**9. References**


Interestingly, Sørensen et al. reported that the effect of vegetable consumption was associated with the *OGG1* Ser326Cys polymorphism [58]. A non-synonymous (associated with an amino acid change) genetic polymorphism at codon 326, Ser326Cys, in the *OGG1* gene is a strong candidate as a genetic factor for cancer risk [59, 60]. In fact, the OGG1 Ser326Cys enzyme exhibited functional defects [61]. OGG1 Ser326Cys excised 8-oxo-Gua from duplex DNA and cleaved abasic sites at rates 2- to 6-fold lower than those of the wildtype enzyme. Yamane et al. reported that 8-oxo-Gua-induced mutations were more efficiently suppressed in OGG1-Ser326 transduced cells than OGG1-Cys326 transduced cells, suggesting that OGG1-Cys326 has reduced ability to prevent mutagenesis by 8-oxo-Gua than OGG1-Ser326 *in vivo* in human cells [62]. Sørensen et al. observed a 54% decrease in lung cancer risk per 50% increase in vegetable intake among homozygous Cys326Cys carriers, and no decrease in risk among carriers of Ser326Ser or Ser326Cys. Therefore, to evaluate the effect of food factors on carcinogenesis, the OGG1 polymorphism should be

As described above, dietary factors influence 8-oxo-Gua generation and its repair systems in a variety of manners. They may contribute to human diseases, including cancer, by causing DNA damage and affecting DNA repair systems. The effects of food factors on the generation of 8-oxo-Gua and the expression of OGG1 must be further clarified, to reduce the

In addition, DNA double-strand break (DAB) is also a well-known DNA damage. Datta *et al*. reported that 8-oxo-formation was associated with 125I-induced double-strand break (DSB) formation. Therefore, analyses of food factors and DSB formation should be interested

The authors thank INTECH OPEN ACCESS PUBLISHER, for inviting us to write this review article, and Elsevier LTD, Blackwell Publishing, and Wiley-Blackwell, for permission to

[1] K.C. Cheng, D.S. Cahill, H. Kasai, S. Nishimura, and L.A. Loeb, "8-Hydroxyguanine, an

[2] T. Tsuzuki, Y. Nakatsu, and Y. Nakabeppu, "Significance of error-avoiding mechanisms

[3] L.J. Marnett, "Oxyradicals and DNA damage," *Carcinogenesis*, vol. 21, pp. 361-370,

abundant form of oxidative DNA damage, causes G-T and A-C substitutions,"

for oxidative DNA damage in carcinogenesis," *Cancer Sciences*, vol. 98, pp. 465-470,

risk of food factor-related diseases, such as cancer or diabetes.

reproduce the material in references [37], [53], and [56], respectively.

*Journal of Biological Chemistry*, vol. 267, pp. 166-172, 1992.

**6. Dietary factors and OGG1 polymorphism** 

considered.

**7. Conclusions** 

as a further study [63].

**9. References** 

2007.

2000.

**8. Acknowledgements** 


Food Factors and Oxidative DNA Damage / DNA Repair Systems 557

[25] M. Wu, J.K. Zhao, X.S. Hu, P.H. Wang, Y. Qin, Y.C. Lu, J. Yang, A.M. Liu, D.L. Wu,

[26] A.L. Klatsky, M.A. Armstrong, and G.D.Friedman, "The relations of alcoholic beverage

[27] J. Ho, T. Lam, and L. Chiu, "Smoking, drinking and colorectal cancer in Hong Kong

[28] J.C. Anderson, Z. Alpern, G. Sethi, C.R. Messina, C. Martin, P.M. Hubbard, R.

[29] P.M. Webb, D.M. Purdie, C.J. Bain, and A.C. Green, "Alcohol, wine, and risk of

[30] N.C. Briggs, R.S. Levine, L.D. Bobo, W.P. Haliburton, E.A. Brann, and C.H. Hennekens,

[31] S. Dragoni, J. Gee, R. Bennett, M. Valoti, and G. Sgaragli, "Red wine alcohol promotes

[32] Y. Wang, K.W. Lee, F.L. Chan, S. Chen, and L.K. Leung, "The red wine polyphenol

[33] S. Mahabir, M.F. Leitzmann, M.J. Virtanen, J. Virtamo, P. Pietinen, D. Albanes, and P.R.

