Obesity is associated with elevated cancer risk, which may be represented by elevated genomic damage. Oxidative stress plays a key role in obesity related detrimental health consequences including DNA oxidation damage. The elevated cancer risk in obesity may be a consequence. Weight loss has been shown to reduce genomic damage, but the role of oxidative stress in that has not been clarified.

The aim of this study is therefore to investigate the influence of bariatric surgery induced weight loss on DNA oxidation damage in morbidly obese subjects. For this aim, we used cryopreserved peripheral blood mononuclear cells in the FPG comet assay. Advanced protein oxidation products and 3-nitrotyrosine were measured as oxidative and nitrative protein stress markers. Furthermore, expression of oxidative stress related proteins HSP70 and Nrf2 as well as mitochondrial enzyme citrate synthase and NADPH oxidase subunit p22 phox were analysed.

Our findings revealed significantly reduced DNA strand breaks, but DNA base oxidation was not reduced. We observed significant reduction in plasma AOPPs and 3-nitrotyrosine, which indicated an improvement in oxidative/nitrative stress. However, expression of HSP70 and Nrf2 were not altered after weight loss. In addition, expression of citrate synthase and p22 phox were also unaltered.

Overall, bariatric surgery induced significant reduction in excess body weight and improved the patients’ health status, including reduced DNA strand breaks and slightly improved antioxidant status in some of the investigated endpoints, while cellular ROS formation and DNA oxidation damage stayed unaltered. This complex situation may be due to combined beneficial effects of weight loss and burdening of the body with fat breakdown products. In the future, collecting samples two years after surgery, when patients have been in a weight plateau for some time, might be a promising approach.

肥胖与癌症风险升高有关，这可能表现为基因组损伤升高。氧化应激在肥胖相关的有害健康后果（包括 DNA 氧化损伤）中起着关键作用。肥胖导致癌症风险升高可能是一个结果。体重减轻已被证明可以减少基因组损伤，但氧化应激在其中的作用尚未阐明。

因此，本研究的目的是调查减肥手术引起的体重减轻对病态肥胖受试者 DNA 氧化损伤的影响。为此，我们在 FPG 彗星试验中使用了冷冻保存的外周血单核细胞。高级蛋白质氧化产物和 3-硝基酪氨酸被测量为氧化和硝化蛋白质应激标志物。此外，还分析了氧化应激相关蛋白 HSP70 和 Nrf2 以及线粒体酶柠檬酸合酶和 NADPH 氧化酶亚基 p22 phox 的表达。

我们的研究结果表明 DNA 链断裂显着减少，但 DNA 碱基氧化并未减少。我们观察到血浆 AOPP 和 3-硝基酪氨酸的显着减少，这表明氧化/硝化应激有所改善。然而，体重减轻后 HSP70 和 Nrf2 的表达没有改变。此外，柠檬酸合酶和 p22 phox 的表达也没有改变。

总体而言，减肥手术显着减少了超重并改善了患者的健康状况，包括减少 DNA 链断裂和一些研究终点的抗氧化状态略有改善，而细胞 ROS 形成和 DNA 氧化损伤保持不变。这种复杂的情况可能是由于减肥和脂肪分解产物对身体造成负担的综合有益影响。在未来，当患者处于体重平稳状态一段时间后，在手术后两年收集样本可能是一种很有前景的方法。