Association between Polymorphisms in Antioxidant Genes and Inflammatory Bowel Disease

Pereira, Cristiana; Durães, Cecília; Coelho, Rosa; Grácio, Daniela; Silva, Marco; Peixoto, Armando; Lago, Paula; Pereira, Márcia S.; Catarino, Telmo; Pinho, Salomé S.; Teixeira, João Paulo; Macedo, Guilherme; Annese, Vito; Magro, Fernando

doi:10.1371/journal.pone.0169102

Cited by 18 publications

(13 citation statements)

References 48 publications

(47 reference statements)

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“…at al. [ 14 ] showed that the A/A genotype of GSHPX1 polymorphism may associated with the risk of ulcerative collitis in the Portuguese population. Crawford A. et al [ 15 ] reported that GSHPX1 Pro/Leu genotype has been related to lung cancer, bladder cancer and diabetic T2DM polyneuropathy.…”

Section: Discussionmentioning

confidence: 99%

Association between SOD1, CAT, GSHPX1 polymorphisms and the risk of inflammatory bowel disease in the Polish population

et al. 2017

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PurposeThe main aim of this study was investigate the association between the genetic polymorphism of antioxidant enzyme genes: SOD1, CAT and GSHPX1 and the risk of inflammatory bowel disease (IBD), including Crohn’s disease and ulcerative colitis in the Polish population.MethodsA total of 445 subjects including 200 patients with IBD and 245 controls were allowed in this study. We determined activity of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx1) and examination their association with the SNPs of respective genes (SOD1 +35A/C, CAT C-262T and GSHPX1 Pro197Leu). RFLP technique was used to determine the selected genes polymorphisms. Antioxidant enzymes activity were evaluated in erythrocyte hemolysate of 23 patients with non-active IBD and 30 healthy participants.ResultsThe A/C genotype and the C allele frequencies of A/C polymorphism of SOD1 gene were significantly associated with the reduced risk of IBD (OR=0.43; 95% CI 0.23; 0.83). Alike, C/T (OR=0.45; 95% CI= 0.29; 0.70) and T/T genotype (OR=0.43; 95% CI= 0.21; 0.87) of GSHPX1 gene polymorphism diminished the susceptibility to IBD. A significant decrease of CAT (P=0.028) and increase of GPx1 (P=0.025) enzyme activities were seen in IBD patients compared to control.ConclusionsOur data confirm dysregulated antioxidant capacity in patients suffering from IBD. Both, the SOD1 A/C genotype as well as GSHPX1 C/T and T/T genotypes may be associated with a reduction risk of IBD in the Polish population.

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Section: Discussionmentioning

confidence: 99%

Association between SOD1, CAT, GSHPX1 polymorphisms and the risk of inflammatory bowel disease in the Polish population

et al. 2017

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“…Oxidative stress, defined as an imbalance between prooxidants and antioxidants, is a key player in the mechanism underpinning mucosal damage in IBD. Oxidative stress has been implicated in the propagation and exacerbation, if not pathogenesis, of IBD as the defective antioxidant system in IBD may be a consequence of genetic variants [5]. Moreover, it has been repeatedly shown that IBD-related oxidative stress is not restricted to the intestinal mucosa but manifests itself at the systemic level as well [6].…”

Section: Introductionmentioning

confidence: 99%

Nonenzymatic Serum Antioxidant Capacity in IBD and Its Association with the Severity of Bowel Inflammation and Corticosteroids Treatment

et al. 2019

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Background and objectives: Oxidative stress signalling plays a monumental role in inflammatory bowel disease (IBD). Reduction of oxidative stress might control inflammation, block tissue damage, and reverse natural history of IBD. We assessed the serum concentrations of free thiols (FT) and uric acid (SUA), together constituting a large part of nonenzymatic serum antioxidant capacity, as well as total antioxidant status (TAS) with reference to IBD phenotype, activity, co-occurrence of anemia, and treatment with azathioprine (AZA) and corticosteroids (CS). Additionally, we appraised the potential of uric acid, thiol stress, and TAS as mucosal healing (MH) markers in ulcerative colitis. Materials and methods: SUA, FT, and TAS were measured colorimetrically using, respectively, uricase, Ellman’s and 2,2′-azino-bis-3-ethylbenzthiazoline-6-sulphonic acid (ABTS) methods. Results: The study group consisted of 175 individuals: 57 controls, 71 ulcerative colitis (UC), and 47 Crohn’s disease (CD) patients. When compared to controls, SUA levels were significantly lower in patients with CD, and FT and TAS levels were significantly lower in patients with CD and UC. In UC patients, SUA, FT, and TAS inversely correlated with the severity of bowel inflammation. As MH markers, SUA displayed better overall accuracy and higher specificity than FT. In active CD, FT, and SUA were significantly lower in patients with anemia. FT was significantly lower in patients treated with corticosteroids. Conclusions: IBD patients, regardless the disease phenotype, have systemic thiol stress, depleted total antioxidant capacity, and reduced concentrations of uric acid, reflecting, to various degrees, clinical and local disease activity as well as presence of anaemia, the most common extraintestinal manifestation of IBD. Evaluation of systemic total antioxidant status may be useful in noninvasive assessment of mucosal healing. Our findings on thiol stress provide an additional aspect on adverse effects of corticosteroids therapy.

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“…These cells are one source of oxidative stress, which induces active mucosal lesions [60]. Single-nucleotide polymorphisms (SNPs) in the antioxidant gene GPX1 are reported to be correlated with UC, while the SOD2 gene was relatively strongly correlated with CD, suggesting that these diseases may be genetically associated with oxidative stress [61]. The mitochondrial DNA mutations in UC and colitic cancer have been analyzed, with marked accumulation noted in UC and even greater accumulation noted in colitic cancer tissue and nontumor adjacent colon tissue [62].…”

Section: Oxidative Stress In the Colonmentioning

confidence: 99%

Paradoxical Roles of Oxidative Stress Response in the Digestive System before and after Carcinogenesis

Takaki

Uchida

Hiraoka

et al. 2019

Cancers

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Oxidative stress is recognized as a cancer-initiating stress response in the digestive system. It is produced through mitochondrial respiration and induces DNA damage, resulting in cancer cell transformation. However, recent findings indicate that oxidative stress is also a necessary anticancer response for destroying cancer cells. The oxidative stress response has also been reported to be an important step in increasing the anticancer response of newly developed molecular targeted agents. Oxidative stress might therefore be a cancer-initiating response that should be downregulated in the precancerous stage in patients at risk of cancer but an anticancer cell response that should not be downregulated in the postcancerous stage when cancer cells are still present. Many commercial antioxidant agents are marketed as “cancer-eliminating agents” or as products to improve one’s health, so cancer patients often take these antioxidant agents. However, care should be taken to avoid harming the anticancerous oxidative stress response. In this review, we will highlight the paradoxical effects of oxidative stress and antioxidant agents in the digestive system before and after carcinogenesis.

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Association between Polymorphisms in Antioxidant Genes and Inflammatory Bowel Disease

Cited by 18 publications

References 48 publications

Association between SOD1, CAT, GSHPX1 polymorphisms and the risk of inflammatory bowel disease in the Polish population

Association between SOD1, CAT, GSHPX1 polymorphisms and the risk of inflammatory bowel disease in the Polish population

Nonenzymatic Serum Antioxidant Capacity in IBD and Its Association with the Severity of Bowel Inflammation and Corticosteroids Treatment

Paradoxical Roles of Oxidative Stress Response in the Digestive System before and after Carcinogenesis

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