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Protective Effects of Extracts from Fructus rhodomyrti against Oxidative DNA Damage In Vitro and In Vivo

DOI: 10.1155/2013/507407

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Abstract:

Objective. To evaluate the potential protective effects of extracts from Fructus rhodomyrti (FR) against oxidative DNA damage using a cellular system and the antioxidant ability on potassium bromate- (KBrO3-) mediated oxidative stress in rats. Methods. The effects of FR on DNA damage induced by hydrogen peroxide (H2O2) were evaluated by comet assay in primary spleen lymphocytes cultures. The effects of FR on the activities of SOD, CAT, and GPx and the levels of GSH, hydroperoxides, and 8-OHdG were determined in the plasma and tissues of rats treated with KBrO3. Results. FR was shown to effectively protect against DNA damage induced by H2O2??in vitro, and the maximum protective effect was observed when FR was diluted 20 times. Endogenous antioxidant status, namely, the activities of SOD, CAT, and GPx and the levels of GSH were significantly decreased in the plasma, the liver, and the kidney of the KBrO3-treated rats, while the pretreatment of FR prevented the decreases of these parameters. In addition, the pretreatment of FR was also able to prevent KBrO3-induced increases in the levels of hydroperoxides and 8-OHdG in the plasma, the liver, and the kidney in rats. Conclusions. Our findings suggested that FR might act as a chemopreventive agent with antioxidant properties offering effective protection against oxidative DNA damage in a concentration-dependent manner in vitro and in vivo. 1. Introduction Plants have played significant roles in maintaining human health and improving the quality of human life for thousands of years [1, 2]. Fructus rhodomyrti (FR) is the fruit of the Rhodomyrtus tomentosa growing on knolls in wilderness and widely distributed in Guangdong, Guangxi, Yunnan, Fujian, and Taiwan. FR has been used for the production of drinks and wine. FR is a traditional Chinese medicine material with antihepatitis property [3]. Cells that live in an oxygen-rich environment are inundated with various endogenous and exogenous sources of reactive oxygen species (ROS) [4]. The most important target for ROS in the carcinogenesis process is DNA [5, 6]. Irreparable DNA damage is involved in carcinogenesis, aging, and other degenerative diseases [4, 7]. However, enzymatic and nonenzymatic systems, which preserve the oxidant/antioxidant status, are disrupted during oxidative stress, a metabolic derangement due to an imbalance caused by excessive generation of ROS or a diminished capacity of the antioxidant defense system. Dietary factors and natural antioxidants that reduce the impact of ROS can protect DNA damage and thus reduce the risk of cancers [8,

References

[1]  J. B. Jeong, E. W. Seo, and H. J. Jeong, “Effect of extracts from pine needle against oxidative DNA damage and apoptosis induced by hydroxyl radical via antioxidant activity,” Food and Chemical Toxicology, vol. 47, no. 8, pp. 2135–2141, 2009.
[2]  B. N. Singh, B. R. Singh, R. L. Singh et al., “Oxidative DNA damage protective activity, antioxidant and anti-quorum sensing potentials of Moringa oleifera,” Food and Chemical Toxicology, vol. 47, no. 6, pp. 1109–1116, 2009.
[3]  R. Huang, N. Li, K. Huang, L. Zheng, S. Lin, and J. Lin, “Anti-radical action and antioxidant function in vivo of flavonoids extracts from Fructus rhodomyrti,” Food Science, vol. 29, pp. 588–590, 2008 (Chinese).
[4]  J. B. Jeong, S. C. Hong, and H. J. Jeong, “3,4-Dihydroxybenzaldehyde purified from the barley seeds (Hordeum vulgare) inhibits oxidative DNA damage and apoptosis via its antioxidant activity,” Phytomedicine, vol. 16, no. 1, pp. 85–94, 2009.
