Abstract
Reactive oxygen and nitrogen species (RONS), including nitric oxide (NO) and superoxide (O2 −), are known to be important signal transduction mediators regulating gene expression, cell differentiation, immune activation, and apoptosis (1). On the other hand, they are potentially toxic to biological systems and chronic production of RONS, in fact, plays causative roles in the onset of a variety of diseases and aging (2). While numerous studies have demonstrated the mutagenicity of RONS (3,4), in most of these experiments target cells or isolated DNA were exposed to chemically generated RONS. The permeation rate and half-life of RONS in vivo are considered to be virtually different from those observed in experiments with the use of RNOS-producing chemicals. Therefore, a model system that can be employed to demonstrate the mutagenic potential of biologically generated RONS needs to be established. In this regard, a co-culture experiment using RONS generating cells, instead of chemically synthesized RONS, may compensate for these insufficient in vitro conditions and thus possibly mimic biological environment in vivo.
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References
Suzuki, Y.J., Forman, H.J. and Sevanian, A. (1997) Oxidants as stimulators of signal transduction. Free Radio. Biol Med., 22, 269–285.
Halliwell, B. and Gutteridge, J.M.C. (1990) The role of free radicals and catalytic metal ions in human diseases: an overview. Methods Enzymol., 186, 1–68.
Palmer, R.M., Ferrige, A.G. and Moncada, S. (1984) Nitric oxide release accounts for the biological activity of endothelial-derived relaxing factor. Nature, 327, 524–526.
Radi, R., Beckmann, J.S., Bush, KM and Freeman, B.A. (1991) Peroxynitrite oxidation of sulfhydryls. The cytotoxic potential of superoxide and nitric oxide. J. Biol. Chem., 266, 4244–4250.
Furchgott. R.F. and Vanhoutte, P.M. (1989) Endothelium-derived relaxing and contracting factors. FASEB J., 3, 2007–2018.
Pedruzzi, E., Fay, M., Elbim, C., Gaudry, M. and Gougerot-Pocidalo, M.A. (2002) Differentiation of PLB- 985 myeloid cells into mature neutrophils, shown by degranulation of terminally differentiated compartments in response to N-formyl peptide and priming of superoxide anion production by granulocyte-macrophage colony-stimulating factor. Br. J. Haematol, 117, 719–726.
Szabo, C. and Ohshima, H. (1997) DNA damage induced by peroxynitrite: Subsequent biological effects. Nitric Oxide, 1, 373–385.
Hsie, A.W., Xu, Z., Yu, Y., Sognier, M.A., Hrelia, P. (1990) Molecular analysis of reactive oxygen species-induced mammalian gene mutation. Teratog. Carcinog. Mutagen., 10, 115–124.
Tindall, K.R., Stankowski, LF. Jr., Machanoff, R. and Hsie, A.W. (1986) Analysis of mutation in pSV2gpt-transformed CHO cells. Mutat. Res., 160, 121–131.
Ariza, M.E. and William, M.V. (1999) Lead and mercury mutagenesis: type of mutation dependent upon metal concentration. J:Biochem. Toxicol, 13, 107–112.
Tindall, K.R. and Stankowski Jr., L.F. (1989) Molecular analysis of spontaneous mutations at the gpt locus in Chinese hamster ovary (AS52) cells. Mutat. Res., 220, 241–253.
Tindall, K.R., Stankowski Jr., LF., Machanoff, R. and Hsie A.W. (1984) Detection of deletion mutations in pS V2gpt-transformed cells. Mol. Cell Biol, 4, 1411–1415.
Ariza, M.E., Obeiyszyn, A.S., Robertson, F.M. and Williams, M.V. (1996) Mutagenic potential of peripheral blood leukocytes: in vivo exposure to the carcinogen 7,12-dimethylbenz[a]anthracene, and the tumor promoter 12–0-tetradecanoylphorbol-13-acetate followed by in vitro co-culture with AS52 cells. Cancer Lett., 106, 9–16.
Kim, H.-W., Murakami, A, Williams M.V., and Ohigashi, H. (2002) Mutagenicity of reactive oxygen and nitrogen species as detected by co-culture of activated inflammatory leukocytes and AS52 cells, Carcinogenesis,in press.
H.-W. Kim, A. Murakami, Y. Nakamura, and H. Ohigashi (2002) Screening of edible Japanese plants for suppressing effects on phorbol ester-induced superoxide generation in differentiated HL-60 cells and AS52 cells, Cancer Lett., 176, 7–16.
Murakami, A., Ohigashi, H. and Koshimizu, K. (1999) Chemoprevention: insights into biological mechanisms and promising food factors., Food Rev. Int., 15, 335–395.
Driscoll, K.E., Deyo, L.C., Carter, J.M., Howard, B.W., Hassenbein, D.G. and Bertram, T.A. (1997) Effects of particle exposure and particle-elicited inflammatory cells on mutation in rat alveolar epithelial cells. Carcinogenesis, 18, 423–430.
Knaapen, A.M, Seiler, F, Schildderman, P.A.E.L., Nehls, P., Bruch, J., Schins, RPF. and Borm, P.J.A. (1999) Neutrophils cause oxidative DNA damage in alveolar epithelial cells. Free Radic. Biol Med., 27. 234–240.
Watanabe, N., Miura, S., Zeki, S. and Ishii, H. (2001) Hepatocellular oxidative DNA injury induced by macrophage-derived nitric oxide. Free Radic. Biol Med., 30. 1019–1028.
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© 2003 Springer Science+Business Media Dordrecht
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Murakami, A., Kim, HW., Williams, M.V., Ohigashi, H. (2003). Suppression of Free Radical-Induced Mutation of Animal Cell Genes by Food Factors. In: Yagasaki, K., Miura, Y., Hatori, M., Nomura, Y. (eds) Animal Cell Technology: Basic & Applied Aspects. Animal Cell Technology: Basic & Applied Aspects, vol 13. Springer, Dordrecht. https://doi.org/10.1007/978-94-017-0726-8_12
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DOI: https://doi.org/10.1007/978-94-017-0726-8_12
Publisher Name: Springer, Dordrecht
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