Comparison of 8-Hydroxy-Deoxyguanosine Levels in Cervical Cancer Advanced Stages Before and After Chemotherapy

Authors

  • Sardina Department of Obstetrics and Gynecology, Faculty of Medicine, Hasanuddin University, Makassar, Indonesia Author
  • Syahrul Rauf Department of Obstetrics and Gynecology, Faculty of Medicine, Hasanuddin University, Makassar, Indonesia Author
  • Rina Previana Amiruddin Department of Obstetrics and Gynecology, Faculty of Medicine, Hasanuddin University, Makassar, Indonesia Author
  • Siti Nur Asni Department of Obstetrics and Gynecology, Faculty of Medicine, Hasanuddin University, Makassar, Indonesia Author
  • Maisuri Tadjuddin Department of Obstetrics and Gynecology, Faculty of Medicine, Hasanuddin University, Makassar, Indonesia Author
  • Sharvianty Arifuddin Department of Obstetrics and Gynecology, Faculty of Medicine, Hasanuddin University, Makassar, Indonesia Author

DOI:

https://doi.org/10.61841/r2wdfq43

Keywords:

8-hydroxy-deoxyguanosine, cervical cancer, advanced stages

Abstract

Cervical cancer is the most commonly diagnosed cancer and the third leading cause of death of women in poor and developing countries. 8-hydroxy-deoxyguanosine (8-OHdG) levels have been widely used as a biomarker of oxidative DNA damage, including cervical cancer. This study aims to compare levels of 8-hydroxy-deoxyguanosine (8-OHdG) as a marker of oxidative stress in advanced cervical cancer (FIGO stages) before and after chemotherapy. This prospective study involved 18 patients stage IIB, 8 patients stage IIIA, 9 patients stage IIIB, and 2 patients stage IIIC of cervical cancer. 8-OHdG levels were measured with the ELISA method. The mean level of 8-OHdG before chemotherapy in stage II was 8.14±9.14 ng/ml and in stage III 8.07±8.79 ng/ml, whereas the mean level of 8-OHdG after chemotherapy in stage II was 24.24±12.46 ng/ml and at stage III 24.67±13.85 ng/ml. 8-OHdG levels increased significantly (p<.05) in stages IIA, IIIA, and IIIB after chemotherapy. In contrast, 8-OHdG levels in stage IIIC were not significantly increased after chemotherapy. In addition, 8-OHdG levels were significantly different between SCC and adenocarcinoma. Likewise, the type of differentiation is good, moderate, and non-classification. 8-OHdG levels increase significantly in advanced stages of cervical cancer after chemotherapy. 

Downloads

Download data is not yet available.

References

1. Torre LA, Bray F, Siegel L, et al. Global Cancer Statistics 2012. Ca Cancer J Clin 2015;65:87–108.

2. Forman D, de Martel C, Lacey CJ, et al. Global burden of human papillomavirus and related diseases.

Vaccine 2012;30:F12-F23.

3. Woodman CBJ, Collins SI, Young LS: The natural history of cervical HPV infection: unresolved issues.

Nat Rev Cancer 2007;7:11-22.

4. zur Hausen H. Papillomaviruses in the causation of human cancers—a brief historical account. Virology

2009;384:260-5.

5. Klaunig JE, Kamendulis LM. The role of oxidative stress in carcinogenesis. Annu Rev Pharmacol

Toxocol 2004;44:29–67.

6. Kolanjiappan K, Manoharan S, Kayalvizhi M. Measurement of erythrocyte lipids, lipid peroxidation,

antioxidants and osmotic fragility in cervical cancer patients. Clin Chim Acta. 2002;326(1-2):143-9.

7. Looi ML, Mohd Dali AZ, Md Ali SA, et al. Oxidative damage and antioxidant status in patients with

cervical intraepithelial neoplasia and carcinoma of the cervix. Eur J Cancer Prev. 2008;17(6):555-560.

