Correlations of circulating levels of oxidants, antioxidants and soluble Fas in breast cancer among Egyptian females

  • Authors

    • Sayed Hamada Madboly professor of medical Biochemistry and Molecular biology- Faculty of Medicine, Al-Azhar University, Cairo
    • Elsaeid Mostafa Elsaeid Elbawab professor of medical Biochemistry and Molecular biology- Faculty of Medicine, Al-Azhar University, Assiut branch
    • Abdallah M. A.A. El-Ebidi Lecturer of Medical Biochemistry and Molecular Biology- Faculty of Medicine- Aswan university
    • Omar Abd-El raheem Sayed Associate professor of General Surgery- Faculty of Medicine- Sohag University
    • Mohammed H. Hassan Lecturer of Medical Biochemistry and Molecular Biology- Qena Faculty of Medicine- South Valley University
    • Tahia H. Saleem professor of medical Biochemistry and Molecular biology- Faculty of Medicine- Assiut University
    • Sameh Salah Eldeen Elsayed Assistant lecturer of medical Biochemistry and Molecular biology- Faculty of Medicine, Al-Azhar University, Assiut branch
    2016-03-14
    https://doi.org/10.14419/ijbas.v5i2.5765
  • Breast Cancer, Egyptian Females, Oxidative Stress, Soluble Fas.
  • Background: Breast cancer is the first most common malignancy in Egyptian females. Oxidative stress is considered to be involved in the pathophysiology of all cancers, especially breast cancer. An inappropriately low rate of apoptosis can give rise to cancer.

    Objectives: The purpose of this study was to asses, compare and correlate the circulatory levels of some oxidants (malondialdehyde "MDA" and nitric oxide "NO"), total antioxidant capacity "TAO") and soluble form of Fas "sFas" in some Egyptian females having breast cancer.

    Methods: A cross sectional case/control study conducted on 50 Egyptian females recruited from outpatient clinics or inpatients department of the general surgery at Sohag university hospital, divided into 30 females with malignant breast lesion and 20 healthy females as a control group. Colorimetric assay of serum levels of NO, MDA and TAO, while, sFas was determined using ELISA method.

    Results: There were significant high levels of NO, MDA, TAO and sFas in malignant group than in control group with p-value < 0.0001, high positive correlation between NO, MDA, TAO and sFas in malignant group ( r= 0.958, 0.807, 0.748 respectively and P< 0.0001 for all). There was high positive correlation between NO and TAO in malignant group (r = 0.78, P < 0.0001).There was also, high positive correlation between MDA and TAO in malignant group (r = 0.81, P < 0.0001).

    Conclusion: These results support the oxidative stress hypothesis and resistance to apoptosis in development and progression of breast cancer.

  • References

    1. [1] J. Ferlay, D.M. Parkin, E. Steliarova-Foucher. Estimates of cancer incidence and mortality in Europe in 2008. European Journal of Cancer, 46 (2010) 765–781. http://dx.doi.org/10.1016/j.ejca.2009.12.014.

      [2] J.H. Breasted, Edwin Smith Surgical Papyrus. The University of Chicago Press, Illinois. Coated from Ebeid NI.; Surgery Chapter 5 in: Egyptian Medicine in the Days of the Pharaohs. The General Egyptian Book Organization, 1999; 403-406.

      [3] A.S. Ibrahim, Epidemiology of breast Cancer. Editors: G .Contesse, S.Omar . Breast cancer. The Cairo Medical Syndicate Scientific Committee; 1984: 1-13.

      [4] A. S. Ibrahim, H. M. Khaled, N. N.H Mikhail, H. Baraka, H. Kamel. Cancer incidence in Egypt: results of the national population-based cancer registry program. Journal of Cancer Epidemiology, 2014 (2014)1-18.http://dx.doi.org/10.1155/2014/437971.

      [5] J. M. Elwood, B. Cox, A.K. Richardson. The effectiveness of breast cancer screening by mammography in younger women. Online J CurrClin Trials, 1 (1993) 32-227.

