British Journal of Nutrition

Research Article

Dietary antioxidants and DNA damage in patients on long-term acid-suppression therapy: a randomized controlled study

K. L. M. Whitea1 c1, D. M. Chalmersa2, I. G. Martina2, S. M. Everetta2, P. M. Nevillea2, G. Naylora2, A. E. Sutcliffea1, M. F. Dixona2, P. C. Turnera1 and C. J. Schoraha1

a1 Molecular Epidemiology Unit, Epidemiology and Health Services Research, University of Leeds, Leeds LS2 9JT, UK

a2 The Centre for Digestive Diseases, The General Infirmary at Leeds, Great George Street, Leeds LS1 3EX, UK


Free radicals and reactive species produced in vivo can trigger cell damage and DNA modifications resulting in carcinogenesis. Dietary antioxidants trap these species limiting their damage. The present study evaluated the role of vitamins C and E in the prevention of potentially premalignant modifications to DNA in the human stomach by supplementing patients who, because of hypochlorhydria and possible depletion of gastric antioxidants, could be at increased risk of gastric cancer. Patients undergoing surveillance for Barrett's oesophagus (n 100), on long-term proton pump inhibitors were randomized into two groups: vitamin C (500 mg twice/d) and vitamin E (100 mg twice/d) for 12 weeks (the supplemented group) or placebo. Those attending for subsequent endoscopy had gastric juice, plasma and mucosal measurements of vitamin levels and markers of DNA damage. Seventy-two patients completed the study. Plasma ascorbic acid, total vitamin C and vitamin E were elevated in the supplemented group consistent with compliance. Gastric juice ascorbic acid and total vitamin C levels were raised significantly in the supplemented group (P=0·01) but supplementation had no effect on the mucosal level of this vitamin. However, gastric juice ascorbic acid and total vitamin C were within normal ranges in the unsupplemented group. Mucosal malondialdehyde, chemiluminescence and DNA damage levels in the comet assay were unaffected by vitamin supplementation. In conclusion, supplementation does not affect DNA damage in this group of patients. This is probably because long-term inhibition of the gastric proton pump alone does not affect gastric juice ascorbate and therefore does not increase the theoretical risk of gastric cancer because of antioxidant depletion.

(Received September 20 2001)

(Revised March 13 2002)

(Accepted April 08 2002)


c1 *Corresponding author:K. L. M. White, fax +44 113 233 6603, email