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评估炎症性肠病患者的 DNA 损伤谱和氧化/抗氧化生物标志物水平。

Assessment of DNA damage profile and oxidative /antioxidative biomarker level in patients with inflammatory bowel disease.

机构信息

Department of Clinical Chemistry and Biochemistry, Medical University, Lodz, Poland.

Chair of Surgery, Department of General and Colorectal Surgery, Medical University, Lodz, Poland.

出版信息

Pol Przegl Chir. 2020 May 26;92(5):8-15. doi: 10.5604/01.3001.0014.1548.

Abstract

<b>Aim:</b> The purpose of this study was to investigate the oxidative DNA damage, pro-antioxidant status in Polish patients with inflammatory bowel disease (IBD). <br><b>Methods:</b> Oxidative DNA damage was measured by comet assay techniques; nitric oxide (NO) and plasmatic lipid peroxidation (MDA) as oxidative stress were valuated by colometric methods; superoxide dismutase (SOD1), catalase (CAT) and glutathione peroxidase (GPx1) as antioxidative defense were determined by spectrophotometric methods. <br><b>Results:</b> The level of oxidative DNA damage in IBD patients was significantly higher in relation to controls (P = 0.01). Alike, in control subject as well as in patients with IBD, lymphocytes are characterized by complete repair of DNA damage. A significant decrease of SOD (P = 0.031), CAT (P = 0.006), GPx1 (P = 0.001) activity was seen in IBD patients vs control. MDA (P = 0.001) and NO (P = 0.001) concentrations were significantly increased in IBD patients as compared to healthy subjects. <br><b>Conclusions:</b> Our results may be due to the induction of DNA repair genes which may occur at the stage of the pathological changes (IBD) that may be caused by excessive oxidative stress. However, the cause of this relationship, and whether it is direct or indirect, remains to be explored.

摘要

目的

本研究旨在探讨波兰炎症性肠病(IBD)患者的氧化 DNA 损伤和前抗氧化状态。
方法:采用彗星试验技术检测氧化 DNA 损伤;比色法评估一氧化氮(NO)和血浆脂质过氧化(MDA)作为氧化应激;分光光度法测定超氧化物歧化酶(SOD1)、过氧化氢酶(CAT)和谷胱甘肽过氧化物酶(GPx1)作为抗氧化防御。
结果:与对照组相比,IBD 患者的氧化 DNA 损伤水平显著升高(P = 0.01)。同样,在对照组和 IBD 患者中,淋巴细胞均表现出 DNA 损伤的完全修复。与对照组相比,IBD 患者的 SOD(P = 0.031)、CAT(P = 0.006)和 GPx1(P = 0.001)活性显著降低。与健康受试者相比,IBD 患者的 MDA(P = 0.001)和 NO(P = 0.001)浓度显著增加。
结论:我们的结果可能是由于诱导 DNA 修复基因所致,这些基因可能发生在病理变化(IBD)阶段,这可能是由过度氧化应激引起的。然而,这种关系的原因,以及它是直接的还是间接的,仍有待探讨。

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