Adenosine deaminase, xanthine oxidase, uric acid, and nitric oxide metabolism in the pathogenesis of disease in patients with colon polyps

Öz

Objective: Protrusion of colonic mucosa to the lumen is called polyp. Since adenomatous polyps are neoplastic polyps, determining the factors contributing to the pathogenesis of the disease would be helpful in terms of reducing mortality and morbidity. Variety studies have showed that increased oxidative stress might play an important role in carcinogenesis. The aim of this study was to investigate the relationship between adenosine deaminase, xanthine oxidase nitric oxide, uric acid levels and oxidative stress in patients with colonic polyps to help the elucidation of pathophysiology of the disease. Methods: The study was conducted at Gastroenterology Clinics of Namik Kemal University Training and Research Hospital. Thirty-five subjects who underwent colonoscopy because of any gastrointestinal symptom and whose pathologic evaluation of colonoscopic biopsy revealed adenomatous polyps were enrolled as patient group. Control group was consisted of 36 healthy subjects. Uric acid was measured by an autoanalyzer using photometric method. Adenosine deaminase, xanthine oxidase, and nitric oxide were measured manually using a spectrophotometric method. Results: Xanthine oxidase, uric acid, and nitric oxide levels were found to be significantly higher in patients with colonic polyp compared that of the healthy controls. (p = 0.007; p = 0.02; p

Anahtar Kelimeler

• Colon polyps
• adenosine deaminase
• xanthine oxidase
• uric acid
• nitric oxide.

Kolon polipli hastalarda hastalığın patogenezinde adenozin deaminaz, ksantin oksidaz, ürik asit ve nitrik oksit metabolizması

Öz

Amaç: Kolonik mukozanın lümene protrüze olması polip olarak adlandırılır. Adenomatöz polipler neoplastik polipler olduğundan dolayı hastalığın patogenezine katkıda bulunabilecek tüm faktörlerin gözden geçirilmesi mortalite ve morbiditenin azaltılması açısından uygun olacaktır. Çeşitli araştırmalar karsinogenezde artmış oksidatif stresin rol oynadığını göstermektedir. Kolon adenomlarının malignleşme potansiyeli taşımasından dolayı oksitatif stresin polip patofizyolojisinde önemli rol oynayabileceği düşünülmektedir. Bu çalışmanın amacı kolon polipli hastalarda adenozin deaminaz, ksantin oksidaz, ürik asit ve nitrik oksit düzeylerinin oksidatif stres ve hastalığın patofizyolojisi ile ilişkisini araştırmaktır Yöntemler: Namık Kemal Üniversitesi Uygulama ve Araştırma Hastanesi Gastroenteroloji Polikliniği\'ne başvuran hastalardan gastrointestinal semptomu olan ve yapılan kolonoskopik biyopsi sonucunda adenomatöz polip saptanan 35 hasta incelendi. Kontrol grubu da 36 sağlıklı kişiden oluşturuldu. Ürik asit ölçümü fotometrik metod ile otomatize sistemde, adenozin deaminaz, ksantin oksidaz ve nitrik oksit (NO) ölçümleri manuel olarak spektrofotometrik yöntemle yapıldı. Bulgular: Kolon polipli hastalar ile sağlıklı kontroller karşılaştırıldığında, kolon polipli hastalarda, ksantin oksidaz, ürik asit ve NO düzeyleri istatistiksel olarak anlamlı oranda yüksek bulundu (sırasıyla p=0.007, p=0.02 ve p

Anahtar Kelimeler

• Kolon polipleri
• adenozin deaminaz
• ksantin oksidaz
• ürik asit
• nitrik oksit

Kaynakça

1. Göral V. Kolorektal Polipler ve Polipozis Sendromları. Gün- cel Gastroenteroloji 2003;7/1.
2. Yamaner S.Colorectal Polyps. Kolon Rektum Hast Derg 2007;17:1-8.
3. Federico A, Morgillo F, Tuccillo C, Ciardiello F, Loguercio C. Chronic inflammation and oxidative stress in human car- cinogenesis. Int J Cancer 2007:121,2381–2386.
4. Bartsch H, Nair J. Chronic inflammation and oxidative stress in the genesis and perpetuation of cancer: role of lipidper- oxidation, DNA damage, and repair Langenbecks Arch Surg 2006;391:499–510.
5. Gutteridge JM. Biological origin of free radicals and mech- anisms of antioxidant protection. Chem Biol Interact 1994;91:133-140.
6. Diaz-Castro J, Alferez MJ, Lopez-Aliaga I, et al. Influence of nutritional iron deficiency anemia on DNA stability and lipid peroxidation in rats. Nutrition 2008;24:1167-1173.
7. Hori A, Mizoue T, Kasai H, et al. Body iron store as predic- torof oxidative DNA damage in healthy men and women. Cancer Sci 2010;101:517-522.
8. Nathan C, Xie OW. Regulation of biosynthesis of nitric ox- ide. J Biol Chem 1994;269:13725–13728.

