title: Free oxygen radical-induced acute pancreatitis. A light and electron microscopic study.
abstract: OBJECTIVE
  To date direct toxic effects of free oxygen radicals in vivo on pancreatic parenchyma have not been studied thoroughly. We aimed to study: 1) the detailed histopathological changes induced by free oxygen radicals in pancreas; and 2) the preventive effect of intraductal catalase in H2O2-induced acute pancreatitis.
  
  
  METHODS
  Wistar Albine rats were randomized into six groups. 1) First experiment: Bile-pancreatic duct was cannulated close to the liver and perfused through the duodenum with (i) normal saline solution, (ii) iron sulfate (FeSO4), (iii) hydrogen peroxide (H2O2), (iv) hydrogen peroxide and iron sulfate simultaneously. 2) Second experiment: Bile pancreatic duct was perfused either with H2O2 or H2O2 + catalase. Serum amylase and pancreas malondialdehyde levels were measured in both experiments after 3 hours of perfusion period. Tissue samples were obtained for histopathological examinations.
  
  
  RESULTS
  1) First experiment: Intraductal perfusion of FeSO4 or H2O2 or H2O2 + FeSO4 induced acute edematous pancreatitis with focal parenchymal necrosis. At the ultrastructural level, intracytoplasmic formation of vacuoles. fusion of the vacuoles and zymogen granules, and autophagosomes containing cellular organelles were found. Serum amylase and pancreas malondialdehyde levels, and morphological score were significantly higher in these groups than control group (p < 0.001). 2) Second experiment: Catalase perfusion simultaneously with H2O2 decreased the serum amylase and pancreas malondialdehyde levels, and morphological score significantly (p < 0.001) and prevented the desquamation of the columnar epithelium and development of gross edema but not parenchymal necrosis.
  
  
  CONCLUSIONS
  Intraductal perfusion of FeSO4 or H2O2 or H2O2 + FeSO4-induced acute pancreatitis with marked light and electronmicroscopic changes. Intraductal perfusion of catalase and H2O2 simultaneously did not prevent or lessen the parenchymal necrosis. These findings have suggested that another mechanism of injury may also play a role in parenchymal injury in oxygen radical-induced acute pancreatitis.
authors.affiliation: Department of Surgery, Celal Bayar University Faculty of Medicine, Manisa, Turkey. coskunt@hotmail.com
authors.forename: Teoman
authors.initials: T
authors.lastname: Coskun
authors.forename: Petek
authors.initials: P
authors.lastname: Korkusuz
authors.forename: Yavuz
authors.initials: Y
authors.lastname: Kaya
authors.forename: Ulken
authors.initials: U
authors.lastname: Ors
authors.forename: Yalçin
authors.initials: Y
authors.lastname: Aker
authors.forename: Kamer
authors.initials: K
authors.lastname: Kilinç
mesh_terms: D000208:Acute Disease; D000818:Animals; D002374:Catalase / Q000627:therapeutic use; D004195:Disease Models, Animal; D005260:Female; D005609:Free Radicals / Q000009:adverse effects*; D008297:Male; D008853:Microscopy; D008854:Microscopy, Electron; D010179:Pancreas / Q000187:drug effects* / Q000473:pathology / Q000648:ultrastructure*; D010195:Pancreatitis / Q000139:chemically induced* / Q000473:pathology* / Q000517:prevention & control; D051381:Rats; D017208:Rats, Wistar; D017382:Reactive Oxygen Species / Q000009:adverse effects*
chemical_list: D005609:Free Radicals; D017382:Reactive Oxygen Species; D002374:Catalase