8. Beevi SS, Rasheed MH, Geetha A. Evidence of oxidative and nitrosative stress in patients with cervical

squamous cell carcinoma. Clin Chim Acta. 2007;375(1-2):119-23.

9. Gao CM, Takezaki T, Wu JZ, et al. Polymorphisms in thymidylate synthase and

methylenetetrahydrofolate reductase genes and the susceptibility to esophageal and stomach cancer with

smoking. Asian Pac J Cancer Prev. 2004;5(2):133-8.

10. Hwang ES, Bowen PE. DNA damage, a biomarker of carcinogenesis: Its measurement and modulation

by diet and environment. Crit Rev Food Sci Nutr 2007;47:27–50.

11. Ock CY, Kim EH, Choi DJ, et al. 8-Hydroxydeoxyguanosine: not mere biomarker for oxidative stres,

but remedy for oxidative stress-implicated gastrointestinal diseases. World J Gastroenterol.

2012;18(4):302-308.

12. Miyake H, Hara I, Kamidono S, Eto H. Oxidative DNA damage in patients with prostate cancer and its

response to treatment. J Urol. 2004;171:1533–36.

13. Weiss JM, Goode EL, Ladiges WC, Ulrich CM. Polymorphic variation in hOGG1 and risk of cancer: A review of the functional and epidemiologic literature. Mol Carcinog 2005;42:127–141.

14. Diakowska D, Lewandowski A, Kopec W, et al. Oxidative DNA damage and total antioxidant status in serum of patients with esophageal squamous cell carcinoma. Hepatogastroenterology 2007;54:1701–4.

15. Tanaka H, Fujita N, Sugimoto R, et al. Hepatic oxidative DNA damage is associated with increased risk

for hepatocellular carcinoma in chronic hepatitis C. Br J Cancer 2008;98:580–586.

16. Romano R, A Sgambato A, Mancini R, et al., 8-hydroxy-2'-deoxyguanosine in Cervical Cells:

Correlation With Grade of Dysplasia and Human Papillomavirus Infection. Carcinogenesis

2000;21(6):1143-1147.

17. Sgambato A, Zannoni GF, Faraglia B, et al. Decreased expression of the CDK in hibitor p27Kip1 and

increased oxidative DNA damage in the multistep process of cervical carcinogenesis. Gynecol Oncol

2004;92(3):776–83.

18. Jelić M, Mandić A, Kladar N, et al. Lipid peroxidation, antioxidative defense and level of 8-hydroxy-2-

deoxyguanosine in cervical cancer patients. J Med Biochem. 2018;37(3):336-345.

19. Cooke MS, Loft S, Olinski R. Measurement and meaning of oxidatively modified DNA lesions in urine.

CEBP 2008;17:3–14.

20. Pylväs-Eerola M, Karihtala P, Puistola U. Preoperative serum 8-hydroxydeoxyguanosine is associated

with chemoresistance and is a powerful prognostic factor in endometrioid-type epithelial ovarian cancer.

BMC Cancer. 2015;15:493.

21. Filippova M, Filippov V, Williams VM, et al. Cellular levels of oxidative stress affect the response of

cervical cancer cells to chemotherapeutic agents. Biomed Res Int. 2014;2014:574659.

22. Liu J, Wang Z. Increased oxidative stress as a selective anticancer therapy. Oxidative Med Cell Longev.

2015;2015:294303.

23. Leone A, Roca MS, Ciardiello C, et al. Oxidative stress gene expression profile correlates with cancer

patient poor prognosis: identification of crucial pathways might select novel therapeutic approaches.

Oxidative Med Cell Longev. 2017;2017:2597581.

24. Postovit L, Widmann C, Huang P, Gibson SB. Harnessing oxidative stress as an innovative target for

cancer therapy. Oxidative Med Cell Longev. 2018;2018:6135739.

