title: [Role of bioantioxidants depression and deficiency of protease inhibitor alpha 1-antitrypsin in mechanisms activating free radical oxidation and proteolysis in chronic pancreatitis].
abstract: OBJECTIVE
  To elucidate the reason and mechanisms of neutralization of protease inhibitors and antioxidants by proteolytic enzymes and oxidants.
  
  
  METHODS
  The trial included 92 patients with exacerbation of chronic pancreatitis. 47 of them had chronic recurrent pancreatitis (CRP), 45 patients had chronic fibrozing pancreatitis (CFP). Measurements were made of blood catalase and ceruloplasmin (according to P. Hubl, R. Breschneider and O. Houchin, respectively), alpha1-antitrypsin (by Reiderman), schiff bases (by B. Fletcher et al.), dienic conjugates (by Z. Placer), serum acid phosphatase (by Bodansky), acid phosphatase of polynuclear cells (by R. Nartsissiv), NBT-test was made according to B. Park.
  
  
  RESULTS
  Exacerbation of CRP was associated with enhancement of free radical lipid peroxidation (FPOL), release of proteolytic and lysosomal enzymes from acinar cells, a fall in catalase level. Catalase depression depends on the level of blood lysosomal enzymes and partially on FPOL activity. In CFP moderate activity of FPOL and trypsin is associated with normal levels of lysosomal enzymes and catalase. In both pancreatitis forms, alpha1-antitrypsin levels are low. This lowering is primary and unrelated with inflammatory process in the pancreas. A trypsin rise in both forms depends on lowering of alpha1-antitrypsin which via trypsin inhibits formation of lysosomal enzymes in polynuclear cells. Inability of protease inhibitor to block proteolytic (lysosomal) enzymes manifests in initial intraacinar activation of trypsin from trypsinogen, in inflammatory focus under polynuclear cells release of lysosomal enzymes and in proteolytic enzymes release from the affected acinar structures.
  
  
  CONCLUSIONS
  Lack of alpha1-antitrypsin--protease inhibitor--and depression of antioxidant catalase are main and intermediate elements in activation of mechanisms of proteolytic aggression and FPOL.
authors.forename: E N
authors.initials: EN
authors.lastname: Zhukova
mesh_terms: D000135:Acid Phosphatase / Q000097:blood; D015415:Biomarkers / Q000097:blood; D002374:Catalase / Q000097:blood; D002570:Ceruloplasmin / Q000378:metabolism; D002908:Chronic Disease; D005609:Free Radicals / Q000378:metabolism; D006801:Humans; D015227:Lipid Peroxidation / Q000502:physiology*; D008247:Lysosomes / Q000201:enzymology; D009504:Neutrophils / Q000201:enzymology; D010088:Oxidoreductases / Q000097:blood*; D010195:Pancreatitis / Q000097:blood* / Q000150:complications; D014357:Trypsin / Q000097:blood; D000515:alpha 1-Antitrypsin / Q000378:metabolism*; D019896:alpha 1-Antitrypsin Deficiency / Q000097:blood* / Q000209:etiology; D011623:gamma-Glutamyl Hydrolase / Q000097:blood
chemical_list: D015415:Biomarkers; D005609:Free Radicals; D000515:alpha 1-Antitrypsin; D010088:Oxidoreductases; D002374:Catalase; D002570:Ceruloplasmin; D000135:Acid Phosphatase; D011623:gamma-Glutamyl Hydrolase; D014357:Trypsin