[34] S. Petti and C. Scully, "Association between different alcoholic beverages and

[35] B.M. Arendt, S. Ellinger, K. Kekic, L. Geus, R. Fimmers, U. Spengler, W.U. Müller, and

[36] R.A.A. Caccetta, V. Burke, V.B. Mori, L.J. Beilin, I.B. Puddey, and K.D. Croft, "Red

study," *European Journal of Cancer*, vol. 42, pp. 521-527, 2006.

*Gastroenterology*, vol. 100, pp. 2049-2055, 2005.

*Toxicological Sciences*, vol. 92, pp. 71-77, 2006.

1693, 2006.

1015, 1988.

pp. 592-599, 2004.

771, 2006.

pp. 170-175, 2005.

2005.

vol. 156, pp. 454-462, 2002.

2004.

Z.F. Zhang, K.J. Frans, and P. van't Veer, "Association of smoking, alcohol drinking and dietary factors with esophageal cancer in high- and low-risk areas of Jiangsu Province, China," *World Journal of Gastroenterology*, vol. 12, pp. 1686-

use to colon and rectal cancer," *American Journal of Epidemiology*, vol. 128, pp. 1007-

Chinese: A case control study," *International Journal of Cancer*, vol. 109, pp. 587-597,

Grimson, P.F. Ells, and R.D. Shaw, "Prevalence and risk of colorectal neoplasia in consumers of alcohol in a screening population," *The American Journal of* 

epithelial ovarian cancer," *Cancer Epidemiology, Biomarkers, and Prevention*, vol. 13,

"Wine drinking and risk of non-Hodgkin's lymphoma among men in the United States: A population-based case-control study," *American Journal of Epidemiology*,

quercetin absorption and directs its metabolism towards isorhamnetin and tamarixetin in rat intestine *in vitro*," *British Journal of Pharmacology*, vol. 147, pp. 765-

resveratrol displays bilevel inhibition on aromatase in breast cancer cells,"

Taylor, "Prospective study of alcohol drinking and renal cell cancer risk in a cohort of Finnish male smokers," *Cancer Epidemiology, Biomarkers, and Prevention*, vol. 14,

leukoplakia among non- to moderate-drinking adults: A matched case-control

R. Goerich, "Single and repeated moderate consumption of native or dealcoholized red wine show different effects on antioxidant parameters in blood and DNA strand breaks in peripheral leukocytes in healthy volunteers: a randomized controlled trial (ISRCTN68505294)," *Nutrition Journal*, vol. 14, p. 33,

wine polyphenols, in the absence of alcohol, reduce lipid peroxidative stress


[15] R. Lu, H.M. Nash, and G.L. Verdine, "A mammalian DNA repair enzyme that excises

[16] T.A. Rosenquist, D.O. Zharkov, and A.P. Grollman, "Cloning and characterization

[17] T. Roldán-Arjona, Y.F. Wei, K.C. Carter, A. Klungland, C. Anselmino, R.P. Wang, M.

[18] J.P. Radicella, C. Dherin, C. Desmaze, M.S. Fox, and S. Boiteux, "Cloning and

[19] M. Bjoräs, L. Luna, B. Johnson, E. Hoff, T. Haug, T. Rongnes, and E. Seeberg, "Opposite

[20] K, Arai, K. Morishita, K. Shinmura, T. Kohno, S.R. Kim, T. Nohmi, M. Taniwaki, S.

[21] H. Aburatani, Y. Hippo, T. Ishida, R. Takashima, C. Matsuba, T. Kodama, M. Takao, A.

functional mutM homologue," *Cancer Research*, vol. 57, pp. 2151-2156, 1997. [22] T. Hirano, K. Higashi, A. Sakai, Y. Tsurudome, Y. Ootsuyama, R. Kido, and H. Kasai,

[23] S.A. Smith-Warner, D. Spiegelman, S.S. Yaun, P.A. van den Brandt, A.R. Folsom,

[24] R.Z. Stolzenberg-Solomon, S.C. Chang, M.F. Leitzmann, K.A. Johnson, C. Johnson, S.S.

*Current Biology*, vol. 7, pp. 397-407, 1997.

*America*, vol. 94, pp. 8016-8020, 1997.

