Oxidative and DNA damage in obese patients undergoing bariatric surgery: A one-year follow-up study

IF 1.5 4区 医学 Q4 BIOTECHNOLOGY & APPLIED MICROBIOLOGY Mutation Research-Fundamental and Molecular Mechanisms of Mutagenesis Pub Date : 2023-07-01 DOI:10.1016/j.mrfmmm.2023.111827
Anna Chiaramonte , Serena Testi , Caterina Pelosini , Consuelo Micheli , Aurora Falaschi , Giovanni Ceccarini , Ferruccio Santini , Roberto Scarpato
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Abstract

The pathogenesis of obesity and related comorbidities has long been associated with oxidative stress. The excess of adipose tissue contributes to the production of free radicals that sustain both a local and a systemic chronic inflammatory state, whereas its reduction can bring to an improvement in inflammation and oxidative stress. In our work, using the fluorescent lipid probe BODIPY® 581/591 C11 and the γH2AX foci assay, a well-known marker of DNA double strand breaks (DSB), we evaluated the extent of cell membrane oxidation and DNA damage in peripheral blood lymphocytes of normal weight (NW) controls and obese patients sampled before and after bariatric surgery. Compared to NW controls, we observed a marked increase in both the frequencies of oxidized cells or nuclei exhibiting phosphorylation of histone H2AX in preoperatory obese patients. After bariatric surgery, obese patients, resampled over one-year follow-up, improved oxidative damage and reduced the presence of DSB. In conclusion, the present study highlights the importance for obese patients undergoing bariatric surgery to also monitor these molecular markers during their postoperative follow-up.

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接受减肥手术的肥胖患者的氧化和DNA损伤:一项为期一年的随访研究
长期以来,肥胖和相关合并症的发病机制一直与氧化应激有关。过量的脂肪组织有助于产生维持局部和全身慢性炎症状态的自由基,而其减少可以改善炎症和氧化应激。在我们的工作中,使用荧光脂质探针BODIPY®581/591 C11和γH2AX焦点分析(一种众所周知的DNA双链断裂(DSB)标记),我们评估了正常体重(NW)对照和肥胖患者在减肥手术前后取样的外周血淋巴细胞中细胞膜氧化和DNA损伤的程度。与NW对照组相比,我们观察到手术前肥胖患者中表现出组蛋白H2AX磷酸化的氧化细胞或细胞核的频率均显著增加。减肥手术后,肥胖患者在一年多的随访中重新取样,改善了氧化损伤,减少了DSB的存在。总之,本研究强调了接受减肥手术的肥胖患者在术后随访期间监测这些分子标记物的重要性。
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来源期刊
CiteScore
4.90
自引率
0.00%
发文量
24
审稿时长
51 days
期刊介绍: Mutation Research (MR) provides a platform for publishing all aspects of DNA mutations and epimutations, from basic evolutionary aspects to translational applications in genetic and epigenetic diagnostics and therapy. Mutations are defined as all possible alterations in DNA sequence and sequence organization, from point mutations to genome structural variation, chromosomal aberrations and aneuploidy. Epimutations are defined as alterations in the epigenome, i.e., changes in DNA methylation, histone modification and small regulatory RNAs. MR publishes articles in the following areas: Of special interest are basic mechanisms through which DNA damage and mutations impact development and differentiation, stem cell biology and cell fate in general, including various forms of cell death and cellular senescence. The study of genome instability in human molecular epidemiology and in relation to complex phenotypes, such as human disease, is considered a growing area of importance. Mechanisms of (epi)mutation induction, for example, during DNA repair, replication or recombination; novel methods of (epi)mutation detection, with a focus on ultra-high-throughput sequencing. Landscape of somatic mutations and epimutations in cancer and aging. Role of de novo mutations in human disease and aging; mutations in population genomics. Interactions between mutations and epimutations. The role of epimutations in chromatin structure and function. Mitochondrial DNA mutations and their consequences in terms of human disease and aging. Novel ways to generate mutations and epimutations in cell lines and animal models.
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