You are in the accessibility menu

Please use this identifier to cite or link to this item: http://acervodigital.unesp.br/handle/11449/16558
Title: 
Mitochondrial alterations and apoptosis in smooth muscle from aged rats
Author(s): 
Institution: 
  • Universidade Federal de São Paulo (UNIFESP)
  • Universidade Estadual Paulista (UNESP)
ISSN: 
0005-2728
Abstract: 
We studied changes in mitochondrial morphology and function in the smooth muscle of rat colon. Under confocal microscopy, tissues loaded with potentiometric dye displayed rapid and spontaneous depolarization. Cyclosporin A (CsA), inhibitor of the permeability transition pore (PTP), caused an increase in mitochondrial membrane potential (DeltaPsi(m)) in tissues from adult young animals. In aged rats these changes were not observed. This suggests that physiological activation of PTP in aged rats is reduced. Electron microscopy showed alterations of the mitochondrial ultrastructure in tissues from aged rats involving a decreased definition of the cristae and fragmentation of the mitochondrial membranes. We also detected an increase in apoptotic cells in the smooth muscle from aged animals. Our results show that the aging process changes PTP activity, the ability to maintain DeltaPsi(m) and mitochondrial morphology. It is suggested that these can be associated with mitochondrial damage and cell death. (C) 2004 Elsevier B.V. All rights reserved.
Issue Date: 
4-Oct-2004
Citation: 
Biochimica Et Biophysica Acta-bioenergetics. Amsterdam: Elsevier B.V., v. 1658, n. 3, p. 187-194, 2004.
Time Duration: 
187-194
Publisher: 
Elsevier B.V.
Keywords: 
  • mitochondria
  • calcium
  • smooth muscle
  • aging
  • mitochondrial dysfunction
Source: 
http://dx.doi.org/10.1016/j.bbabio.2004.05.011
URI: 
http://hdl.handle.net/11449/16558
Access Rights: 
Acesso aberto
Type: 
outro
Source:
http://repositorio.unesp.br/handle/11449/16558
Appears in Collections:Artigos, TCCs, Teses e Dissertações da Unesp

There are no files associated with this item.
 

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.