[5]  W. Lopaczynski and S. H. Zeisel, “Antioxidants, programmed cell death, and cancer,” Nutrition Research, vol. 21, no. 1-2, pp. 295–307, 2001.
[6]  S. Muthukumaran, A. R. Sudheer, V. P. Menon, and N. Nalini, “Protective effect of quercetin on nicotine-induced prooxidant and antioxidant imbalance and DNA damage in Wistar rats,” Toxicology, vol. 243, no. 1-2, pp. 207–215, 2008.
[7]  B. Bowerman, “Oxidative stress and cancer: a β-catenin convergence,” Science, vol. 308, no. 5725, pp. 1119–1120, 2005.
[8]  N. Khan and S. Sultana, “Inhibition of potassium bromate-induced renal oxidative stress and hyperproliferative response by Nymphaea alba in Wistar rats,” Journal of Enzyme Inhibition and Medicinal Chemistry, vol. 20, no. 3, pp. 275–283, 2005.
[9]  Y. Ke, X. Duan, F. Wen et al., “Association of melamine exposure with urinary stone and oxidative DNA damage in infants,” Archives of Toxicology, vol. 84, no. 4, pp. 301–307, 2010.
[10]  K. S. McDorman, B. F. Pachkowski, J. Nakamura, D. C. Wolf, and J. A. Swenberg, “Oxidative DNA damage from potassium bromate exposure in Long-Evans rats is not enhanced by a mixture of drinking water disinfection by-products,” Chemico-Biological Interactions, vol. 152, no. 2-3, pp. 107–117, 2005.
[11]  M. Raschke, I. R. Rowland, P. J. Magee, and B. L. Pool-Zobel, “Genistein protects prostate cells against hydrogen peroxide-induced DNA damage and induces expression of genes involved in the defence against oxidative stress,” Carcinogenesis, vol. 27, no. 11, pp. 2322–2330, 2006.
[12]  R. Yin, D. Zhang, Y. Song, B. Z. Zhu, and H. Wang, “Potent DNA damage by polyhalogenated quinones and H2O2via a metal-independent and Intercalation-enhanced oxidation mechanism,” Scientific Reports, vol. 3, Article ID 1269, pp. 1–6, 2013.
[13]  A. Maroz, R. F. Anderson, R. A. J. Smith, and M. P. Murphy, “Reactivity of ubiquinone and ubiquinol with superoxide and the hydroperoxyl radical: implications for in vivo antioxidant activity,” Free Radical Biology and Medicine, vol. 46, no. 1, pp. 105–109, 2009.
[14]  M. Khan, F. Yi, A. Rasul et al., “Alantolactone induces apoptosis in glioblastoma cells via GSH depletion, ROS generation, and mitochondrial dysfunction,” IUBMB Life, vol. 64, no. 9, pp. 783–794, 2012.
[15]  J. T. Rotruck, A. L. Pope, H. E. Ganther, A. B. Swanson, D. G. Hafeman, and W. G. Hoekstra, “Selenium: biochemical role as a component of glatathione peroxidase,” Science, vol. 179, no. 4073, pp. 588–590, 1973.
[16]  Y. Chen, J. Zhang, Y. Lin et al., “Tumour suppressor SIRT3 deacetylates and activates manganese superoxide dismutase to scavenge ROS,” EMBO Reports, vol. 12, no. 6, pp. 534–541, 2011.
[17]  E. Pick and Y. Keisari, “Superoxide anion and hydrogen peroxide production by chemically elicited peritoneal macrophages: induction by multiple nonphagocytic stimuli,” Cellular Immunology, vol. 59, no. 2, pp. 301–308, 1981.
[18]  A. K. Sinha, “Colorimetric assay of catalase,” Analytical Biochemistry, vol. 47, no. 2, pp. 389–394, 1972.
[19]  J.-L. Li, H.-X. Li, S. Li, Z.-X. Tang, S.-W. Xu, and X.-L. Wang, “Oxidative stress-mediated cytotoxicity of cadmium in chicken splenic lymphocytes,” Polish Journal of Environmental Studies, vol. 19, no. 5, pp. 947–956, 2010.
