title: Ultrastructural aspects of acute pancreatitis induced by 2, 2'-azobis (2-amidinopropane) dihydrochloride (AAPH) in rats.
abstract: Pathophysiology of acute pancreatitis (AP) has not been clearly established;  nevertheless, accumulating evidence implicates highly reactive oxygen species  (ROS) as important mediators of exocrine tissue damage. In this study, we used  a water-soluble radical initiator, 2,2 -azobis-(2-amidinopropane) dihydrochloride  (AAPH), to investigate the consequences of oxidative stress insult to the rat  pancreas. The detailed characterisation of acini ultrastructural changes in the  early course (3, 6, 12, 24 h) of AAPH-induced pancreatitis (40 mg/1 kg body  weight) was performed. Considerable damage to the mitochondria in acinar  cells manifested by increased translucence of the matrix, partial destruction of  cristae, and formation of myelin figures were noted. At the same time, focal  dilation, degranulation of rough endoplasmic reticulum, and reduced number  of zymogen granules was observed. The most prominent ultrastructural feature  was accumulation of highly polymorphic cytoplasmic vacuoles in acinar  cells. Double membrane-bound autophagosomes, different in size and shape,  with sequestered organelles, autophagolysosomes, and large, empty, single-membrane-bound vacuoles were observed within the cytoplasm. The results  indicate that intensive and impaired autophagy mediates pathological accumulation  of vacuoles in acinar cells. The rat model of acute pancreatitis induced  by AAPH is useful to investigate the early events of oxidative stress insult  to the pancreas.
authors.affiliation: Department of Electron Microscopy, Medical University of Gdansk, Poland. ctukaj@gumed.edu.pl
authors.forename: C
authors.initials: C
authors.lastname: Tukaj
authors.forename: A
authors.initials: A
authors.lastname: Olewniak-Adamowska
authors.forename: M I
authors.initials: MI
authors.lastname: Pirski
authors.forename: M
authors.initials: M
authors.lastname: Woźniak
mesh_terms: D061354:Acinar Cells / Q000378:metabolism / Q000648:ultrastructure*; D000208:Acute Disease; D000578:Amidines / Q000009:adverse effects* / Q000494:pharmacology; D000818:Animals; D001343:Autophagy / Q000187:drug effects; D004721:Endoplasmic Reticulum / Q000378:metabolism / Q000648:ultrastructure; D008297:Male; D008928:Mitochondria / Q000378:metabolism / Q000648:ultrastructure; D009153:Mutagens / Q000009:adverse effects* / Q000494:pharmacology; D018384:Oxidative Stress / Q000187:drug effects; D010179:Pancreas / Q000378:metabolism / Q000648:ultrastructure*; D010195:Pancreatitis / Q000139:chemically induced / Q000378:metabolism / Q000473:pathology*; D051381:Rats; D017208:Rats, Wistar; D022142:Secretory Vesicles / Q000378:metabolism / Q000648:ultrastructure; D014617:Vacuoles / Q000378:metabolism / Q000648:ultrastructure
chemical_list: D000578:Amidines; D009153:Mutagens; C046728:2,2'-azobis(2-amidinopropane)