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The effect of vitamin C or vitamin E supplementation on basal and H2O2-induced DNA damage in human lymphocytes

Published online by Cambridge University Press:  09 March 2007

Lisa A. Brennan
Affiliation:
Cancer and Ageing Research Group, School of Biomedical Sciences, University of Ulster, Coleraine BT52 1SA, Northern Ireland
Gerard M. Morris
Affiliation:
Cancer and Ageing Research Group, School of Biomedical Sciences, University of Ulster, Coleraine BT52 1SA, Northern Ireland
Gillian R. Wasson
Affiliation:
Cancer and Ageing Research Group, School of Biomedical Sciences, University of Ulster, Coleraine BT52 1SA, Northern Ireland
Bernadette M. Hannigan
Affiliation:
Cancer and Ageing Research Group, School of Biomedical Sciences, University of Ulster, Coleraine BT52 1SA, Northern Ireland
Yvonne A. Barnett*
Affiliation:
Cancer and Ageing Research Group, School of Biomedical Sciences, University of Ulster, Coleraine BT52 1SA, Northern Ireland
*
*Corresponding author: Dr Yvonne Barnett, fax +44 (0) 1265 324965, email [email protected]
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Abstract

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There is a wealth of epidemiological information on antioxidants and their possible prevention of disease progression but very little of the research on antioxidants has involved intervention studies. In this study, the potential protective effect of vitamin C or E supplementation in vivo against endogenous and H2O2-induced DNA damage levels in lymphocytes was assessed. The supplementation involved fourteen healthy male and female non-smokers mean age 25·53 (SD 1·82) years, who were asked to supplement an otherwise unchanged diet with 1000 mg vitamin C daily for 42 d or 800 mg vitamin E daily for 42 d. DNA damage in H2O2-treated peripheral blood lymphocytes (PBL) and untreated PBL before and after supplementation, and during a 6-week washout period was assessed using an ELISA. At each sampling time-point, the red cell concentrate activities of superoxide dismutase, catalase and glutathione peroxidase were also determined. Supplementation with vitamin C or vitamin E decreased significantly H2O2-induced DNA damage in PBL, but had no effect on endogenous levels of DNA damage. The activities of the antioxidant enzymes superoxide dismutase and glutathione peroxidase were suppressed during the supplementation period. These supplementation regimens may be used to limit the possible adverse effects of reactive oxygen species (including those produced during the course of an immune response) on lymphocytes in vivo, and so help to maintain their functional capacity.