      [6] G.N. Hortobagyi, L.Esserman, T.A.Buchholz. Neoplasms of the Breast. In: Kufe DW, Bast RC, Hait WN, et al, eds. Cancer Medicine. 7th ed. Hamilton, Ontario: BC Decker, 2006; 1584-1643.

      [7] M. Morrow. Magnetic resonance imaging in breast cancer: one step forward, tow steps back? The Journal of the American Medical Association, 292 (2004) 779-80.http://dx.doi.org/10.1001/jama.292.22.2779.

      [8] N. Hylton. Magnetic resonance imaging of breast: Opportunities to improve breast cancer management. Journal of Clinical Oncology 23 (2005)1678-84.http://dx.doi.org/10.1200/JCO.2005.12.002.

      [9] J.C.Reed, M. Pellecchi. Apoptosis-based therapies for hematologic malignancies. Blood, 106 (2005) 408-418.http://dx.doi.org/10.1182/blood-2004-07-2761.

      [10] J. Zipprich, M.B.Terry, Y.Liao, M. Agrawal, I. Gurvich, R.Senie, R.M. Santella. Plasma protein carbonyls and breast cancer risk in sisters discordant for breast cancer from the New York site of the breast cancer family registry. Cancer Res, 69 (2009) 2966-72.http://dx.doi.org/10.1158/0008-5472.CAN-08-3418.

      [11] T. Aghvami, M. Djalali, A. Keshavarz, M.R. Sadeghi, H. Zeraati,H.S.Yeganeh, M. Negahdar. Plasma level of antioxidant vitamins and lipid peroxidation in breast cancer patients. Iranian J Publ Health, 35(2006) 42-47.

      [12] E.K. Pauwels, P.A.Erba, M. Kostkiewicz. Antioxidants: A tale of two stories. Drug News Perspect, 20 (2007) 579–585.http://dx.doi.org/10.1358/dnp.2007.20.9.1162242.

      [13] D.E. Sener, A. Gonenc, M. Akinci, M. Torun. Lipid peroxidation and total antioxidant status in patients with breast cancer. Cell BiochemFunct, 25(2007) 377-82.http://dx.doi.org/10.1002/cbf.1308.

      [14] J.L. do Val Carneiro, S.L.Nixdorf, M.S. Mantovani, H.A.C. da Silva do Amaral, M.N. Aoki, M.K. Amarante, B.A. Fabris, F.M.H. Pelegrinelli, W.M.A. Ehara. Plasma malondialdehyde levels and CXCR4 expression in peripheral blood cells of breast cancer patients. J Cancer Res ClinOncol, 135 (2009) 997-1004.http://dx.doi.org/10.1007/s00432-008-0535-7.

      [15] G. Ray, S.A. Husain. Oxidants, antioxidants and carcinogenesis. Indian J ExpBiol, 40(2002) 1213-32.

      [16] N. Tuteja , M.Chandra, R. Tuteja , M.K. Misra . Nitric Oxide as a Unique Bioactive Signaling Messenger in Physiology and Pathophysiology.J Biomed Biotechnol, 4(2004): 227-237.http://dx.doi.org/10.1155/S1110724304402034.

      [17] B. Brüne, A. von Knethen, K.B.Sandau. Nitric oxide (NO): an effector of apoptosis. Cell Death Differ, 6 (1999) 969-75.http://dx.doi.org/10.1038/sj.cdd.4400582.

      [18] S. Pervin, R. Singh, G. Chaudhuri. Nitric oxide, N omega-hydroxy-L-arginine and breast cancer. Nitric Oxide, 19 (2008)103-6.http://dx.doi.org/10.1016/j.niox.2008.04.016.

      [19] M. Valko, C.J. Rhodes, J. Moncol, M. Izakovic, M. Mazur. Free radicals, metals and antioxidants in oxidative stress-induced cancer. ChemBiol Interact, 160 (2006)1–40. http://dx.doi.org/10.1016/j.cbi.2005.12.009.

      [20] B. Fadeel, S. Orrenius. Apoptosis: a basic biological phenomenon with wide-ranging implications in human disease. J Intern Med, 258 (2005) 479–517.http://dx.doi.org/10.1111/j.1365-2796.2005.01570.x.

