title: Nitric oxide protects against pancreatic subcellular damage in acute pancreatitis.
abstract: OBJECTIVE
  Oxidative stress involvement in damage to the pancreas in acute pancreatitis (AP) is well documented. However, little is known about oxidative damage occurring in the different subcellular fractions of pancreatic cells. The aim of this study was to ascertain the main targets of oxidative damage inside cells after AP and the role of endogenous nitric oxide (NO) in it.
  
  
  METHODS
  A model of cerulein-induced AP in rats was used and N-nitro-l-arginine methyl ester (l-NAME) was administered as an NO production inhibitor. After pancreatitis induction, indicative parameters of lipid peroxidation and protein oxidation together with some enzymatic and nonenzymatic endogenous free radical scavengers were assessed in serum and pancreatic subcellular fractions.
  
  
  CONCLUSIONS
  In pancreatitic rats, malondialdehyde and protein carbonyl group concentrations were significantly increased (P < 0.05) in serum and some fractions. The increases were higher in l-NAME-treated rats (P < 0.05). Superoxide dismutase and catalase activities were also increased (P < 0.05) but were decreased (P < 0.05) with l-NAME. The alpha-tocopherol concentration diminished (P < 0.05) in serum and all the studied subcellular fractions and the decrease was stronger in l-NAME-treated rats. Our data suggest that microsomes followed by lysosomal + mitochondrial are the fractions most susceptible to oxidative damage in AP. Endogenous NO plays a protective role against oxidative damage to subcellular fractions.
authors.affiliation: Department of Molecular Biochemistry and Biology, Edificio Departamental, University of Salamanca, Salamanca. Spain.
authors.forename: Carmen
authors.initials: C
authors.lastname: Sánchez-Bernal
authors.forename: Onel H
authors.initials: OH
authors.lastname: García-Morales
authors.forename: Carmen
authors.initials: C
authors.lastname: Domínguez
authors.forename: Pilar
authors.initials: P
authors.lastname: Martin-Gallán
authors.forename: José Julian
authors.initials: JJ
authors.lastname: Calvo
authors.forename: Laura
authors.initials: L
authors.lastname: Ferreira
authors.forename: Nieves
authors.initials: N
authors.lastname: Pérez-González
mesh_terms: D000208:Acute Disease; D000818:Animals; D002374:Catalase / Q000097:blood / Q000378:metabolism; D002108:Ceruletide; D004791:Enzyme Inhibitors / Q000494:pharmacology; D008054:Lipid Peroxides / Q000097:blood / Q000378:metabolism; D008297:Male; D008315:Malondialdehyde / Q000097:blood / Q000378:metabolism; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D009569:Nitric Oxide / Q000502:physiology*; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors / Q000378:metabolism; D010179:Pancreas / Q000737:chemistry* / Q000187:drug effects / Q000473:pathology; D010195:Pancreatitis / Q000097:blood / Q000139:chemically induced / Q000503:physiopathology*; D011506:Proteins / Q000737:chemistry; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D013347:Subcellular Fractions / Q000737:chemistry / Q000187:drug effects; D013482:Superoxide Dismutase / Q000097:blood / Q000378:metabolism; D024502:alpha-Tocopherol / Q000097:blood / Q000378:metabolism
chemical_list: D004791:Enzyme Inhibitors; D008054:Lipid Peroxides; D011506:Proteins; D009569:Nitric Oxide; D008315:Malondialdehyde; D002108:Ceruletide; D002374:Catalase; D019001:Nitric Oxide Synthase; D013482:Superoxide Dismutase; D024502:alpha-Tocopherol; D019331:NG-Nitroarginine Methyl Ester