Effect of Dietary EGCG on Normal and Vitamin E and Selenium Deficient Rats

Abstract

The tea catechin EGCG has been postulated to provide health benefits in humans, to some extent, as an antioxidant. The dose-response effect of dietary EGCG (0, 30, 60, or 120 mg/kg diet) was tested in rats under high versus low oxidative stress conditions that were created by feeding diets adequate in vitamin E and Se (Lox), or deficient in both (Hox) for six weeks. Effects on growth, quinone reductase (NQO1) activity, F2-isoprostanes and nutrient antioxidant amounts in the liver were evaluated as markers of nutrient deficiency and oxidative status. Under Hox conditions consumption of EGCG only at the lowest dose was partially associated with a protection against oxidative stress, reflected by a delay in growth deceleration, but no protection against lipid oxidation. Elevated liver NQO1 activity was observed in this group (>4-fold) increasing with the dose; but it was not associated with antioxidant protection. In contrast, under Lox conditions consumption of EGCG was associated with antioxidant activity reflected in a reduction (>30%) in F2-isoprostanes and protection of CoQ reduced status in the liver. Overall these results suggest that the antioxidant effect of EGCG in vivo depends on the level of oxidative stress and the presence of other nutrient antioxidants.

Share and Cite:

J. Andrade and J. Burgess, "Effect of Dietary EGCG on Normal and Vitamin E and Selenium Deficient Rats," Food and Nutrition Sciences, Vol. 4 No. 8A, 2013, pp. 163-173. doi: 10.4236/fns.2013.48A020.

Conflicts of Interest

The authors declare no conflicts of interest.