      [21] S. Fulda, K.M. Debatin. Extrinsic versus intrinsic apoptosis pathways in anticancer chemotherapy. Oncogene, 25(2006) 4798-811.http://dx.doi.org/10.1038/sj.onc.1209608.

      [22] I.N. Lavrik, A. Golks, P.H. Krammer. Caspases: pharmacological manipulation of cell death. J Clin Invest, 115(2005) 2665–2672.http://dx.doi.org/10.1172/JCI26252.

      [23] M. Villa-Morales, J. Fernández-Piqueras. Targeting the Fas/FasL signaling pathway in cancer therapy.Expert Opin Ther Targets, 16(2012)85-101. http://dx.doi.org/10.1517/14728222.2011.628937.

      [24] Z.Peng, Y.Zhang, W.Gu, Z.Wang, D.Li, F.Zhang, G.Qiu, K.Xie. Integration of the hepatitis B virus X fragment in hepatocellular carcinoma and its effects on the expression of multiple molecules: a key to the cell cycle and apoptosis. Int J Oncol, 26 (2005) 467â€473.

      [25] S. Nagata, P. Golstein. The Fas death factor [review]. Science, 267 (1995) 1449-1456.http://dx.doi.org/10.1126/science.7533326.

      [26] C.A.Smith, T. Farrah, R.G.Goodwin. The TNF receptor superfamily of cellular and viral proteins: activation, co stimulation, and death. Cell, 76(1994) 959-962.http://dx.doi.org/10.1016/0092-8674(94)90372-7.

      [27] S. Nagata. Apoptosis by death factor. Cell, 88 (1997)355-365.http://dx.doi.org/10.1016/S0092-8674(00)81874-7.

      [28] R. Watanabe-Fukunaga, C.I. Brannan, N. Itoh, et al. The cDNA structure, expression, and chromosomal assignment of the mouse Fas antigen. J Immunol, 148 (1992)1274-1279.

      [29] E. Leitha, F. user, J. Dhein, G. Mechtersheimer, et al. Constitutive and induced expression of APO-1, a new member of the nerve growth factor/tumor necrosis factor receptor superfamily, in normal and neoplastic cells. Lab Invest, 69(1993) 415-429.

      [30] J.Cheng, T.Zhou, C.Liu, J.P.Shapiro, M.J.Brauer, M.C.Kiefer, P.J.Barr, J.D. Mountz. Protection fr-om Fasâ€mediated apoptosis by asoluble form of the Fas molecule. Science, 263 (1994) 1759†1762.http://dx.doi.org/10.1126/science.7510905.

      [31] I. Cascino, G. Fiucci, G. Papoff, G. Ruberti. Three functional soluble forms of the human apoptosis-inducing Fas molecule are produced by alternative splicing. J Immunol, 154 (1995) 2706–2713.

      [32] S.L.B. Owen, L.S. Angelo, R. Radinsky, C.F. Ware, T.G. Gesner, D.P. Bartos. Soluble Fas/APO1 in tumor cells: a potential regulator of apoptosis? .Cancer Lett, 94 (1995)1–8.http://dx.doi.org/10.1016/0304-3835(95)03834-J.

      [33] I. Cascino, G. Fiucci, G. Papoff, G. Ruberti. Three functional soluble forms of the human apoptosis inducing Fas molecule are produced by alternative splicing. J.Immunol , 154 (1995) 2706–2713.

      [34] G. Natoli , A. Innai , A. Costanzo , G. De Petrillo , I. Ilai , C. Chirillo , C. Balsano, M. Levero. Resistance to Fas mediated apoptosis in human hepatoma cells. Oncogene, 10 (1995) 1157–1164.

      [35] T. Suda, T. Takahahi, P. Golstein, S. Nagata. Molecular cloning and expression of the Fas ligand, a novel member of the tumor necrosis factor family. Cell, 75(1993)1169–1178.http://dx.doi.org/10.1016/0092-8674(93)90326-L.

      [36] N. Kayagaki, A. Kawasaki, T. Ebata, et al. Metallo-proteinase mediated release of human Fas ligand. J Exp Med, 182 (1995)1777–1783.http://dx.doi.org/10.1084/jem.182.6.1777.

