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

2020 ◽  
Vol 92 (4) ◽  
pp. 1-5
Author(s):  
Małgorzata Mrowicka ◽  
Jerzy Mrowicki ◽  
Michał Mik ◽  
Łukasz Dziki ◽  
Adam Dziki ◽  
...  

Aim: The purpose of this study was to investigate the oxidative DNA damage, pro- antioxidant status in Polish patients with inflammatory bowel disease (IBD). Method: Oxidative DNA damage were 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 defence were determined by spectrophotometric methods. Results: 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 than in healthy subjects. Conclusion: Our results may be due to induction of DNA repair genes may occur at the stage of the pathological changes pathway (IBD), that may be caused by excessive oxidative stress. However, the reasons for these relationship, and whether it is direct or indirect, remains to be explored.

2016 ◽  
Vol 10 (11) ◽  
pp. 1316-1323 ◽  
Author(s):  
Cristiana Pereira ◽  
Rosa Coelho ◽  
Daniela Grácio ◽  
Cláudia Dias ◽  
Marco Silva ◽  
...  

BioFactors ◽  
2007 ◽  
Vol 31 (3-4) ◽  
pp. 191-200 ◽  
Author(s):  
Mojgan Najafzadeh ◽  
P. Dominic Reynolds ◽  
Adolf Baumgartner ◽  
David Jerwood ◽  
Diana Anderson

2007 ◽  
Vol 52 (7) ◽  
pp. 1636-1641 ◽  
Author(s):  
Yıldız Dincer ◽  
Yusuf Erzin ◽  
Solen Himmetoglu ◽  
Kezban Nur Gunes ◽  
Kadir Bal ◽  
...  

2020 ◽  
Vol 8 (Suppl 3) ◽  
pp. A38-A38
Author(s):  
Shilpa Ravindran ◽  
Heba Sidahmed ◽  
Harshitha Manjunath ◽  
Rebecca Mathew ◽  
Tanwir Habib ◽  
...  

BackgroundPatients with inflammatory bowel disease (IBD) have increased risk of developing colorectal cancer (CRC), depending on the duration and severity of the disease. The evolutionary process in IBD is driven by chronic inflammation leading to epithelial-to-mesenchymal transition (EMT) events in colonic fibrotic areas. EMT plays a determinant role in tumor formation and progression, through the acquisition of ‘stemness’ properties and the generation of neoplastic cells. The aim of this study is to monitor EMT/cancer initiating tracts in IBD in association with the deep characterization of inflammation in order to assess the mechanisms of IBD severity and progression towards malignancy.Methods10 pediatric and 20 adult IBD patients, admitted at Sidra Medicine (SM) and Hamad Medical Corporation (HMC) respectively, have been enrolled in this study, from whom gut tissue biopsies (from both left and right side) were collected. Retrospectively collected tissues (N=10) from patients with malignancy and history of IBD were included in the study. DNA and RNA were extracted from fresh small size (2–4 mm in diameter) gut tissues using the BioMasher II (Kimble) and All Prep DNA/RNA kits (Qiagen). MicroRNA (miRNA; N=700) and gene expression (N=800) profiling have been performed (cCounter platform; Nanostring) as well as the methylation profiling microarray (Infinium Methylation Epic Bead Chip kit, Illumina) to interrogate up to 850,000 methylation sites across the genome.ResultsDifferential miRNA profile (N=27 miRNA; p<0.05) was found by the comparison of tissues from pediatric and adult patients. These miRNAs regulate: i. oxidative stress damage (e.g., miR 99b), ii. hypoxia induced autophagy; iii. genes associated with the susceptibility to IBD (ATG16L1, NOD2, IRGM), iv. immune responses, such as TH17 T cell subset (miR 29). N=6 miRNAs (miR135b, 10a196b, 125b, let7c, 375) linked with the regulation of Wnt/b-catenin, EM-transaction, autophagy, oxidative stress and play role also in cell proliferation and mobilization and colorectal cancer development were differentially expressed (p<0.05) in tissues from left and right sides of gut. Gene expression signature, including genes associated with inflammation, stemness and fibrosis, has also been performed for the IBD tissues mentioned above. Methylation sites at single nucleotide resolution have been analyzed.ConclusionsAlthough the results warrant further investigation, differential genomic profiling suggestive of altered pathways involved in oxidative stress, EMT, and of the possible stemness signature was found. The integration of data from multiple platforms will provide insights of the overall molecular determinants in IBD patients along with the evolution of the disease.Ethics ApprovalThis study was approved by Sidra Medicine and Hamad Medical Corporation Ethics Boards; approval number 180402817 and MRC-02-18-096, respectively.