References

[1] J. M. Gutteridge and B. Halliwell, “Free Radicals and Antioxidants in the Year 2000. A Historical Look to the Future,” Annals of the New York Academy of Sciences, Vol. 899, 2000, pp. 136-147. doi:10.1111/j.1749-6632.2000.tb06182.x
[2] B. Halliwell, “Antioxidants in Human Health and Disease,” Annual Review of Nutrition, Vol. 16, 1996, pp. 3350. doi:10.1146/annurev.nu.16.070196.000341
[3] P. M. Kris-Etherton, K. D. Hecker, A. Bonanome, S. M. Coval, A. E. Binkoski, K. F. Hilpert, A. E. Griel and T. D. Etherton, “Bioactive Compounds in Foods: Their Role in the Prevention of Cardiovascular Disease and Cancer,” American Journal of Medicine, Vol. 113, No. S9B, 2002, pp. 71S-88S. doi:10.1016/S0002-9343(01)00995-0
[4] C. Rice-Evans, “Flavonoid Antioxidants,” Current Medicinal Chemistry, Vol. 8, No. 7, 2001, pp. 797-807. doi:10.2174/0929867013373011
[5] V. Crespy and G. Williamson, “A Review of the Health Effects of Green Tea Catechins in in Vivo Animal Models,” Journal of Nutrition, Vol. 134, No. 12S, 2004, pp. 3431S-3440S.
[6] J. V. Higdon and B. Frei, “Tea Catechins and Polyphenols: Health Effects, Metabolism, and Antioxidant Functions,” Critical Reviews in Food Science and Nutrition, Vol. 43, No. 1, 2003, pp. 89-143. doi:10.1080/10408690390826464
[7] C. S. Yang, P. Maliakal and X. Meng, “Inhibition of Carcinogenesis by Tea,” Annual Review of Pharmacology and Toxicology, Vol. 42, 2002, pp. 25-54. doi:10.1146/annurev.pharmtox.42.082101.154309
[8] H. H. Chow, Y. Cai, I. A. Hakim, J. A. Crowell, F. Shahi, C. A. Brooks, R. T. Dorr, Y. Hara and D. S. Alberts, “Pharmacokinetics and Safety of Green Tea Polyphenols after Multiple-Dose Administration of Epigallocatechin Gallate and Polyphenon E in Healthy Individuals,” Clinical Cancer Research, Vol. 9, No. 9, 2003, pp. 3312-3319.
[9] C. F. Kuo, S. Cheng and J. R. Burgess, “Deficiency of Vitamin E and Selenium Enhances Calcium-Independent Phospholipase A2 Activity in Rat Lung and Liver,” Journal of Nutrition, Vol. 125, No. 6, 1995, pp. 1419-1429.
[10] S. M. Henning, C. Fajardo-Lira, H. W. Lee, A. A. Youssefian, V. L. Go and D. Heber, “Catechin Content of 18 Teas and a Green Tea Extract Supplement Correlates with the Antioxidant Capacity,” Nutrition and Cancer, Vol. 45, No. 2, 2003, pp. 226-235. doi:10.1207/S15327914NC4502_13
[11] W. A. McCrehan, “Determination of Retinal, a-Tocopherol, and b-Carotene in Serum by Liquid Chromatography,” Methods in Enzymology, Vol. 189, 1990, pp. 172-181. doi:10.1016/0076-6879(90)89288-S
[12] ESA, “Simultaneous Analysis of Carotenoids, Retinoids, Tocopherols, Vitamin K1 and Coenzyme Q10 in Plasma,” 1996.
[13] D. Stempak, S. Dallas, J. Klein, R. Bendayan, G. Koren and S. Baruchel, “Glutathione Stability in Whole Blood: Effects of Various Deproteinizing Acids,” Therapeutic Drug Monitoring, Vol. 23, No. 5, 2001, pp. 542-549. doi:10.1097/00007691-200110000-00008
[14] B. S. Kristal, K. E. Vigneau-Callahan and W. R. Matson, “Simultaneous Analysis of the Majority of Low-Molecular-Weight, Redox-Active Compounds from Mitochondria,” Analytical Biochemistry, Vol. 263, No. 1, 1998, pp. 18-25. doi:10.1006/abio.1998.2831
[15] H. Prochaska and A. B. Santamaria, “Direct Measurement of NAD(P)H: Quinone Reductase from Cells Cultured in Microtiter Wells: A Screening Assay for Anticarcinogenic Enzyme Inducers,” Analytical Biochemistry, Vol. 169, No. 2, 1998, pp. 328-336. doi:10.1016/0003-2697(88)90292-8
