Effects of Insulin-Like Growth Factor-1 on Rotenone-InducedApoptosis in Human Lymphocyte Cells
ABSTRACT: Human peripheral blood lymphocytes have been useful as a putative model of oxidative stress-induced apoptosisfor Parkinson’s disease. The present work shows that rotenone, a mitochondrial complex I inhibitor, induced time- and con-centration-dependent apoptosis in lymphocytes which was med...
- Autores:
-
Ávila Gómez, Isabel Cristina
Vélez Pardo, Carlos Alberto
Jiménez Del Río, Marlene
- Tipo de recurso:
- Article of investigation
- Fecha de publicación:
- 2009
- Institución:
- Universidad de Antioquia
- Repositorio:
- Repositorio UdeA
- Idioma:
- eng
- OAI Identifier:
- oai:bibliotecadigital.udea.edu.co:10495/25916
- Acceso en línea:
- http://hdl.handle.net/10495/25916
- Palabra clave:
- Apoptosis
Linfocitos
Lymphocytes
Rotenona
Rotenone
Insulina
Insulin
- Rights
- openAccess
- License
- http://creativecommons.org/licenses/by-nc-nd/2.5/co/
Summary: | ABSTRACT: Human peripheral blood lymphocytes have been useful as a putative model of oxidative stress-induced apoptosisfor Parkinson’s disease. The present work shows that rotenone, a mitochondrial complex I inhibitor, induced time- and con-centration-dependent apoptosis in lymphocytes which was mediated by anion superoxide radicals (O2•)) ⁄ hydrogen peroxide,depolarization of mitochondria, caspase-3 activation, concomitantly with the nuclear translocation of transcription factorssuch as NF-jB, p53, c-Jun and nuclei fragmentation. Since insulin-like growth factor-1 (IGF-1) interferes with a cell’s apopto-tic machinery when subjected to several stressful conditions, it is demonstrated here for the first time that IGF-1 effectivelyprotects lymphocytes against rotenone through PI-3K ⁄ Akt activation, down-regulation of p53 and maintenance of mitochon-drial membrane potential independently of ROS generation. These data might contribute to understanding the role played byIGF-1 against oxidative stress stimuli |
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