The relation of SOD, GPx, MDA concentration and TAS with histopathological characteristic in chronic gastritis patients
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Abstract
Objective: To study the relation of serum SOD, GPx, MDA concentration and TAS with histopathological characteristics in patients with chronic gastritis. Subject and method: A descriptive, cross-sectional study was conduted on 136 patient with chronic gastritis. Result: SOD activity in the group with atrophic inflammation 348.54 ± 458.19ng/ml was lower than the group without atrophic inflammation 406.95 ± 309.61ng/ml (p=0.04). SOD activity in the inflammatory group was active highest at 326.27 ± 450.79ng/ml, lower than the active inflammatory group with a mild level of 449.09 ± 481.27ng/ml (p=0.03). GPx activity in the group with atrophic inflammation was 182.71 ± 223.58pg/ml, lower than the group without atrophic inflammation 209.98 ± 159.53pg/ml (p=0.005). GPx activity in the group with dysplasia 94.2 ± 84.23pg/ml was lower than the group without dysplasia 199.97 ± 222.37pg/ml (p=0.03). TAS activity was lowest in the group of severe inflammation and highest in mild inflammation group (p=0.03). TAS activity in the group with atrophic inflammation was 2.02 ± 3.48U/ml higher than the group without atrophic 1.12 ± 1.46U/ml (p=0.002). MDA activity in the group with atrophic inflammation was 5.19 ± 6.84mmol/l lower than the group without inflammation at 7.19 ± 4.96mmol/l (p=0.006). MDA activity in the active inflammation group was low at 7.42 ± 8.34mmol/l, higher than the inflammatory group at the severity of 4.64 ± 5.22mmol/l (p=0.04). Conclusion: The activity of antioxidants in plasma is the lowest in cases of atrophic inflammation, at the same time the activity of antioxidants decreases with the degree of inflammation activity.
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2. Dröge W (2003) Oxidative stress and aging. Adv Exp Med Biol 543: 191-200.
3. Dulger AC, Aslan M, Nazligul Y et al (2011) Peripheral lymphocyte DNA damage and oxidative status after eradication therapy in patients infected with Helicobacter pylori. Polskie archiwum medycyny wewnĘtrznej 121(12): 428-431.
4. Hahm KB, Lee KJ, Kim YS et al (1998) Augmented eradication rates of Helicobacter pylori by new combination therapy with lansoprazole, amoxicillin, and rebamipide. Digestive Diseases and Sciences 43(2): 235-240.
5. Marjanović K, Dovhanj J, Kljaić K et al (2010) Role of zinc in chronic gastritis. Coll. Antropol 34(2): 599-603.
6. Noyan T, Guducuoglu H, and Ilhan M (2009) A study of oxidative stress parameters in anti-Helicobacter pylorus immunoglobuling positive and negative gastric cancer patients. Yonsei Med J 50(5): 677-682.
7. Pignatelli B, Bancel B, Plummer M et al (2001) Helicobacter pylori eradication attenuates oxidative stress in human gastric mucosa. Am J Gastroenterol 96(6): 1758-1766.
8. Schlemper RJ, Riddell RH, Kato Y et al (2000) The Vienna classification of gastrointestinal epithelial neoplasia. Gut 47(2): 251-255.
9. Rugge M, Pennelli G, Pilozzi E et al (2011) Gastritis: The histology report. Digestive and Liver Diseas 43: 373-384.
10. Sasaki M and Joh T (2007) Oxidative stress and ischemia-reperfusion injury in gastrointestinal tract and antioxidant, protective agents. J. Clin. Biochem. Nutr 40: 1-12.