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

Published online by Cambridge University Press:  09 March 2007

K. L. M. White*
Affiliation:
Molecular Epidemiology Unit, Epidemiology and Health Services Research, University of Leeds, Leeds LS2 9JT, UK
D. M. Chalmers
Affiliation:
The Centre for Digestive Diseases, The General Infirmary at Leeds, Great George Street, Leeds LS1 3EX, UK
I. G. Martin
Affiliation:
The Centre for Digestive Diseases, The General Infirmary at Leeds, Great George Street, Leeds LS1 3EX, UK
S. M. Everett
Affiliation:
The Centre for Digestive Diseases, The General Infirmary at Leeds, Great George Street, Leeds LS1 3EX, UK
P. M. Neville
Affiliation:
The Centre for Digestive Diseases, The General Infirmary at Leeds, Great George Street, Leeds LS1 3EX, UK
G. Naylor
Affiliation:
The Centre for Digestive Diseases, The General Infirmary at Leeds, Great George Street, Leeds LS1 3EX, UK
A. E. Sutcliffe
Affiliation:
Molecular Epidemiology Unit, Epidemiology and Health Services Research, University of Leeds, Leeds LS2 9JT, UK
M. F. Dixon
Affiliation:
The Centre for Digestive Diseases, The General Infirmary at Leeds, Great George Street, Leeds LS1 3EX, UK
P. C. Turner
Affiliation:
Molecular Epidemiology Unit, Epidemiology and Health Services Research, University of Leeds, Leeds LS2 9JT, UK
C. J. Schorah
Affiliation:
Molecular Epidemiology Unit, Epidemiology and Health Services Research, University of Leeds, Leeds LS2 9JT, UK
*
*Corresponding author:K. L. M. White, fax +44 113 233 6603, email [email protected]
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Abstract

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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.

Type
Research Article
Copyright
Copyright © The Nutrition Society 2002

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