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01.04.2012 | Original Research Paper

Functional polymorphisms in XRCC-1 and APE-1 contribute to increased apoptosis and risk of ulcerative colitis

verfasst von: Avinash Bardia, Santosh K. Tiwari, Sivaram Gunisetty, Farha Anjum, Pratibha Nallari, Md. Aejaz Habeeb, Aleem A. Khan

Erschienen in: Inflammation Research | Ausgabe 4/2012

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Abstract

Objective

The present study was designed to investigate the role of X-ray cross-complementing group 1 (XRCC1) and apurinic/apyrimidinic endonuclease 1 (APE1) polymorphisms in apoptosis and the risk of ulcerative colitis (UC).

Materials and methods

Blood samples from 384 unrelated subject (age range 18–65 years; 171 with UC, 213 healthy controls) were collected after colonoscopy. Genomic DNA was isolated and genotyped for XRCC1 Arg399Gln and APE1 Asp148Glu using a confronting two-pair primers polymerase chain reaction. Apoptosis and intracellular reactive oxygen species (ROS) levels in peripheral blood mononuclear cells were measured using annexin-V and H₂DCFDA assay, respectively.

Results

The frequency of genotype Arg399Gln (heterozygous) of XRCC1 gene was significantly higher in patients with UC than the controls (odds ratio [OR] 1.73; 95% confidence interval [CI] 1.13–2.64; p = 0.01). Similarly the genotypic frequency of APE1 Asp148Glu showed statistically significant incidence among UC subjects (OR 1.54; 95% CI 1.02–2.33; p = 0.04). Polymorphism in XRCC1 Arg399Gln and APE1 Asp148Glu together considerably increased the risk of UC (OR 2.303; 95% CI 1.43–3.69; p = 0.0007). ROS levels were high in UC subjects compared with controls (p = 0.01).

Conclusion

Polymorphisms in XRCC1 Arg399Gln and APE1 Asp148Glu significantly increased the rate of apoptosis and risk of ulcerative colitis.

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Titel: Functional polymorphisms in XRCC-1 and APE-1 contribute to increased apoptosis and risk of ulcerative colitis
verfasst von: Avinash Bardia
Santosh K. Tiwari
Sivaram Gunisetty
Farha Anjum
Pratibha Nallari
Md. Aejaz Habeeb
Aleem A. Khan
Publikationsdatum: 01.04.2012
Verlag: SP Birkhäuser Verlag Basel
Erschienen in: Inflammation Research / Ausgabe 4/2012
Print ISSN: 1023-3830
Elektronische ISSN: 1420-908X
DOI: https://doi.org/10.1007/s00011-011-0418-2

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