*America*, vol. 94, pp. 8010-8015, 1997.

*Research*, vol. 91, pp. 681-695, 2000.

pp.535-540, 1998.

904, 2006.

pp. 6314-6322, 1997.

2861, 1997.

1997.

oxidatively damaged guanines maps to a locus frequently lost in lung cancer,"

of a mammalian 8-oxoguanine DNA glycosylase," *Proceedings of the National Academy of Sciences of the United States of America*, vol. 94, pp. 7429-7434,

Augustus, and T. Lindahl, "Molecular cloning and functional expression of a human cDNA encoding the antimutator enzyme 8-hydroxyguanine-DNA glycosylase," *Proceedings of the National Academy of Sciences of the United States of* 

characterization of hOGG1, a human homolog of the OGG1 gene of *Saccharomyces cerevisiae*," *Proceedings of the National Academy of Sciences of the United States of* 

base-dependent reactions of a human base excision repair enzyme on DNA containing 7, 8-dihydro-8-oxoguanine and abasic sites," *The EMBO Journal*, vol. 16,

Ohwada, and J. Yokota, "Cloning of a human homolog of the yeast OGG1 gene that is involved in the repair of oxidative DNA damage," *Oncogene*, vol. 14, pp. 2857-

Yasui, K. Yamamoto, M. Asano, K. Fukasawa, T. Yoshinari, H. Inoue, E. Ohtsuka, and S. Nishimura, "Cloning and characterization of mammalian 8 hydroxyguanine-specific DNA glycosylase/apurinic, apyrimidinic lyase, a

"Analyses of oxidative DNA damage and its repair activity in the livers of 3' methyl-4-dimethylaminoazobenzene-treated rodents," *Japanese Journal of Cancer* 

A. Goldbohm, S. Graham, L. Holmberg, G.R. Howe, J.R. Marshall, A.B. Miller, J.D. Potter, F.E. Speizer, W.C. Willett, A. Wolk, and D.J. Hunter, "Alcohol and breast cancer in women; A pooled analysis of cohort studies," *JAMA*, vol. 279,

Buys, R.N. Hoover, and R.G. Ziegler, "Folate intake, alcohol use, and postmenopausal breast cancer risk in the prostate, lung, colorectal, and ovarian cancer screening trial," *The American Journal of Clinical Nutrition*, vol. 83, pp. 895-


Food Factors and Oxidative DNA Damage / DNA Repair Systems 559

[50] B.N. Ames and E.S. Gold, "Environmental pollution, pesticide, and the prevention of cancer: misconceptions," *The FASEB Journal*, vol. 11, pp. 1041-1052, 1997. [51] S.C. Larsson, E. Giovannucci, and A. Wolk, "Coffee consumption and stomach cancer

[52] M. Akagawa, T. Shigemitsu, and K. Suyama, "Production of hydrogen

[53] H. Morii, A. Kuboyama, T. Nakashima, K. Kawai, H. Kasai, K. Tamae, and T.

[54] N. Yoshioka, H. Nakashima, K. Hosoda, Y. Eitaki, N. Shimada, and K. Omae, "Urinary

[55] M.C. Cooke, P.T. Henderson, and M.D. Evans, "Sources of extracellular, oxidatively-

[56] K. Tamae, K. Kawai, S. Yamasaki, K. Kawanami, M. Ikeda, K. Takahashi, T. Miyamoto,

[57] S. Guarrera, C. Sacerdote, L. Fiorini, R. Marsala, S. Polidoro, S. Gamberini, F. Saletta, C.

[58] M. Sørensen, O. Raaschou-Nielsen, R.D. Hansen, A. Tjønneland, K. Overvad, and U.

[59] T. Kohno, K. Shinmura, M. Tosaka, M. Tani, S.R. Kim, H. Sugimura, T. Nohmi, H.

[60] C. Dherin, J.P. Radicella, M. Dizdaroglu, and S. Boiteux, "Excision of oxidatively

[61] J.W. Hill and M. Evans, "Dimerization and opposite base-dependent catalytic

populations," *Nucleic Acids Research*, vol. 27, pp. 4001-4007, 1999.

*Clinical Biochemistry and Nutrition*, vol. 45, pp. 255-270, 2009.

2186-2189, 2006.

pp. H155-H161, 2009.