2017 ◽  
Vol 2017 ◽  
pp. 1-18 ◽  
Author(s):  
Tian Tian ◽  
Ziling Wang ◽  
Jinhua Zhang

Inflammatory bowel disease (IBD) is a chronic gastrointestinal disease whose incidence has risen worldwide in recent years. Accumulating evidence shows that oxidative stress plays an essential role in the pathogenesis and progression of IBD. This review highlights the generation of reactive oxygen species (ROS) and antioxidant defense mechanisms in the gastrointestinal (GI) tract, the involvement of oxidative stress signaling in the initiation and progression of IBD and its relationships with genetic susceptibility and the mucosal immune response. In addition, potential therapeutic strategies for IBD that target oxidative stress signaling are reviewed and discussed. Though substantial progress has been made in understanding the role of oxidative stress in IBD in humans and experimental animals, the underlying mechanisms are still not well defined. Thus, further studies are needed to validate how oxidative stress signaling is involved in and contributes to the development of IBD.


2016 ◽  
Vol 88 (6) ◽  
Author(s):  
Jerzy Mrowicki ◽  
Małgorzata Mrowicka ◽  
Ireneusz Majsterek ◽  
Michał Mik ◽  
Adam Dziki ◽  
...  

AbstractInflammatory bowel disease (IBD) are a heterogeneous group of disorders in the course dominated by chronic, recurrent gastrointestinal inflammation. It is believed that the activation of IBD occurs in patients with a genetic predisposition to their development. Chronic inflammation develops as a result of an excessive reaction of the immune system principally under the influence of environmental risk factors. Among them, it has been shown that the mechanism of oxidative stress is associated with the pathophysiology of inflammatory bowel disease, responsible for the commencement and progress of these diseases.was the relationship between single nucleotide polymorphisms (SNPs) of individual antioxidant enzymes, and the prevalence of inflammatory bowel disease that may be associated with increased levels of oxidative stress.A total of 111 IBD patients, including 65 patients with ulcerative colitis (UC) and 46 with Crohn’s disease (CD) and 125 healthy controls recruited from the Polish population, were genotyped forThe performed analysis of genetic polymorphisms of antioxidant enzymes showed that polymorphic variant of the CAT -262 C / T may have protective effects in patients with ulcerative colitis in the range of genotype C / T; OR = 0.49 (0.25-0.99), p = 0.044. Trend protective, but statistically unrelated, it was also observed for genotype T / T and T allele of the same polymorphism and genotypes and allelesIt has been shown that the polymorphism of antioxidant enzymes


2016 ◽  
Vol 70 ◽  
pp. 265-271 ◽  
Author(s):  
Małgorzata Zielińska-Przyjemska ◽  
Anna Olejnik ◽  
Agnieszka Dobrowolska-Zachwieja ◽  
Michał Łuczak ◽  
Wanda Baer-Dubowska

2020 ◽  
Vol 26 (11) ◽  
pp. 1034-1046 ◽  
Author(s):  
Arno R. Bourgonje ◽  
Martin Feelisch ◽  
Klaas Nico Faber ◽  
Andreas Pasch ◽  
Gerard Dijkstra ◽  
...  

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