Research article

Dietary antioxidants protect gut epithelial cells from oxidant-induced apoptosis

Mark JS Miller¹ , Fausto M Angeles¹ , Brian K Reuter¹ , Paul Bobrowski² and Manuel Sandoval¹

¹Center for Cardiovascular Sciences, Albany Medical College, Albany, New York, USA

²Rainforest Phytoceuticals, LLC, Delmar, New York, USA

author email corresponding author email

BMC Complementary and Alternative Medicine 2001, 1:11doi:10.1186/1472-6882-1-11

Published:	10 December 2001

Abstract

Background

The potential of ascorbic acid and two botanical decoctions, green tea and cat's claw, to limit cell death in response to oxidants were evaluated in vitro.

Methods

Cultured human gastric epithelial cells (AGS) or murine small intestinal epithelial cells (IEC-18) were exposed to oxidants – DPPH (3 μM), H₂O₂ (50 μM), peroxynitrite (300 μM) – followed by incubation for 24 hours, with antioxidants (10 μg/ml) administered as a 1 hour pretreatment. Cell number (MTT assay) and death via apoptosis or necrosis (ELISA, LDH release) was determined. The direct interactions between antioxidants and DPPH (100 μM) or H₂O₂ (50 μM) were evaluated by spectroscopy.

Results

The decoctions did not interact with H₂O₂, but quenched DPPH although less effectively than vitamin C. In contrast, vitamin C was significantly less effective in protecting human gastric epithelial cells (AGS) from apoptosis induced by DPPH, peroxynitrite and H₂O₂ (P < 0.001). Green tea and cat's claw were equally protective against peroxynitrite and H₂O₂, but green tea was more effective than cat's claw in reducing DPPH-induced apoptosis (P < 0.01). Necrotic cell death was marginally evident at these low concentrations of peroxynitrite and H₂O₂, and was attenuated both by cat's claw and green tea (P < 0.01). In IEC-18 cells, all antioxidants were equally effective as anti-apoptotic agents.

Conclusions

These results indicate that dietary antioxidants can limit epithelial cell death in response to oxidant stress. In the case of green tea and cat's claw, the cytoprotective response exceed their inherent ability to interact with the injurious oxidant, suggestive of actions on intracellular pathways regulating cell death.