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Expression of reactive oxygen species in reflux disease

Kapitel i bok
Författare Emma Andreasson
Anna Casselbrant
Publicerad i Gastrointestinal Endoscopy
Sidor 79-90
ISBN 978-953-307-385-9
Förlag InTech
Förlagsort Rijeka, Croatia
Publiceringsår 2011
Publicerad vid Institutionen för kliniska vetenskaper, Avdelningen för gastrokirurgisk forskning och utbildning
Sidor 79-90
Språk en
Länkar dx.doi.org/10.5772/24676
Ämnesord reactive-oxygen species, gastroesophageal reflux disease, red streak, nitric oxide
Ämneskategorier Patologi

Sammanfattning

Background: High levels of nitric oxide (NO) are formed when nitrite in swallowed saliva meets acidic refluxates in the distal esophagus. In inflamed tissue with production of reactive-oxygen-species (ROS) it is reasonable to assume that luminal NO will react with particularly superoxide and form the extremely labile oxidising compound peroxynitrite. Such oxidative species have potential roles in all steps of carcinogenesis. The aim of the present study is to elucidate the presence of radical producing enzymes, and elucidate the histological changes and number of inflammatory cells in human esophageal mucosa. Material and Methods: Biopsies from healthy volunteers and patients with erosive reflux disease (ERD) were analysed for myeloperoxidase (MPO), inducible nitric oxide synthase (iNOS) and NADPH oxidase, well as the expression of inflammatory markers IL1β and IL6 by western blot technique. Expression of nitrotyrosine was used as an indicator of peroxynitrite activity, thus mirroring the foregoing radical formation. A histological evaluation of inflammation and a morphometric investigation were performed on mucosal specimens. Results: Expression of MPO and nitrotyrosine formation was up regulated in the ERD-patients compared healthy controls. No significant differences in expression of iNOS, NADPH oxidase, IL1β or IL6 were detected. No signs of active inflammation, defined as presence of inflammatory cells were observed, whereas histological signs of erosive mucosal disease were confirmed in the esophageal mucosa. Conclusion: There were clear signs of increased radical forming capacity in the epithelium despite absence of histological inflammation, in association to ERD. During acidified refluxes, epithelial ROS production in combination with luminal NO formation, may constitute aggravated factors in the carcinogenic process.

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