Assessment of Biomarkers of Oxidative Stress among Patients with Lymphoma

Journal of Chemical Health Risks

دوره 11، شماره 2، شهریور 2021، صفحه 163-167   

نوع مقاله: Original Article

شناسه دیجیتال (DOI): 10.22034/jchr.2021.1916955.1228

نویسندگان

Hosnie Hoseini¹؛ Parichehreh Yaghmaei^{* 2}؛ Gholamrezagh Bahari^{3، 4}؛ Saeed Aminzadeh⁵

¹Department of Biology, Science and Research Branch,Islamic Azad University,Tehran,Iran

²Department of Biology,Science and Research Branch,Islamic Azad University,Tehran,Iran

³Department of Clinical Biochemistry,School of Medicin,Zahedan University of Medical Sciences,Zahedan,Iran

⁴Children and Adolescent Health Research Center, Resistant Tuberculosis Institute, Zahedan University of Medical Sciences, Zahedan, Iran

⁵Bioprocess Engineering Group,National Institute for Genetic Engineering and Biotechnology,Tehran, Iran

چکیده

The role of oxidative stress is one of the most important factors in the development of cancer. In this study, the catalase activity and total antioxidant capacity in NHL patients were measures and compared with those in healthy subjects. The population of this study consisted of 25 patients with non-Hodgkin's lymphoma, diagnosed based on pathological findings. Total antioxidant capacity (TAC) and catalase catalytic activity (CAT) were determined by spectrophotometry.  Based on the results, the CAT activity  was significantly lower and TAC was lower (0.29±0.04 vs. 2.69±0.15; P-value=0.01) in NHL patients than in healthy subjects. The findings showed that these markers could be used as a prognosis in non-Hodgkin's lymphoma that oxidative stress may also be related to the NHL or increase the risk of disease.

کلیدواژه‌ها

Non-Hodgkin lymphoma؛ Catalytic activity catalase؛ Total antioxidant capacity

مراجع

1. Müller A., Ihorst G., Mertelsmann R., Engelhardt M., 2005. Epidemiology of non-Hodgkin’s lymphoma (NHL): trends, Geographic distribution and aetiology. Ann Hematol. 84,1–12.

 2. Armitage J., Longo D., 2008. Malignancies of lymphoid cells. Harrison's Principles of Internal Medicine. 641–56.

 3. Durackova Z., 2009 . Some current insights into oxidative stress. Physiol Res. Reactive oxygen intermediates as mediators of programmed necrobiosis in plants and animals. BiochemPharmacol. 57,231–245.

 4. Boscia F., Grattagliano I., Vendemiale G., Micelli-Ferrari T., Altomare E., 2000. Protein oxidation in humans. Investigative Ophthalmology and Visual Science. 41,2461–2465.

 5. Taylor A., Nowell T., 1997. Oxidative stress and antioxidant function in relation to NHL. Advances in Pharmacology. 38,515–536.

 6. Sun Y., Oberley L.W., Li Y., 1988. A simple method for clinical assay of SOD. Clinical Chemistry. 34,497–500.

 7. Paglia D.E., Valentine W.N., 1967. Studies on the quantitative and qualitative characterization of erythrocyte peroxidase . The Journal of Laboratory and Clinical Medicine. 70,158–169.

 8. Aebi H., 1984. Catalase in vitro . Methods in Enzymology. 105,121–126.

 9. Witko-Sarsat V., Friedlander M., Capeillère-Blandin C., 1996. Advanced oxidation protein products as a completely unique marker of oxidative stress in uremia. Kidney International. 49,1304–1313.

 10. Reznick A.Z., Packer L., 1994. Oxidative damage to proteins: spectrophotometric method for carbonyl assay. Methods in Enzymology. 233,357–363.

 11. Sasaki H., Jonasson F., Shui Y.B., 2002. High prevalence of nuclear cataract within the population of tropical and subtropical areas. Developments in Ophthalmology. 35,60–69.

 12. Betteridge D.J., 2000.What is oxidative stress? Metabolism. 49,3–8.

 13. Huang L., Yappert M.C., Jumblatt M.M., Borchman D., 2008. Hyperoxia and thyroxine treatment and therefore the relationships between reactive oxygen species generation, mitochondrial membrane potential, and cardiolipin in human lens somatic cell cultures. Current Eye Research. 33,575–586.