      [37] M. Tanaka, T. Suda, T. Takahashi, S. Nagata. Expression of the functional soluble form of human Fas ligand inactivated lymphocytes. EMBO J, 14 (1995) 1129–1135.

      [38] G.Papoff, I.Cascino, A. Eramo, G.Starace G, D.H.Lynch, G.Ruberti. An Nâ€terminal domain shared by Fas/Apoâ€1 (CD95) soluble variants prevents cell death invitro. J Immunol, 156 (1996) 4622â€4630.

      [39] . N. Kavathia, A. Jain, J. Walston, A.B. Beamer, S.N. Fedarko.Serum markers of apoptosis decrease with age and cancer stage. J AGING, 1 (2009) 652-663.http://dx.doi.org/10.18632/aging.100069.

      [40] S. Nagata. Fas and Fas ligand: a death factor and its receptor. Adv.Immunol, 57 (1994)12–144.http://dx.doi.org/10.1016/S0065-2776(08)60672-0.

      [41] T. Sato,S. Irie, S. Kitada, J.C.Reed. FAP1: a protein tyrosine phosphatase that associates with Fas. Science, 268 (1995)411–415.http://dx.doi.org/10.1126/science.7536343.

      [42] G. Natoli, A. Innai, A. Costanzo, G. DePetrillo, I. Ilai, C. Chirillo, C. Balsano, M. Levero. Resistance to Fas mediated apoptosis in human hepatoma cells. Oncogene, 10 (1995)1157–1164.

      [43] M. Zornig, A. Grzeschizek, M.B. Kowalsky, K.U. Hartmann, T. Moroy. Loss of Fas/APO-1 receptor accelerates lymphoma-genesis in EmL-MYC transgenic mice but not in animals infected with Mo MuLV. Oncogene, 10(1995) 2397–2401.

      [44] M.I. Othman, M.I. Majid, M. Singh, S. Subathra, L. Seng, L.H. Gam. Proteomics of Grade 3 infiltrating ductal carcinoma in Malaysian Chinese breast cancer patients. BiotechnolApplBiochem, 52(2009) 209-19.http://dx.doi.org/10.1042/BA20070271.

      [45] R. Farag, M. Ahmed, M. El-Gendy, I. Mohamed. Evaluation of oxidative stress and apoptosis in breast cancer. Egyptien Journal of Biochemistry and Molecular Biology, 27(2009) 63-82.

      [46] G.N. Ray, M. Shahid, S.A. Husain. Effect of nitric oxide and malondialdehyde on sister-chromatid exchanges in breast cancer. Br J Biomed Sci 58 (2001) 169-76.

      [47] A. Gönenç, D. Erten, S. Aslan, M. Akinci, B. Simşek, M. Torun. Lipid peroxidation and antioxidant status in blood and tissue of malignant breast tumor and benign breast disease. Cell BiolInt, 30 (2006) 376-80.http://dx.doi.org/10.1016/j.cellbi.2006.02.005.

      [48] A. Nassar, D. Lawson, G. Cotsonis, C. Cohen. Survivin and caspase-3 expression in breast cancer: correlation with prognostic parameters, proliferation, angiogenesis, and outcome. ApplImmunohistochemMolMorphol, 16 (2008) 113-20.http://dx.doi.org/10.1097/PAI.0b013e318032ea73.

      [49] A. Ates, G. Kihikli, M. Turgay, N. Duman. The levels of serum-soluble Fas in patients with rheumatoid arthritis and systemic sclerosis, Clin. Rheumatol, 23 (2004) 421-425.http://dx.doi.org/10.1007/s10067-004-0909-4.

  • Downloads

  • How to Cite

    Madboly, S. H., Elsaeid Elbawab, E. M., El-Ebidi, A. M. A., Sayed, O. A.-E. raheem, Hassan, M. H., Saleem, T. H., & Elsayed, S. S. E. (2016). Correlations of circulating levels of oxidants, antioxidants and soluble Fas in breast cancer among Egyptian females. International Journal of Basic and Applied Sciences, 5(2), 110-114. https://doi.org/10.14419/ijbas.v5i2.5765