Dietary antioxidants protect gut epithelial cells from oxidant-induced apoptosis: green tea, cat's claw, ascorbic acid

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*Dietary antioxidants protect gut epithelial cells from oxidant-induced

apoptosis

* MJ, Angeles FM, Reuter BK, Bobrowski P, Sandoval M.

Center for Cardiovascular Sciences, Albany Medical College, Albany, New

York, USA. millermj@...

BMC Complement Altern Med. 2001;1:11

http://www.biomedcentral.com/1472-6882/1/11

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 microM), H2O2 (50 microM), peroxynitrite

(300 microM) - followed by incubation for 24 hours, with antioxidants

(10 microg/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

microM) or H2O2 (50 microM) 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.

PMID: 11749672