9. Anggard E. Nitric oxide: mediator, murderer and medicine. The Lancet 1994; 343:1199-1206.
10. Waugh WH: Inhibition of iron-catalyzed oxidations by attainable uric acid and ascorbic acid levels: therapeutic implications for Alzheimer’s disease and late cognitive im- pairment. Gerontology 2008;54:238–243.
11. Gurel A, Altinyazar HC, Unalacak M, et al. Purine cata- bolic enzymes and nitric oxide in patients with recurrent aphthous ulceration. Oral Dis 2007;13:570-574.
12. Giuisti G. Enzyme activities. Bergmeyer U. (Ed.), Methods of Enzymatic Analysis, Verlog Chemie, Gmblt Weinheim, Bergest 1974;1092–1098.
13. Prajda N, Weber G. Malign transformation-linked imbal- ance: decreased XO activity in hepatomas. FEBS Lett 1975;59:245-249.
14. Cortas NK, Wakid NW. Determination of inorganic nitrate in serum and urineby a kinetic cadmium-reduction method. Clin Chem 1990;36: 1440–1443.
15. Ikeda K, Mutoh M, Teraoka N, et al. Increase of oxidant- related triglycerides and phosphatidyl cholines in serum and small intestinal mucosa during development of intes- tinal polyp formation in mice. Cancer Sci 2011;102:79-87.
16. Nagababu E, Chrest FJ, Rifkind JM. Hydrogen-peroxide- induced heme degradation in red blood cells: the protective roles of catalase and glutathione peroxidase. Biochim Bio- phys Acta 2003;1620: 211-217.
17. Li H, Horke S, Förstermann U. Oxidative stress in vascular disease and its pharmacological prevention. Trends Phar- macol Sci 2013;34: 313-319.
18. Bras A, Sanches R, Cristovao L, et al. Oxidative stress in familial adenomatous polyposis. Eur J Cancer Prev 1999;8: 305-310.
19. Yildirim A, Altinkaynak K, Aksoy H, et al. Plasma xanthin eoxidase, superoxide dismutase andglutathione peroxidase activities and uric acid levels in severe and mild pre-ec- lampsia. Cell Biochem Funct 2004; 22: 213–217.
20. Kaya EB, Yorgun H, Canpolat U. Serum uric acid levels predict the severity and morphology of coronary athero- sclerosis detected by multidetector computed tomography. Atherosclerosis 2010; 213: 178-183.
21. Cheng TH, Lin JW, Chao HH. Uric acid activates extra- cellular signal-regulated kinases and thereafter endothe- lin-1 expression in rat cardiac fibroblasts. Int J Cardiol 2010;139:42-49.
22. Sogut S, Aydin E, Elyas H, et al. The activities of serum adenosine deaminase and xanthine oxidase enzymes in Be- hcet’s disease. Clin Chim Acta 2002: 325;133–138.
23. Dennis KL, Wang Y, Blatner NR, et al. Adenomatous pol- yps are driven bymicrobe-instigated focal inflammation and are controlled by IL-10 producing T-cells. Cancer Res 2013;1;73:5905-5913.
24. Gounaris E, Blatner NR, Dennis K, et al. T-regulatory cells shift from a protective anti-inflammatory to a cancer-pro- moting proinflammatory phenotype in polyposis. Cancer Res 2009;69:5490-5497.
25. Gersch C, Palii SP, Kim KM, et al. Inacti-vation of nitri- coxide by uricacid. Nucleosides Nucleotides Nucleic Acids 2008;27:967-978.
26. Kanabrocki EL, Sothern RB, Messmore HL, et al. Circa- dian relationship of serum uric acid and nitric oxide. J Am Med Assoc 2000; 283;2240–2241.