 14. Stadtman E.R., 1992. Protein oxidation and aging. Science. 257,1220–1224.

 15. Alderman C.J.J., Shah S., Foreman J.C., Chain B.M., Katz D.R., 2002. The role of advanced oxidation protein products in regulation of dendritic cell function. Free Radical Biology and Medicine. 32,377–385.

16. deZwart L.L., Meerman J.H.N., Commandeur J.N.M., 1999. Vermeulen NPE. Biomarkers of radical damage applications in experimental animals and in humans. Free Radical Biology and Medicine. 26,202–226.

 17. Kalousová M., Skrha J., Zima T., 2002. Advanced glycation end-products and advanced oxidation protein products in patients with DM . Physiological Research. 51,597–604.

 18. Witko-Sarsat V., Friedlander M., Khoa T.N., 1998. Advanced oxidation protein products as novel mediators of inflammation and monocyte activation in chronic renal failure . Journal of Immunology. 161,2524–2532.

 19. Pan H.Z., Zhang H., Chang D., Li H., Sui H., 2008.The change of oxidative stress products in DM and diabetic retinopathy. British Journal of Ophthalmology. 92,548–551.

20. Garland D., 1990. Role of site-specific, metal-catalyzed oxidation in lens aging and cataract. a hypothesis. Experimental Eye Research. 50,677–682.

21. Wolf N., Pendergrass W., Singh N., Swisshelm K., Schwartz J., 2008. Radiation cataracts: mechanisms involved in their long delayed occurrence on the opposite hand rapid progression. Molecular Vision. 14, 274–285.

 22.Alonso de Vega J.M., Diaz J., Serrano E., Carbonell L.F., 2002.Oxidative stress in critically ill patients with systemic inflammatory response syndrome. Crit Care Med.30,1782–1786.

23.Alonso de Vega J.M., Diaz J., Serrano E., Carbonell L.F., 2000. Plasma redox status relates to severity in critically ill patients. Crit Care Med. 28,1812–1814.

 24.Ghiselli A., Serafini M., Natella F., Scaccini C., 2000.Total antioxidant capacity as a tool to assess redox status: critical view and experimental data. Free Rad Biol Med. 29,1106–1114.

25.Motoyama T., Okamoto K., Kukita I., Hamaguchi M., Kinoshita Y., Ogawa H., 2003. Possible role of increased oxidant stress in multiple organ failure after systemic inflammatory response syndrome. Crit Care Med. 31,1048–1052.

 26.Tsai K., Hsu TG., Kong C.W., Lin K., Lu F., 2000. Is the endogenous peroxyl-radical scavenging capacity of plasma protective in systemic inflammatory disorders in humans? Free Rad Biol Med. 28,926–933.

27.MacKinnon KL., Molnar Z., Lowe D., Watson I.D., Shearer E., 1999. Measures of total radical activity in critically ill patients. ClinBiochem. 32,263–268.

 28.Teng R.J., Ye Y.Z., Parks D.A., Beckman J.S., 2002. Urate produced during hypoxia protects heart proteins from peroxynitrite-mediated protein nitration. Free Rad Biol Med. 33,1243–1249.

29.Anker S.D., Doehner W., Rauchhaus M., Sharma R., Francis D., Knosalla C., Davos C.H., Cicoira M., Shamim W., Kemp M., 2003. Uric acid and survival in chronic heart failure: validation and application in metabolic, functional, and hemodynamic staging.Circulation.107,1991–1997.

 30.Whitehead T.P., Thorpe G.H.G., Maxwell S.R.J., 1992.Enhanced chemiluminescent assay for antioxidant capacity in biological fluids. AnalyticaChimicaActa. 266,265–277.

 31.Altman D.G., 2000.Confidence intervals in practice. In: Altman DG, Machin D, Bryant TN, Gardner MJ, editor. Statistics with Confidence: Confidence Intervals and Statistical Guidelines. 6–14.

32.Dasgupta A., Malhotra D., Levy H., Marcadis D., Blackwell W., Johnston D., 1997. Decreased total antioxidant capacity but normal lipid hydroperoxide concentrations in sera of critically ill patients. Life Sciences. 60,335–340.