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Effect of physiological concentrations of vitamin C on gastric cancer cells and Helicobacter pylori

Digestive Diseases Research Centre, St Bartholomew's and the Royal London School of Medicine and Dentistry, London, UK

Correspondence to:
Correspondence to:
Dr Z W Zhang, Level 7, Bristol Royal Infirmary, University of Bristol, Bristol BS2 8HW, UK;
z.w.zhang{at}bristol.ac.uk

Background: Gastric juice vitamin C may be protective against gastric carcinogenesis but concentrations are significantly reduced by Helicobacter pylori infection. We investigated the in vitro effects of vitamin C at concentrations comparable with those found in gastric juice on gastric cancer cells and H pylori.

Methods: Gastric cancer cell lines and various H pylori strains were treated with L-ascorbic acid for up to 72 hours. Cell viability, and protein and DNA synthesis were determined. Flow cytometry was used for assessment of H pylori adherence, cell cycle distribution, and apoptosis. H pylori growth and its haemagglutination activity were determined using viability count and microtitration assay.

Results: Vitamin C induced a significant dose dependent growth inhibition of gastric AGS and MKN45 cells but this effect was significantly reduced at levels similar to those in gastric juice of H pylori infected patients (<50 µM). Although vitamin C had no obvious effect on H pylori growth, haemagglutination activity, or adherence ability to gastric AGS cells compared with untreated controls, it significantly enhanced H pylori associated apoptosis and induced cell cycle arrest in these cells.

Conclusion: Vitamin C may inhibit gastric cancer cell growth and alter H pylori induced cell cycle events at concentrations comparable with those in gastric juice, but has no effect on H pylori growth or pathogenicity. However, the inhibitory effect on gastric cancer cells was lost at vitamin C concentrations found in patients with H pylori infection.

Keywords: Helicobacter pylori; vitamin C; gastric cancer

Abbreviations: BrdU, bromodeoxyuridine; DHA, dehydroascobic acid; FITC, fluorescein isothiocyanate; NOC, N-nitroso compounds; PBS, phosphate buffered saline; RBCs, red blood cells; ROM, reactive oxygen metabolites

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