Evaluation of glutathione peroxidase and superoxide dismutase enzyme polymorphisms in celiac disease patients      
Yazarlar (4)
Doç. Dr. Muzaffer KATAR Tokat Gaziosmanpaşa Üniversitesi, Türkiye
A. F. Ozugurlu
Tokat Gaziosmanpaşa Üniversitesi, Türkiye
H. Ozyurt
Tokat Gaziosmanpaşa Üniversitesi, Türkiye
I. Benli
Tokat Gaziosmanpaşa Üniversitesi, Türkiye
Makale Türü Açık Erişim Özgün Makale
Makale Alt Türü SSCI, AHCI, SCI, SCI-Exp dergilerinde yayınlanan tam makale
Dergi Adı Genetics and Molecular Research
Dergi ISSN 1676-5680 Wos Dergi Scopus Dergi
Dergi Tarandığı Indeksler SCI-Expanded
Dergi Grubu Q4
Makale Dili İngilizce
Basım Tarihi 02-2014
Cilt No 13
Sayı 1
Sayfalar 1030 / 1037
DOI Numarası 10.4238/2014.February.20.4
Makale Linki https://www.geneticsmr.com/articles/2901
Özet
Celiac disease (CD) is a multifactorial, inflammatory small bowel disorder characterized by nutrient malabsorption resulting from mucosal damage, the latter induced by cereal products like barley, oat, and wheat. Oxidative stress has previously been reported to play an important role in the pathogenesis of CD. In the present study, we aimed to evaluate the frequency of polymorphisms that affects the structure of the enzymes superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), with levels being dependent on the amount of oxidative stress and whether or not there is an association with the mutations DQA1* 0501, DQB1* 0201, and DRB1* 04 that are frequently reported for CD. SOD and GSH-Px polymorphisms were investigated by realtime quantitative polymerase chain reaction in 265 cases. Of the 117 cases that had at least one of DQA1* 0501, DQB1* 0201, or DRB1* 04, 98 (83.75%) also had SOD enzyme polymorphisms and 68 (58.12%) also had GSH-Px polymorphisms. In conclusion, although the etiology of CD is not yet entirely clear, many mechanisms have been suggested. This study supports the notion that SOD and GSH-Px polymorphisms are involved in CD development, even though our findings were not
Anahtar Kelimeler
Antioxidant | Inflammation | Mutation | Oxidative stress | Polymorphism | Small bowel