[20]  M. Cavia-Saiz, M. D. Busto, M. C. Pilar-Izquierdo, N. Ortega, M. Perez-Mateos, and P. Mu?iz, “Antioxidant properties, radical scavenging activity and biomolecule protection capacity of flavonoid naringenin and its glycoside naringin: a comparative study,” Journal of the Science of Food and Agriculture, vol. 90, no. 7, pp. 1238–1244, 2010.
[21]  T. B. Nguelefack, F. H. K. Mbakam, L. A. Tapondjou et al., “A dimeric triterpenoid glycoside and flavonoid glycosides with free radical-scavenging activity isolated from Rubus rigidus var. camerunensis,” Archives of Pharmacal Research, vol. 34, no. 4, pp. 543–550, 2011.
[22]  R. Amorati and L. Valgimigli, “Modulation of the antioxidant activity of phenols by non-covalent interactions,” Organic and Biomolecular Chemistry, vol. 10, pp. 4147–4158, 2012.
[23]  J. Dong, M. Zhang, L. Lu, L. Sun, and M. Xu, “Nitric oxide fumigation stimulates flavonoid and phenolic accumulation and enhances antioxidant activity of mushroom,” Food Chemistry, vol. 135, pp. 1220–1225, 2012.
[24]  I. E. Orhan, B. ?ener, and S. G. Musharraf, “Antioxidant and hepatoprotective activity appraisal of four selected Fumaria species and their total phenol and flavonoid quantities,” Experimental and Toxicologic Pathology, vol. 64, no. 3, pp. 205–209, 2012.
[25]  Y.-C. Tsai, Y.-H. Wang, C.-C. Liou, Y.-C. Lin, H. Huang, and Y.-C. Liu, “Induction of oxidative DNA damage by flavonoids of propolis: its mechanism and implication about antioxidant capacity,” Chemical Research in Toxicology, vol. 25, no. 1, pp. 191–196, 2012.
[26]  C. F. Skibola and M. T. Smith, “Potential health impacts of excessive flavonoid intake,” Free Radical Biology and Medicine, vol. 29, no. 3-4, pp. 375–383, 2000.
[27]  B. Lipinski, M. Ghyczy, and M. Boros, “Evidence in support of a concept of reductive stress (multiple letters),” British Journal of Nutrition, vol. 87, no. 1, pp. 93–94, 2002.
[28]  G. ?ener, A. ?. ?ehirli, Y. Ip?i et al., “Taurine treatment protects against chronic nicotine-induced oxidative changes,” Fundamental and Clinical Pharmacology, vol. 19, no. 2, pp. 155–164, 2005.
[29]  M. Zhang, S. G. Swarts, L. Yin et al., “Antioxidant properties of quercetin,” Advances in Experimental Medicine and Biology, vol. 701, pp. 283–289, 2011.
[30]  M. Lee, B.-M. Kwon, K. Suk, E. McGeer, and P. L. McGeer, “Effects of obovatol on GSH depleted glia-mediated neurotoxicity and oxidative damage,” Journal of Neuroimmune Pharmacology, vol. 7, pp. 173–186, 2012.
[31]  P. R. Rom?o, J. Tovar, S. G. Fonseca et al., “Glutathione and the redox control system trypanothione/trypanothione reductase are involved in the protection of Leishmania spp. against nitrosothiol-induced cytotoxicity,” Brazilian Journal of Medical and Biological Research, vol. 39, no. 3, pp. 355–363, 2006.
[32]  C. Luchese, E. C. Stangherlin, B. M. Gay, and C. W. Nogueira, “Antioxidant effect of diphenyl diselenide on oxidative damage induced by smoke in rats: involvement of glutathione,” Ecotoxicology and Environmental Safety, vol. 72, no. 1, pp. 248–254, 2009.
