Kabzinski Jacek, Walczak Anna, Dziki Adam, Mik Michał, Majsterek Ireneusz
Department of Clinical Chemistry and Biochemistry, Head of the Department prof. dr hab. n. med. Ireneusz Majsterek, Medical University of Lodz, Poland.
Department of General and Colorectal Surgery, Head of the Department prof. dr hab. n. med. Adam Dziki, Medical University of Lodz, Military Medical Academy University Teaching Hospital-Central Veterans' Hospital, Łódź, Poland.
Pol Przegl Chir. 2018 Apr 30;90(2):13-15. doi: 10.5604/01.3001.0011.7486.
As a result of reactive oxygen species operation, cell damage occurs in both cellular organelles and molecules, including DNA. Oxidative damage within the genetic material can lead to accumulation of mutations and consequently to cancer transformation. OGG1 glycosylase, a component of the Base Excision Repair (BER) system, is one of the enzymes that prevents excessive accumulation of 8-oxoguanine (8-oxG), the most common compound formed by oxidative DNA damage. In case of structural changes of OGG1 resulting from polymorphic variants, we can observe a significant increase in the concentration of 8-oxG. Linking individual polymorphisms to DNA repair systems with increased risk of colorectal cancer will allow patients to be classified as high risk and included in a prophylactic program. The aim of the study was to determine the level of oxidative DNA damage and to analyze the distribution of Ser326Cys polymorphism of the OGG1 gene in a group of patients with colorectal cancer and in a control group in the Polish population.
DNA was isolated from the blood of 174 patients with colorectal cancer. The control group consisted of 176 healthy individuals. The level of oxidative damage was determined by analyzing the amount of 8-oxguanine using the HT 8-oxo-dG ELISA II Kit. Genotyping was performed via the TaqMan method.
The obtained results indicate that Ser326Cys polymorphism of the OGG1 gene increases the risk of RJG and is associated with significantly increased levels of 8-oxoguanine.
Based on the results obtained, we conclude that Ser326Cys polymorphism of the OGG1 gene may modulate the risk of colorectal cancer by increasing the level of oxidative DNA damage.
由于活性氧的作用,细胞内的细胞器和分子(包括DNA)都会受到损伤。遗传物质内的氧化损伤会导致突变积累,进而引发癌症转化。OGG1糖基化酶是碱基切除修复(BER)系统的一个组成部分,是防止8-氧代鸟嘌呤(8-oxG)过度积累的酶之一,8-oxG是氧化DNA损伤形成的最常见化合物。如果OGG1因多态性变体而发生结构变化,我们会观察到8-oxG浓度显著增加。将个体多态性与患结直肠癌风险增加的DNA修复系统联系起来,将有助于把患者归类为高风险人群,并纳入预防计划。本研究的目的是确定一组波兰结直肠癌患者和对照组中氧化DNA损伤的水平,并分析OGG1基因Ser326Cys多态性的分布情况。
从174例结直肠癌患者的血液中分离DNA。对照组由176名健康个体组成。使用HT 8-氧代-dG ELISA II试剂盒通过分析8-氧代鸟嘌呤的量来确定氧化损伤水平。通过TaqMan方法进行基因分型。
所得结果表明,OGG1基因的Ser326Cys多态性会增加直肠癌的风险,并与8-氧代鸟嘌呤水平的显著升高有关。
根据所得结果,我们得出结论,OGG1基因的Ser326Cys多态性可能通过增加氧化DNA损伤水平来调节结直肠癌的风险。