about the physiological or biochemical factors present in the GI tract that may influence the biological properties of ITCs. The current study was undertaken to determine the effects of H2S on PEITC mediated apoptosis in colon cancer cells.

METHODS: Induction of apoptosis by PEITC in human colon cancer HCT116 cells was assessed using classic apoptotic markers namely SubG1 population analysis, caspase-3 like activity and nuclear fragmentation and condensation coupled with the MTT [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrasodium bromide] viability assay and LDH leakage.

RESULTS: PEITC significantly induced apoptosis in HCT116 cells as assessed by SubG1 population formation, nuclear condensation, LDH leakage and caspase-3 activity after 24 h, these data being significant from control groups (P < 0.01). In contrast, co-treatment of cells with physiological concentrations of H2S (0.1-1 mmol/L) prevented PEITC mediated apoptosis as assessed using the parameters described.

CONCLUSION: PEITC effectively induced cell death in the human adenocarcinoma cell line HCT116 in vitro through classic apoptotic mechanisms. However, in the presence of H2S, apoptosis was abolished. These data suggest that H2S may play a significant role in the response of colonic epithelial cells to beneficial as well as toxic agents present within the GI tract.

Keywords: Apoptosis; Colon cancer; Hydrogen sulfide; β-phenylethyl isothiocyanate