[33]  K. Husain, B. R. Scott, S. K. Reddy, and S. M. Somani, “Chronic ethanol and nicotine interaction on rat tissue antioxidant defense system,” Alcohol, vol. 25, no. 2, pp. 89–97, 2001.
[34]  Q. Liang, Y. Sheng, P. Jiang et al., “The gender-dependent difference of liver GSH antioxidant system in mice and its influence on isoline-induced liver injury,” Toxicology, vol. 280, no. 1-2, pp. 61–69, 2011.
[35]  T. W. Fischer, K. Kleszczynski, L. H. Hardkop, N. Kruse, and D. Zillikens, “Melatonin enhances antioxidative enzyme gene expression (CAT, GPx, SOD), prevents their UVR-induced depletion, and protects against the formation of DNA damage (8-hydroxy-2′-deoxyguanosine) in ex vivo human skin,” Journal of Pineal Research, vol. 54, pp. 303–312, 2012.
[36]  M. Y. Moridani, J. Pourahmad, H. Bui, A. Siraki, and P. J. O'Brien, “Dietary flavonoid iron complexes as cytoprotective superoxide radical scavengers,” Free Radical Biology and Medicine, vol. 34, no. 2, pp. 243–253, 2003.
[37]  G. Cao, E. Sofic, and R. L. Prior, “Antioxidant and prooxidant behavior of flavonoids: structure-activity relationships,” Free Radical Biology and Medicine, vol. 22, no. 5, pp. 749–760, 1997.
[38]  E. J. Lien, S. Ren, H.-H. Bui, and R. Wang, “Quantitative structure-activity relationship analysis of phenolic antioxidants,” Free Radical Biology and Medicine, vol. 26, no. 3-4, pp. 285–294, 1999.
[39]  M.-R. Kim, J. Y. Lee, H.-H. Lee et al., “Antioxidative effects of quercetin-glycosides isolated from the flower buds of Tussilago farfara L,” Food and Chemical Toxicology, vol. 44, no. 8, pp. 1299–1307, 2006.
[40]  Q. Cai, R. O. Rahn, and R. Zhang, “Dietary flavonoids, quercetin, luteolin and genistein, reduce oxidative DNA damage and lipid peroxidation and quench free radicals,” Cancer Letters, vol. 119, no. 1, pp. 99–107, 1997.
[41]  R. K. Bhattacharya and P. F. Firozi, “Effect of plant flavonoids on microsome catalyzed reactions of aflatoxin B1 leading to activation and DNA adduct formation,” Cancer Letters, vol. 39, no. 1, pp. 85–91, 1988.
[42]  R. Dixit and B. Gold, “Inhibition of N-methyl-N-nitrosourea-induced mutagenicity and DNA methylation by ellagic acid,” Proceedings of the National Academy of Sciences of the United States of America, vol. 83, no. 21, pp. 8039–8043, 1986.
[43]  K. L. Khanduja and S. Majid, “Ellagic acid inhibits DNA binding of benzo(a)pyrene activated by different modes,” Journal of Clinical Biochemistry and Nutrition, vol. 15, pp. 1–9, 1993.
[44]  A. W. Wood, M. T. Huang, R. L. Chang, et al., “Inhibition of the mutagenicity of bay-region diol epoxides of polycyclic aromatic hydrocarbons by naturally occurring plant phenols: exceptional activity of ellagic acid,” Proceedings of the National Academy of Sciences of the United States of America, vol. 79, no. 18, pp. 5513–5517, 1982.
[45]  H. Dok-Go, K. H. Lee, H. J. Kim et al., “Neuroprotective effects of antioxidative flavonoids, quercetin, (+)-dihydroquercetin and quercetin 3-methyl ether, isolated from Opuntia ficusindica var. saboten,” Brain Research, vol. 965, no. 1-2, pp. 130–136, 2003.

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