[16] P. K. Smith, R. I. Krohn, G. T. Hermanson, A. K. Mallia, F. H. Gartner, M. D. Provenzano, E. K. Fujimoto, N. M. Goeke, B. J. Olson and D. C. Klenk, “Measurement of Protein Using Bicinchoninic Acid,” Analytical Biochemistry, Vol. 150, No. 1, 1985, pp. 76-85. doi:10.1016/0003-2697(85)90442-7
[17] J. R. Burgess and C. F. Kuo, “Increased Calcium-Independent Phospholipase A2 Activity in Vitamin E and Selenium-Deficient Rat Lung, Liver and Spleen Cytosol Is Time-Dependent and Reversible,” Journal of Nutritional Biochemistry, Vol. 7, No. 7, 1996, pp. 366-374. doi:10.1016/S0955-2863(96)00057-5
[18] R. D. Cabo, J. R. Burgess and P. Navas, “Adaptations to Oxidative Stress Induced by Vitamin E Deficiency in Rat Liver,” Journal of Bioenergetics and Biomembranes, Vol. 38, No. 5-6, 2006, pp. 309-317. doi:10.1007/s10863-006-9050-1
[19] J. E. Andrade and J. R. Burgess, “Effect of the Citrus Flavanone Naringenin on Oxidative Stress in Rats,” Journal of Agricultural and Food Chemistry, Vol. 55, No. 6, 2007, pp. 2142-2148. doi:10.1021/jf061714h
[20] K. Matsumoto, I. Ui, K. Satoh, T. Tobe, F. Ushio and K. Endo, “Evaluation of Oxidative Damage in the Liver of Selenium-Deficient Rats,” Redox Report, Vol. 7, No. 5, 2002, pp. 351-354. doi:10.1179/135100002125000974
[21] J. K. Willcox, G. L. Catignani and L. J. Roberts, “Dietary Flavonoids Fail to Suppress F2-Isoprostane Formation in Vivo,” Free Radical Biology & Medicine, Vol. 34, No. 7, 2003, pp. 795-799. doi:10.1016/S0891-5849(02)01425-9
[22] E. J. Lien, S. Ren, H. H. Bui and R. Wang, “Quantitative Structure-Activity Relationship Analysis of Phenolic Antioxidants,” Free Radical Biology & Medicine, Vol. 26, No. 3-4, 1999, pp. 285-294. doi:10.1016/S0891-5849(98)00190-7
[23] E. J. Choi, K. M. Chee and B. H. Lee, “Antiand Prooxidant Effects of Chronic Quercetin Administration in Rats,” European Journal of Pharmacology, Vol. 482, No. 1-3, 2003, pp. 281-285. doi:10.1016/j.ejphar.2003.09.067
[24] F. Lucesoli, M. Caligiuri, M. F. Roberti, J. C. Perazzo and C. G. Fraga, “Dose-Dependent Increase of Oxidative Damage in the testes of Rats Subjected to Acute Iron Overload,” Archives of Biochemistry and Biophysics, Vol. 372, No. 1, 1999, pp. 37-43. doi:10.1006/abbi.1999.1476
[25] L. Miles, M. V. Miles, P. H. Tang, P. S. Horn, J. G. Quinlan, B. Wong, A. Wenisch and K. E. Bove, “Ubiquinol: A Potential Biomarker for Tissue Energy Requirements and Oxidative Stress,” Clinica Chimica Acta, Vol. 360, No. 1-2, 2005, pp. 87-96. doi:10.1016/j.cccn.2005.04.009
[26] A. Galinier, A. Carriere, Y. Fernandez, A. M. Bessac, S. Caspar-Bauguil, B. Periquet, M. Comtat, J. P. Thouvenot and L. Casteilla, “Biological Validation of Coenzyme Q Redox State by HPLC-EC Measurement: Relationship between Coenzyme Q Redox State and Coenzyme Q Content in Rat Tissues,” FEBS Letters, Vol. 578, No. 1-2, 2004, pp. 53-57. doi:10.1016/j.febslet.2004.10.067
[27] F. Navarro, P. Navas, J. R. Burgess, R. I. Bello, R. De Cabo, A. Arroyo and J. M. Villalba, “Vitamin E and Selenium Deficiency Induces Expression of the UbiquinoneDependent Antioxidant System at the Plasma Membrane,” FASEB Journal, Vol. 12, No. 15, 1998, pp. 1665-1673.
[28] G. Lenaz, M. D’Aurelio, M. Merlo Pich, M. L. Genova, B. Ventura, C. Bovina, G. Formiggini and G. Parenti Castelli, “Mitochondrial Bioenergetics in Aging,” Biochimica et Biophysica Acta (BBA)—Bioenergetics, Vol. 1459, No. 2-3, 2000, pp. 397-404. doi:10.1016/S0005-2728(00)00177-8
[29] L. Ernster, P. Forsmark and K. Nordenbrand, “The Mode of Action of Lipid-Soluble Antioxidants in Biological Membranes: Relationship between the Effects of Ubiquinol and Vitamin E as Inhibitors of Lipid Peroxidation in Submitochondrial Particles,” Biofactors, Vol. 3, No. 4, 1992, pp. 241-248.