Type
Research Article
Copyright
Copyright © The Nutrition Society 2000

References

Aebi, ABH (1974) Catalase. In Methods in Enzymatic Analysis, vol 2, pp. 643684 ]Bergmeyer, E, editor]. New York, NY: Academic Press.Google Scholar
Anderson, D, Phillips, BJ, Yu, TW, Ayesh, R and Butterworth, KR (1997) The effects of vitamin C supplementation on biomarkers of oxygen radical generated damage in human volunteers with "low" or "high" cholesterol levels. Environmental and Molecular Mutagenesis 30, 161274.3.0.CO;2-Q>CrossRefGoogle ScholarPubMed
Barnett, YA and Barnett, CR (1998) DNA damage and mutations: Contributors to the age-related alterations to T-cell mediated immune responses. Mechanisms of Ageing and Development 102, 165175.CrossRefGoogle Scholar
Barnett, YA and King, CM (1995) An investigation of in vivo antioxidant status, DNA repair capacity and mutation as a function of age in humans. Mutation Research 338, 115128.CrossRefGoogle ScholarPubMed
Bradford, MM (1976) A rapid and sensitive method for the quantitation of microgram quantities of protein utilising the principle of protein-dye binding. Analytical Biochemistry 72, 248254.CrossRefGoogle ScholarPubMed
Cheeseman, KH (1993) Lipid peroxidation and cancer. In DNA and Free Radicals pp. 211228 ]Halliwell, B & Aruoma, OI, editors]. West Sussex: Ellis Horwood Ltd.Google ScholarPubMed
Cole, J, Waugh, APW & Beare, DM (1991) HPRT mutant frequencies in circulating lymphocytes: population studies using normal donors, exposed groups and cancer prone syndromes. In New Horizons in Biological Dosimetry, pp. 319328 ]Gledhill, BL & Mauro, F, editors]. New York, NY: Wiley–Liss.Google Scholar
Dacie, J & Lewis, SM (1991) Practical Haematology, 7th ed. Edinburgh: Churchill Livingstone U.K. Limited.Google Scholar
Dizdaroglu, M (1993) Chemistry of free radical damage to DNA and nucleoproteins. In DNA and Free Radicals pp. 1941 ]Halliwell, B & Aruoma, OI, editors]. West Sussex: Ellis Horwood Ltd.Google ScholarPubMed
Duthie, SJ, Ma, A, Ross, MA and Collins, AR (1996) Antioxidant supplementation decreases oxidative DNA damage in human lymphocytes. Cancer Research 56, 12911295.Google ScholarPubMed
Fenech, M and Morley, AA (1985) The effect of donor age on spontaneous and induced micronuclei. Mutation Research 148, 99105.CrossRefGoogle ScholarPubMed
Frei, B (1989) Ascorbate is an outstanding antioxidant in human blood plasma. Proceedings of the National Academy of Sciences, USA 86, 63776381.CrossRefGoogle ScholarPubMed
Gregory, SH, Wing, EJ, Hoffman, RA and Simmons, RL (1993) Reactive nitrogen intermediates suppress the primary immunologic response to Listeria. Journal of Immunology 150, 29012909.CrossRefGoogle ScholarPubMed
Helliger, F (1980) Ascorbic acid analysis by LCEC. Current Separations (BAS) 2, 45.Google Scholar
Jones, DG and Suttle, NF (1981) Some effects of copper deficiency on leucocyte function in sheep and cattle. Research Veterinary Science 31, 151156.CrossRefGoogle ScholarPubMed
King, CM, Gillespie, ES, McKenna, PG and Barnett, YA (1994) An investigation of mutation as a function of age in humans. Mutation Research 316, 7990.CrossRefGoogle ScholarPubMed
Ma, L, Hoeijmakers, JHJ and van der Eb, AJ (1995) Mammalian excision repair. Biochimica et Biophysica Acta 124, 137164.Google Scholar
Meneghini, R & Martins, S (1993) Hydrogen peroxide and DNA damage. In DNA and Free Radicals pp. 211228 ]Halliwell, B & Aruoma, OI, editors]. West Sussex: Ellis Horwood Ltd.Google Scholar
Metzger, Z, Hoffeld, JT and Oppenheim, JJ (1980) Macrophage-mediated suppression: Evidence for participation of both hydrogen peroxide and prostaglandins in suppression of murine lymphocyte proliferation. Journal of Immunology 124, 983988.CrossRefGoogle ScholarPubMed
Meyer, M, Schreck, R and Baeuerle, PA (1993) H2O2 and antioxidants have opposite effects on activation of NF-κB and AP-1 in intact cells: AP-1 as secondary antioxidant-responsive. The EMBO Journal 12, 20052015.CrossRefGoogle ScholarPubMed
Moser, U (1987) Uptake of ascorbic acid by leukocytes. Annals of the New York Academy of Science 201, 215.Google Scholar
Packer, L (1992) Interactions among antioxidants in health and disease: Vitamin E and its redox cycle. Proceedings of Society for Experimental Biology 200, 271276.CrossRefGoogle ScholarPubMed
Paglia, DE and Valentine, KJA (1967) Characterisation of erythrocyte glutathione peroxidase. Journal of Laboratory and Clinical Laboratory Medicine 70, 158.Google ScholarPubMed
Pawelec, G, Remarque, E, Barnett, Y and Solana, R (1998) T cells and ageing. Frontiers in Bioscience 3, 3999.CrossRefGoogle Scholar
Pohl, H and Reidy, JA (1989) Vitamin C intake influences the bleomycin-induced chromosome damage assay: implications for detection of cancer susceptibility and chromosome breakages syndromes. Mutation Research 224, 247252.CrossRefGoogle ScholarPubMed
Schraufstätter, I, Hyslop, PA, Jackson, JH and Cochrane, CG (1988) Oxidant-induced DNA damage of target cells. Journal of Clinical Investigation 82, 10401250.CrossRefGoogle ScholarPubMed
Schreck, R, Reiber, P and Baeuerle, PA (1992) Reactive oxygen intermediates as apparently widely used messengers in the activation of the NFκB transcription factor and HIV-1. The EMBO Journal 10, 22472258.CrossRefGoogle Scholar
Singh, NP, Danner, DB, Tice, RR, Pearson, JD, Brant, LJ, Morrell, CH and Schneider, EL (1991) Basal DNA damage in individual human lymphocytes with age. Mutation Research 256, 16.CrossRefGoogle ScholarPubMed
Strain, JJ, Hannigan, BM and McKenna, PG (1991) The pathophysiology of oxidant damage. Journal of Biomedical Sciences 2, 1924.Google Scholar
Sweetman, SF, Strain, JJ and McKelvey-Martin, VJ (1997) Effect of antioxidant supplementation on DNA damage and repair in human lymphoblastoid cells. Nutrition and Cancer 27, 122130.CrossRefGoogle ScholarPubMed
Tates, AD, Van Dam, FJ and Van Mossel, H (1991) Use of the clonal assay for the measurement of frequencies of HPRT mutants in T-lymphocytes from five control populations. Mutation Research 253, 199213.CrossRefGoogle ScholarPubMed
Thurnham, DI, Smith, E and Flora, PS (1988) Concurrent liquid-chromatographic assay of retinol, α-tocopherol, β-carotene, α-carotene, lycopene and β-cryptoxanthin in plasma, with tocopherol acetate as internal standard. Clinical Chemistry 34, 337381.CrossRefGoogle ScholarPubMed
Trainor, KJ, Wigmore, DJA, Chrysostomou, J, Dempsey, R, Seshadri, R and Morley, AA (1984) Mutation frequency in human lymphocytes increases with age. Mechanisms of Ageing and Development 27, 8386.CrossRefGoogle ScholarPubMed
van Loon, AAWM, Groenendijk, RH, Timmerman, AJ, Van der Schans, GP, Lohman, PHM and Baan, RA (1992) Quantitative detection of DNA damage in cells after exposing to ionising radiation by means of an improved immunochemical assay. Mutation Research 274, 1927.CrossRefGoogle Scholar
Vuilleumieur, JP and Keck, E (1989) Fluorometric assay of vitamin C in biological materials using a centrifugal analyser with fluorescence attachment. Journal of Micronutrient Analysis 5, 2534.Google Scholar
Washko, P, Rotrosen, D and Levine, M (1989) Ascorbic acid transport and accumulation in human neutrophils. Journal of Biological Chemistry 264, 1899619002.CrossRefGoogle ScholarPubMed