open access

Vol 71, No 3 (2012)
ORIGINAL ARTICLES
Published online: 2012-08-31
Submitted: 2012-05-08
Accepted: 2012-06-19
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Ultrastructural aspects of acute pancreatitis induced by 2, 2'-azobis (2-amidinopropane) dihydrochloride (AAPH) in rats

C. Tukaj, A. Olewniak-Adamowska, M. I. Pirski, M. Woźniak
Folia Morphol 2012;71(3):136-141.

open access

Vol 71, No 3 (2012)
ORIGINAL ARTICLES
Published online: 2012-08-31
Submitted: 2012-05-08
Accepted: 2012-06-19

Abstract

Background. 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.

Methods. In this study, we used a water-soluble radical initiator, 2,2'-azobis-(2-amidinopropane) dihydrochloride (AAPH), to investigate consequences of oxidative stress insult to rats pancreas. Detailed ultrastructural characterization of exocrine pancreatic changes that involved a time course of AAPH (40 mg/1kg body weight) induction from 3 to 24 hours was performed.

Results. 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 (RER), and reduced number of zymogen granules was observed. The most prominent ultrastructural feature was accumulation of highly polymorphic cytoplasmic vacuoles in acinar cells. Different in size and shape double membrane-bound autophagosomes with sequestered organelles, autophagolisosomes, and also large, empty, single-membrane-bound vacuoles were observed within the cytoplasm.

Conclusions. The results indicate that intensive but impaired autophagy mediates pathological accumulation of vacuoles in acinar cells. Rat model of acute pancreatitis induced by AAPH  is useful to investigate the early events of oxidative stress insult to pancreas.

Abstract

Background. 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.

Methods. In this study, we used a water-soluble radical initiator, 2,2'-azobis-(2-amidinopropane) dihydrochloride (AAPH), to investigate consequences of oxidative stress insult to rats pancreas. Detailed ultrastructural characterization of exocrine pancreatic changes that involved a time course of AAPH (40 mg/1kg body weight) induction from 3 to 24 hours was performed.

Results. 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 (RER), and reduced number of zymogen granules was observed. The most prominent ultrastructural feature was accumulation of highly polymorphic cytoplasmic vacuoles in acinar cells. Different in size and shape double membrane-bound autophagosomes with sequestered organelles, autophagolisosomes, and also large, empty, single-membrane-bound vacuoles were observed within the cytoplasm.

Conclusions. The results indicate that intensive but impaired autophagy mediates pathological accumulation of vacuoles in acinar cells. Rat model of acute pancreatitis induced by AAPH  is useful to investigate the early events of oxidative stress insult to pancreas.

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Keywords

acute pancreatitis; oxidative stress; AAPH; Ultrastructure; autophagy

About this article
Title

Ultrastructural aspects of acute pancreatitis induced by 2, 2'-azobis (2-amidinopropane) dihydrochloride (AAPH) in rats

Journal

Folia Morphologica

Issue

Vol 71, No 3 (2012)

Pages

136-141

Published online

2012-08-31

Bibliographic record

Folia Morphol 2012;71(3):136-141.

Keywords

acute pancreatitis
oxidative stress
AAPH
Ultrastructure
autophagy

Authors

C. Tukaj
A. Olewniak-Adamowska
M. I. Pirski
M. Woźniak

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