[30] K. E. Hill and R. F. Burk, “Effect of Selenium Deficiency and Vitamin E Deficiency on Glutathione Metabolism in Isolated Rat Hepatocytes,” Journal of Biological Chemistry, Vol. 257, No. 18, 1982, pp. 10668-10672.
[31] J. Frank, T. Lundh, R. S. Parker, J. E. Swanson, B. Vessby and A. Kamal-Eldin, “Dietary (+)-Catechin and BHT Markedly Increase Alpha-Tocopherol Concentrations in Rats by a Tocopherol-Omega-Hydroxylase-Independent Mechanism,” Journal of Nutrition, Vol. 133, No. 10, 2003, pp. 3195-3199.
[32] J. Frank, A. Budek, T. Lundh, R. S. Parker, J. E. Swanson, C. F. Lourenco, B. Gago, J. Laranjinha, B. Vessby and A. Kamal-Eldin, “Dietary Flavonoids with a Catechol Structure Increase Alpha-Tocopherol in Rats and Protect the Vitamin from Oxidation in Vitro,” Journal of Lipid Research, Vol. 47, No. 12, 2006, pp. 2718-2725. doi:10.1194/jlr.M600291-JLR200
[33] L. Fremont, M. T. Gozzelino, M. P. Franchi and A. Linard, “Dietary Flavonoids Reduce Lipid Peroxidation in Rats Fed Polyunsaturated or Monounsaturated Fat Diets,” Journal of Nutrition, Vol. 128, No. 9, 1998, pp. 14951502.
[34] F. Nanjo, M. Honda, K. Okushio, N. Matsumoto, F. Ishigaki, T. Ishigami and Y. Hara, “Effects of Dietary Tea Catechins on Alpha-Tocopherol Levels, Lipid Peroxidation, and Erythrocyte Deformability in Rats Fed on High Palm Oil and Perilla Oil Diets,” Biological & Pharmaceutical Bulletin, Vol. 16, No. 11, 1993, pp. 1156-1159. doi:10.1248/bpb.16.1156
[35] M. A. Colucci, C. J. Moody and G. D. Couch, “Natural and Synthetic Quinones and Their Reduction by the Quinone Reductase Enzyme NQO1: From Synthetic Organic Chemistry to Compounds with Anticancer Potential,” Organic & Biomolecular Chemistry, Vol. 6, No. 4, 2008, pp. 637-656. doi:10.1039/b715270a
[36] K. B. Storey, “Oxidative Stress: Animal Adaptations in Nature,” Brazilian Journal of Medical and Biological Research, Vol. 29, No. 12, 1996, pp. 1715-1733.
[37] A. K. Jaiswal, “Regulation of Genes Encoding NAD(P)H: Quinone Oxidoreductases,” Free Radical Biology & Medicine, Vol. 29, No. 3-4, 2000, pp. 254-262. doi:10.1016/S0891-5849(00)00306-3
[38] Y. J. Moon, X. Wang and M. E. Morris. “Dietary Flavonoids: Effects on Xenobiotic and Carcinogen Metabolism,” Toxicology In Vitro, Vol. 20, No. 2, 2006, pp. 187-210. doi:10.1016/j.tiv.2005.06.048
[39] A. D. Kinghorn, B. N. Su, D. S. Jang, L. C. Chang, D. Lee, J. Q. Gu, E. J. Carcache-Blanco, A. D. Pawlus, S. K. Lee, E. J. Park, M. Cuendet, J. J. Gills, K. Bhat, H. S. Park, E. Mata-Greenwood, L. L. Song, M. Jang and J. M. Pezzuto, “Natural Inhibitors of Carcinogenesis,” Planta Medica, Vol. 70, No. 8, 2004, pp. 691-705. doi:10.1055/s-2004-827198
[40] C. Chen, R. Yu, E. D. Owuor and A. N. Kong. “Activation of Antioxidant-Response Element (ARE), MitogenActivated Protein Kinases (MAPKs) and Caspases by Major Green Tea Polyphenol Components During Cell Survival and Death,” Archives of Pharmacal Research, Vol. 23, No. 6, 2000, pp. 605-612. doi:10.1007/BF02975249
[41] H. Y. Chan, H. Wang, D. S. Tsang, Z. Y. Chen and L. K. Leung, “Screening of Chemopreventive Tea Polyphenols against PAH Genotoxicity in Breast Cancer Cells by a XRE-Luciferase Reporter Construct,” Nutrition and Cancer, Vol. 46, No. 1, 2003, pp. 93-100. doi:10.1207/S15327914NC4601_12
[42] S. K. Katiyar, R. Agarwal, M. T. Zaim and H. Mukhtar, “Protection against N-Nitrosodiethylamine and Benzo[a] Pyrene-Induced Forestomach and Lung Tumorigenesis in A/J Mice by Green Tea,” Carcinogenesis, Vol. 14, No. 5, 1993, pp. 849-855. doi:10.1093/carcin/14.5.849