25. Conklin KA. Chemotherapy-associated oxidative stress: impact on chemotherapeutic effectiveness.

Integr Cancer Ther 2004; 3: 294-300.

26. Wang J, Lin D, Peng H, et al. Cancer-derived immunoglobulin G promotes LPS-induced

proinflammatory cytokine production via binding to TLR4 in cervical cancer cells. Oncotarget

2014;5(20):9727–43.

27. Lovell MA, Gabbita P, Markesbery WR. Increased DNA oxidation and decreased levels of repair

products in Alzheimer’s disease ventricular CSF. J Neurochem 1999;72:771–776.

28. Hata I, Kaji M, Hirano S, et al. Urinary oxidative stres markers in young patients with type 1 diabetes.

Pediatr Int 2006;48:58–61.

29. Wong RH, Kuo CY, Hsu ML, et al. Increased levels of 8-hydroxy-20-deoxyguanosine attributable to

carcinogenic metal exposure among school children. Environ Health Perspect 2005;113:1386–1390.

30. Irie M, Tamae K, Iwamoto-Tanaka N, Kasai H. Occupational and lifestyle factors and urinary 8-

hydroxydeoxyguanosine. Cancer Sci. 2005;96:600–606.

31. Rodic S, Vincent DM, Reactive oxygen species (ROS) are key determinant of cancer’s metabolic phenotype. IJC. 2018 :440-448.

32. Mizutani H, Tada-Oikawa S, Hiraku Y, Kojima M, Kawanishi S. Mechanism of apoptosis induced by doxorubicin through the generation of hydrogen peroxide. Life Sci. 2005;76:1439–53.

33. Shi H, Shi X, Liu KJ. Oxidative mechanism of arsenic toxicity and carcinogenesis. Mol Cell Biochem.

2004;255:67–78.

34. Brozovic A, Ambriović-Ristov A, Osmak M. The relationship between cisplatin-induced reactive

oxygen species, glutathione, and BCL-2 and resistance to cisplatin. Crit Rev Toxicol. 2010;40(4):347–

359.

35. Raudenska M, Balvan J, Fojtu M, et al. Unexpected therapeutic effects of cisplatin. Metallomics.

2019;11(7):1182–1199.

36. Apel K, Hirt H. Reactive oxygen species: metabolism, oxidative stress, and signal transduction. Annu

Rev Plant Biol. 2004;55:373–99.

37. Yang H, Villani RM, Wang H, et al. The role of cellular reactive oxygen species in cancer

chemotherapy. J Exp Clin Cancer Res. 2018;37(1):266.

38. Maiti AK. Gene network analysis of oxidative stress-mediated drug sensitivity in resistant ovarian

carcinoma cells. Pharmacogenomics J. 2010;10:94–104.

39. Chou WC, Jie C, Kenedy AA, et al. Role of NADPH oxidase in arsenic-induced reactive oxygen species formation and cytotoxicity in myeloid leukemia cells. Proc Natl Acad Sci U S A. 2004;101:4578–83.

40. Dixon SJ, Lemberg KM, Lamprecht MR, et al. Ferroptosis: an irondependent form of nonapoptotic cell death. Cell. 2012;149:1060–72.

41. Sallmyr A, Fan J, Datta K, et al. Internal tandem duplication of FLT3 (FLT3/ITD) induces increased ROS production, DNA damage, and misrepair: implications for poor prognosis in AML. Blood. 2008;111:3173–82.

Downloads

Published

31.05.2020

How to Cite

Sardina, Rauf, S., Previana Amiruddin, R., Nur Asni, S., Tadjuddin, M., & Arifuddin, S. (2020). Comparison of 8-Hydroxy-Deoxyguanosine Levels in Cervical Cancer Advanced Stages Before and After Chemotherapy. International Journal of Psychosocial Rehabilitation, 24(3), 3971-3978. https://doi.org/10.61841/r2wdfq43