2640, 2003.

2008.

715-721, 2009.

885-891, 2006.

vol. 98, pp. 525-533, 2007.

34, pp. 1620-1632, 2006.

DNA," *Oncogene*, vol. 16, pp. 3219-3225, 1998.

risk in a cohort of Swedish women," *International Journal of Cancer*, vol. 119, pp.

peroxide by polyphenols and polyphenol-rich beverages under *quasi*-physiological conditions," *Bioscience, Biotechnology, and Biochemistry*, vol. 67, pp. 2632-

Hirano, "Effects of instant coffee consumption on oxidative DNA damage, DNA repair, and redox system in mouse liver," *Journal of Food Sciences*, vol. 74,

excretion of an oxidative stress marker, 8-hydroxyguanine (8-OH-Gua), among nickel-cadmium battery workers," *Journal of Occupational Health*, vol. 50, 229-235,

modified DNA lesions: implications for their measurement in urine," *Journal of* 

N. Kato, and H. Kasai, "Effect of age, smoking and other lifestyle factors on urinary 7-methylguanine and 8-hydroxydeoxyguanosine," *Cancer Sciences*, vol. 100, pp.

Malaveille, G. Talaska, P. Vineis, and G. Matullo, "Expression of DNA repair and metabolic genes in response to a flavonoid-rich diet," *British Journal of Nutrition*,

Vogel, "Interaction between the OGG1 Ser326Cys polymorphism and intake of fruit and vegetables in relation to lung cancer," *Free Radical Research*, vol. 40, pp.

Kasai, and J. Yokota, "Genetic polymorphisms and alternative splicing of the hOGG1 gene, that is involved in the repair of 8-hydroxyguanine in damaged

damaged DNA bases by the human alpha-hOgg1 protein and the polymorphic alpha-hOgg1 (Ser326Cys) protein which is frequently found in human

impairment of polymorphic S326C OGG1 glycosylase," *Nucleic Acids Research*, vol.

in smoking subjects," *Free Radical and Biological Medicine*, vol. 30, pp. 636-642, 2001.


[37] T. Hirano, A. Sakai, Y. Ootsuyama, and H. Kasai, "Chronic alcohol consumption

[38] T. Hirano, Y. Yamaguchi, H. Hirano, and H. Kasai, "8-Hydroxyguanine levels in

[39] T.K. Hazra, J.W. Hill, T. Izumi, and S. Mitra, "Multiple DNA glycosylases for repair of

[40] G.B. Keijzers, C.J. Tack, B.E. De Galan, and P. Smits, "Caffeine can decrease insulin

[41] H. Iso, C. Date, K. Wakai, M. Fukui, A. Tamakoshi, and the JACC Study Group, "The

[42] S. Gallus, M. Bertuzzi, A. Tavani, C. Bosetti, E. Negri, C.L. Vecchia, P. Lagiou, and D.

[43] Y. Kurozawa, I. Ogimoto, A. Shibata, T. Nose, T. Yoshimura, H. Suzuki, R. Sakata, Y.

[44] S.R. Brown, P.A. Cann, and N.W. Read, "Effect of coffee on distal colon function," *Gut*,

[45] K.J. Lee, M. Inoue, T. Otani, M. Iwasaki, S. Sasazuki, S. Tsugami, and the JPHC Study

[46] A. Nehlig and G. Debry, "Potential genotoxic, mutagenic and antimutagenic effects of

[47] S.C. Larsson, L. Bergkvist, E. Giovannucci, and A. Wolk, "Coffee consumption

[48] T. Naganuma, S. Kuriyama, M. Akhter, M. Kakizaki, N. Nakaya, K. Matsuda-Ohmori,

[49] M. Nagao, Y. Fujita, K. Wakabayashi, H. Nukaya, T. Kosuge, and T. Sugimura,

coffee: a review," *Mutation Research*, vol. 317, pp. 145-162, 1994.

*Research Communications*, vol. 387, pp. 316-320, 2009.

*Research and Molecular Biology*, vol. 68, pp. 193-205, 2001.

sensitivity in humans," *Diabetes Care*, vol. 25, pp. 364-369, 2002.

*Gerontology*, vol. 51A, pp. B303-B307, 1996.

*Journal of Cancer*, vol. 87, pp. 956-959, 2002.