[43] S. G. Khan, S. K. Katiyar, R. Agarwal and H. Mukhtar, “Enhancement of Antioxidant and Phase II Enzymes by Oral Feeding of Green Tea Polyphenols in Drinking Water to SKH-1 Hairless Mice: Possible Role in Cancer Chemoprevention,” Cancer Research, Vol. 52, No. 14, 1992, pp. 4050-4052.
[44] L. Qi and C. Han, “Induction of NAD(P)H: Quinone Reductase by Anticarcinogenic Ingredients of Tea,” Wei Sheng Yan Jiu, Vol. 27, No. 5, 1998, pp. 323-326.
[45] D. J. Morre, D. M. Morre, H. Sun, R. Cooper, J. Chang and E. M. Janle, “Tea Catechin Synergies in Inhibition of Cancer Cell Proliferation and of a Cancer Specific Cell Surface Oxidase (ECTO-NOX),” Pharmacology and Toxicology, Vol. 92, No. 5, 2003, pp. 234-241. doi:10.1034/j.1600-0773.2003.920506.x
[46] S. Itoh, S. Nagaoka and K. Mukai, “Kinetic Study of the Tocopherol Regeneration Reaction by Biological Hydroquinones in Micellar Solution,” Journal of Physical Chemistry A, Vol. 112, No. 3, 2008, pp. 448-456. doi:10.1021/jp075894p
[47] J. Kaikkonen, K. Nyyssonen, A. Tomasi, A. Iannone, T. P. Tuomainen, E. Porkkala-Sarataho and J. T. Salonen, “Antioxidative Efficacy of Parallel and Combined Supplementation with Coenzyme Q10 and d-Alpha-Tocopherol in Mildly Hypercholesterolemic Subjects: A Randomized Placebo-Controlled Clinical Study,” Free Radical Research, Vol. 33, No. 3, 2000, pp. 329-340. doi:10.1080/10715760000301501
[48] B. Zhou, L. M. Wu, L. Yang and Z. L. Liu, “Evidence for Alpha-Tocopherol Regeneration Reaction of Green Tea Polyphenols in SDS Micelles,” Free Radical Biology & Medicine, Vol. 38, No. 1, 2005, pp. 78-84. doi:10.1016/j.freeradbiomed.2004.09.023
[49] F. Dai, W. F. Chen and B. Zhou, “Antioxidant Synergism of Green Tea Polyphenols with Alpha-Tocopherol and LAscorbic Acid in SDS Micelles,” Biochimie, Vol. 90, No. 10, 2008, pp. 1499-1505. doi:10.1016/j.biochi.2008.05.007
[50] Y. Kadoma, M. Ishihara, N. Okada and S. Fujisawa, “Free Radical Interaction between Vitamin E (Alpha-, Beta-, Gammaand Delta-Tocopherol), Ascorbate and Flavonoids,” In Vivo, Vol. 20, No. 6B, 2006, pp. 823-827.
[51] Q. Y. Zhu, Y. Huang, D. Tsang and Z. Y. Chen, “Regeneration of Alpha-Tocopherol in Human Low-Density Lipoprotein by Green Tea Catechin,” Journal of Agricultural and Food Chemistry, Vol. 47, No. 5, 1999, pp. 2020-2025. doi:10.1021/jf9809941
[52] S. V. Jovanovic and M. G. Simic, “Antioxidants in Nutrition,” Annals of the New York Academy of Sciences, Vol. 899, 2000, pp. 326-334. doi:10.1111/j.1749-6632.2000.tb06197.x
[53] K. Furuno, T. Akasako and N. Sugihara, “The Contribution of the Pyrogallol Moiety to the Superoxide Radical Scavenging Activity of Flavonoids,” Biological & Pharmaceutical Bulletin, Vol. 25, No. 1, 2002, pp. 19-23. doi:10.1248/bpb.25.19
[54] M. Muzolf-Panek, A. Gliszczynska-Swiglo, L. de Haan, J. M. Aarts, H. Szymusiak, J. M. Vervoort, B. Tyrakowska and I. M. Rietjens, “Role of Catechin Quinones in the Induction of EpRE-Mediated Gene Expression,” Chemical Research in Toxicology, Vol. 21, No. 12, 2008, pp. 2352-2360. doi:10.1021/tx8001498
[55] J. George, “Elevated Serum Beta-Glucuronidase Reflects Hepatic Lysosomal Fragility Following Toxic Liver Injury in Rats,” Biochemistry and Cell Biology, Vol. 86, No. 3, 2008, pp. 235-243. doi:10.1139/O08-038

Copyright © 2023 by authors and Scientific Research Publishing Inc.

Creative Commons License

This work and the related PDF file are licensed under a Creative Commons Attribution 4.0 International License.