title: Inflammation, oxidative stress and L-fucose as indispensable participants in schistosomiasis-associated colonic dysplasia.
abstract: BACKGROUND
  Schistosomiasis is a parasitic disease causing chronic ill health in humans with a serious consequences for socio-economic development in tropical and subtropical regions. There is also evidence linking Schistosoma mansoni to colonic carcinoma occurrence. The aim of this study was to evaluate some inflammatory and oxidative stress biomarkers, as well as L-fucose as linkers between intestinal schistosomiasis and colonic dysplasia development in mice.
  
  
  METHODS
  This study was conducted upon 80 mice that were divided the control group (10 non infected mice) and infected group which was subdivided into 7 sub-groups (10 mice each) according to the time of sacrifaction in the post infection (p.i.) period, 10 mice being sacrificed every two weeks from 6 weeks p.i. to 18 weeks p.i. Tumor necrosis factor alpha (TNF-α), inducible nitric oxide synthase (iNOS), and pentraxin 3 (PTX3) levels were estimated by immunoassay. The L-fucose level, and thioredoxin reductase (TrxR) and lactate dehydrogenase (LDH) activities were also evaluated in colonic tissue.
  
  
  RESULTS
  The current study revealed statistically significant elevation in the studied biochemical markers especially at 16 and 18 weeks p.i. The results were confirmed by histopathological examination that revealed atypical architectural and cytological changes in the form of epithelial surface serration and nuclear hyper-chromatizia at 14, 16 and 18 weeks p.i.
  
  
  CONCLUSIONS
  inflammation, oxidative stress and L-fucose together may form an important link between Schistosomal mansoni infection and colonic dysplasia and they can be new tools for prediction of colonic dysplasia development in experimental schistosomiasis.
authors.affiliation: Departments of Medical Biochemistry, Faculty of Medicine, Tanta University, Tanta, Egypt E-mail : nemaali2006@yahoo mail.com.
authors.forename: Nema Ali
authors.initials: NA
authors.lastname: Soliman
authors.forename: Walaa Arafa
authors.initials: WA
authors.lastname: Keshk
authors.forename: Zeinab Salah
authors.initials: ZS
authors.lastname: Shoheib
authors.forename: Dalia Salah
authors.initials: DS
authors.lastname: Ashour
authors.forename: Maha Moustafa
authors.initials: MM
authors.lastname: Shamloula
mesh_terms: D000818:Animals; D002097:C-Reactive Protein / Q000096:biosynthesis; D003106:Colon / Q000473:pathology; D003110:Colonic Neoplasms / Q000473:pathology*; D005643:Fucose / Q000097:blood*; D005759:Gastroenteritis / Q000473:pathology*; D006801:Humans; D007249:Inflammation / Q000473:pathology*; D007770:L-Lactate Dehydrogenase / Q000096:biosynthesis; D051379:Mice; D052247:Nitric Oxide Synthase Type II / Q000096:biosynthesis; D018384:Oxidative Stress; D012550:Schistosoma mansoni; D012552:Schistosomiasis / Q000473:pathology*; D000683:Serum Amyloid P-Component / Q000096:biosynthesis; D013880:Thioredoxin-Disulfide Reductase / Q000096:biosynthesis; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis; D000099153:Pentraxins
chemical_list: D002097:C-Reactive Protein; D005643:Fucose; D007770:L-Lactate Dehydrogenase; D052247:Nitric Oxide Synthase Type II; D000683:Serum Amyloid P-Component; D013880:Thioredoxin-Disulfide Reductase; D014409:Tumor Necrosis Factor-alpha; D000099153:Pentraxins