2001.

554-562, 2006.

vol. 93, pp. 607-610, 2005.

vol. 31, pp. 450-453, 1990.

vol. 121, pp. 1312-1318, 2007.

2006.

pp. 1542-1547, 2007.

67, pp. 89-91, 1986.

in smoking subjects," *Free Radical and Biological Medicine*, vol. 30, pp. 636-642,

prevents 8-hydroxyguanine accumulation in 3'-methyl-4 dimethylaminoazobenzene-treated mouse liver," *Biochemical and Biophysical* 

nuclear DNA and its repair activity in rat organs associated with age," *Journal of* 

8-oxoguanine and their potential in vivo functions," *Progress in Nucleic Acid* 

relationship between green tea and total caffeine intake and risk for self-reported type 2 diabetes among Japanese adults," *Annals of Internal Medicine*, vol. 144, pp.

Trichopoulos, "Does coffee protect against hepatocellular carcinoma?," *British* 

Fujita, S. Ichikawa, N. Iwai, and A. Tamakoshi, "Coffee and risk of death from hepatocellular carcinoma in a large cohort study in Japan," *British Journal of Cancer*,

Group, "Coffee consumption and risk of colorectal cancer in a population-based prospective cohort of Japanese men and women," *International Journal of Cancer*,

and incidence of colorectal cancer in two prospective cohort studies of Swedish women and men," *American Journal of Epidemiology*, vol. 163, pp. 638-644,

T. Shimazu, A. Fukao, and I. Tsuji, "Coffee consumption and the risk of colorectal cancer: a prospective cohort study in Japan," *International Journal of Cancer*, vol. 120,

"Mutagens in coffee and other beverages," *Environmental Health Perspectives*, vol.


**26** 

Ronald W. Pero

*Sweden* 

**Enhancing DNA Repair by Combining only** 

Here this presentation embraces dietary supplement compositions containing resveratrol material, carotenoid material, nicotinamide material, DMAE material, zinc source material, and qjuinic acid-containing material , where no other known bioactive nutrient agents having competing modes of action to these specified agents are intentionally excluded from mixtures containing at least two of these DNA repair enhancing ingredients. The compositions may be embodied in formulations for oral administration, or alternatively, in

The combined composition may be selected from the group consisting of resveratrol (3, 5, 4' trihydroxy-stilbene or an equivalent polyphenol in pure chemical form); the carotenoid material may be alpha carotene, beta carotene, canthaxanthin, lycopene and mixtures thereof; the nicotinamide material may be selected from the group consisting of nicotinamide, niacin, and mixtures thereof; the DMAE material selected from a group consisting of other choline analogs that pass the blood brain barrier; the zinc source material may be one or more zinc salts; and the quinic acid-containing material selected from a group consisting of quinic acid compounds that can enhance DNA repair by enhancing the uptake

of tryptophan and nicotinamide ingredients (Pero et al 2009b; Pero and Lund 2011).

For human administration, the resveratrol material, carotenoid material, nicotinamide material, zinc source material, DMAE material, and quinic acid material may be present in proportions effective, in combination, to improve resistance to DNA damage, enhance DNA repair capacity, and stimulate immune function in a human subject to whom the composition is administered as a daily dosage (Pero et al 2009b; Pero and Lund 2011). This formulation named Nutra-Reservatrol (Pero and Garret 2010) also contemplates the provision of a method of treating a human or other animal subject, consisting of administering resveratrol material, carotenoid material, nicotinamide material, DMAE material, zinc source material and quinic acid material to the subject to selectively supplement the subject's dietary intake thereof (i.e. without supplementing the dietary intake of any other active nutrient agents having competing modes of action) and repeating

**1. Introduction** 

formulations for peritoneal administration.

the administration on a substantially daily basis.

**Dietary Supplement Ingredients that** 

**do not Metabolically Compete in** 

*Section of Immunology, BMC: D14 Lund University, Lund,* 

**Order to Achieve Synergism** 


[63] K. Datta, P. Jaruga, M. Dizdaroglu, R.D. Neumann, and T.A. Winters, "Molecular analysis of base damage clustering associated with a site-specific radiation-induced DNA double-strand break," *Radiation Research*, vol. 166, pp. 767-781, 2006.
