DNA damage, oxidative stress, and inflammation in children with celiac disease

Abstract

The objective of this study was to evaluate the level of genomic instability in patients with celiac disease and to establish a relationship between inflammation, oxidative stress, and DNA damage in these patients. Myeloperoxidase (MPO) activity, adenosine deaminase, nitric oxide (NOx), thiobarbituric acid, catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx), and DNA damage were evaluated in peripheral blood samples from 47 celiac disease patients and 31 controls. Patients with celiac disease presented higher levels of DNA damage in comparison to controls (p=0.023). This difference was also observed for markers of oxidative stress, such as CAT (p=0.011) and SOD (p=0.013), and inflammatory markers such as MPO (p < 0.001) and NOx (p=0.009). Positive correlations were found between DNA damage levels and the values of CAT (r=0.405; p=0.009) and SOD (r=0.516; p < 0.001). Positive correlations were also found between GPx and NOx (r=0.349; p=0.030) and MPO and NOx (r=0.239; p=0.039). CAT and NOx showed a negative correlation (r=-0.315; p=0.042). In conclusion, intestinal inflammation can have systemic effects, causing an imbalance between oxidant and antioxidant markers, which may promote increased levels of DNA damage.

Apple Pomace as a Source of Bioactive Polyphenol Compounds in Gluten-Free Breads

“…It should be noted that oxidative stress is significantly higher in patients shortly after diagnosis, who have not yet started a gluten-free diet [9]. The findings suggest that it is gliadin that disrupts the pro-oxidant-antioxidant balance in the small intestinal mucosa of affected individuals through overproduction of ROS [49].…”

“…Gluten-free products are deficient in nutritional and especially pro-health constituents, resulting in the occurrence of many disorders, such as osteoporosis, esophageal cancer, and infertility [5,6]. It should be noted that many authors [7][8][9][10] have indicated oxidative stress and cellular redox status as potential factors in the pathogenesis of celiac disease. People with CD usually exhibit significant oxidative stress and impaired performance of antioxidant enzymes (glutathione peroxidase, glutathione reductase, superoxide dismutase (SOD), and catalase), which form an important antioxidant barrier in the body, and are therefore prone to oxidant-antioxidant imbalance and DNA damage.…”

Programmed Cell Death in the Small Intestine: Implications for the Pathogenesis of Celiac Disease

“…In parallel, ROS and nitric oxide production are increased in circulating erythrocytes and the small intestine of untreated CD patients, together with reduced levels of GSH, the principal substrate of GPX4 [ 75 , 76 , 77 ]. Increases in other markers of oxidation, including catalase, superoxide dismutase, myeloperoxidase and DNA instability have also been detected in peripheral blood of untreated CD patients [ 115 ]. A further factor which could lead to reduced GPX4 activity in untreated CD may be the deficiency in selenium uptake which occurs in these patients [ 116 ].…”

“…Cell death pathways also are interconnected and influence each other. For instance, there is evidence that lipid peroxidation changes associated with ferroptosis may occur in CD [ 75 , 76 , 77 , 115 ] and it has been shown that these mediators can induce apoptosis in the presence of a competent antioxidant system (GSH and thioredoxin systems). However, when the antioxidant system is deficient, both apoptosis and pro-inflammatory PCDs may occur because oxidative conditions activate factors such as MLKL, RIPK1/3, NLRP3, caspase-1 and GSDMD.…”

Pigmented Corn Varieties as Functional Ingredients for Gluten-Free Products

“…Some authors suggested that patients on a strict GFD showed a pattern of ongoing disease, in terms of inflammation and persistent villus atrophy [9,10]. Moreover, the oxidative imbalance, identified as one of the pathogenetic mechanisms of CD [11][12][13], seems to be only partially reverted by the gluten-free diet [14,15].…”