Background: Our aim is to investigate whether brucellosis causes carcinogenesis through studying the oxidative/anti-oxidative level and DNA damage in different serological titers of brucellosis.

Material and Methods: In the different serological test titers of brucellosis standard agglutination test (SAT): 1/40 = 12 people, 1/80 = 13 people, 1/160 = 13 people, 1/320 = 12 people, 1/640 = 12 people) and 19 healthy people were included in the study. DNA damage was investigated through 8-hydroxy-2'-deoxyguanosine Cayman’s ELISA kit method. The total oxidative status (TOS), total antioxidant capacity (TAC), total thiol (SH) and lipid hydroperoxide (LOOH) levels were analyzed through colorimetric method. Also, oxidative stress index (OSI) was found via calculation.

Results: It was realized that the TOS, LOOH, OSI and DNA damage gradually increased beginning from the control group and brucella SAT 1/40 titer and gained statistical significance (respectively at the 1/160, 1/640, 1/160, 1/80 titers). (p < 0.001). The TAC and SH however, was found to gradually decrease beginning from the control group and brucella SAT 1/40 titer and gain statistical significance (respectively, at the 1/320, 1/640 titers). (p < 0.001). There was a significantly positive correlation between serum brucella SAT titers and DNA damage, TOS, OSI and LOOH (respectively, rho = 0.796, 0.810, 0.389, 0.717). And there was significantly negative correlation between brucella SAT titers and TAC and SH (respectively, rho = -0.540, -0.503).

Conclusion: The serological antibody titer increased in brucellosis, oxidative stress and DNA damage also increased in relation to it. And this DNA damage might lead to brucellosis-related mutation and carcinogenesis. Therefore, these patients must be treated urgently to counteract the DNA damage.

Keywords: Brucellosis; Oxidative Stress; DNA Damage; Carcinogenesis

References

1. Coussens LM and Werb Z. “Inflammation and cancer”. Nature 420 (2002): 860-867.
2. Kawanishi S and Hiraku Y. “Oxidative and nitrative DNA damage as biomarker for carcinogenesis with special reference to inflammation”. Antioxidants and Redox Signaling 8 (2006): 1047-1058.
3. Murata M., et al. “Role of nitrative and oxidative DNA damage in inflammation-related carcinogenesis”. Journal of Biomedicine and Biotechnology 2012 (2012): 623019.
4. IARC. “Chronic infections”. In: Stewart BW, Kleihues P, editors. World cancer report. Lyon: IARC Press (2008): 128-135.
5. Kawanishi S., et al. “Nitrative and oxidative DNA damage in infection-related carcinogenesis in relation to cancer stem cells”. Genes and Environment 1.39 (2017): 8.
6. Selek S., et al. “Peripheral DNA Damage in Active Pulmonary Tuberculosis”. Environmental Toxicology 27.6 (2012): 380-384. 
7. Kocyigit A., et al. “Increased DNA damage and oxidative stress in patients with cutaneous leishmaniasis”. Mutation Research 585.1-2 (2005): 71-78.
8. Karsen H., et al. “Serum paraoxonase and arylesterase activities and oxidant status in patients with brucellosis”. African Journal of Microbiology Research 5.13 (2011): 1701-1706.
9. Usta M., et al. “Oxidant and antioxidant parameters in patients with Brucella canis”. Clinical Biochemistry 45 (2012): 366-367.
10. Karaagac L., et al. “Decreasing oxidative stress in response to treatment in patients with brucellosis: could it be used to monitor treatment?” International Journal of Infectious Diseases 15 (2011): 346-349.
11. Nourooz Zadeh J. “Ferrous ion oxidation in presence of xylenol orange for detection of lipid hydroperoxides in plasma”. Methods in Enzymology 300 (1999): 58-62. 
12. Ellman GL. “Tissue sulfhydryl groups”. Archives of Biochemistry and Biophysics 82 (1959): 70-77.
13. Hu ML. “Measurement of protein thiol groups and glutathione in plasma”. Methods in Enzymology 233 (1994): 380-385.
14. Da Costa CM., et al. “A simple automated procedure for thiol measurement in human serum samples”. Jornal Brasileiro de Patologia e Medicina Laboratorial 42 (2006): 345-350.
15. Erel O. “A novel automated direct measurement method for total antioxidant capacity using a new generation, more stable ABTS radical cation”. Clinical Biochemistry 37 (2004): 277-285.
16. Erel O. “A new automated colorimetric method for measuring total oxidant status”. Clinical Biochemistry 38 (2005): 1103-1111.
17. Young EJ. “Brucella species”. In: Mandell GL, Bennett JE, Dolin R, editors. Principles and practice of infectious diseases. 6th ed, Philadelphia: Churchill Livingstone (2005): 2669- 2672.
18. Franco MP., et al. “Human brucellosis”. Lancet Infection Disease 7 (2007): 775-786.
19. Kataria N., et al. “Evaluation of oxidative stress in brucella infected cows”. Journal of Stress Physiology and Biochemistry 6 (2010): 19-25.
20. Liautard JP., et al. “Interactions between professional phagocytes and Brucella spp”. Microbiologia 12 (1996): 197-206.
21. Nathan C and Xie QW. “Regulation of biosynthesis of nitric oxide”. Journal of Biological Chemistry 269 (1994): 13725-13728. 
22. Jiang X and Baldwin CL. “Macrophage control of Brucella abortus: role of reactive oxygen intermediates and nitric oxide”. Cell Immunology 151 (1993): 309-319.
23. Cadet J., et al. “Formation and repair of oxidatively generated damage in cellular DNA”. Free Radical Biology and Medicine (2017).
24. Halliwell B and Aruoma O. “DNA damage by oxygen-derived species: Its mechanism and measurement in mammalian systems”. FEBS Letter 281 (1991): 9-19.
25. Valko M., et al. “Role of oxygen radicals in DNA damage and cancer incidence”. Molecular and Cellular Biochemistry 266 (2004): 37-56.
26. Paz-Elizur T., et al. “DNA repair of oxidative DNA damage in human carcinogenesis: Potential application for cancer risk assessment and prevention”. Cancer Letter 266 (2008): 60-72.

Citation

Citation: Hasan Karsen., et al. “Increased DNA Damage and Oxidative Stress in Patients with Brucellosis". Acta Scientific Nutritional Health 4.4 (2020): 02-06.

Copyright

Copyright: © 2020 Hasan Karsen., et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.