Short-term exposure of 4-hydroxynonenal induces mitochondria-mediated apoptosis in PC12 cells.
Hum Exp Toxicol
; 31(4): 336-45, 2012 Apr.
Article
en En
| MEDLINE
| ID: mdl-22241629
4-Hydroxynonenal (4-HNE) is one of the most reactive aldehydic by-products of lipid peroxidation. The role of 4-HNE in the etiology of various neurodegenerative disorders including cerebral ischemia/reperfusion, Alzheimer's disease, Parkinson's disease, etc. has been documented. We and others have reported that long-term toxic insults of 4-HNE triggers apoptotic signals and oxidative stress in various cells. However, the status of apoptosis following short-term exposure and underlying mechanisms has not been explored so far. We studied the apoptotic changes in PC12 cells receiving short-term exposure of 4-HNE. A significant dose-dependent induction in reactive oxygen species (ROS) and early response markers (c-Fos, c-Jun, and GAP-43) were observed in cells exposed to 4-HNE (10, 25, and 50 µM) for 1h. Following the exposure of PC12 cells to 4-HNE, the levels of protein and messenger RNA expressions of P(53), Bax, and caspase 3 were significantly upregulated, whereas the levels of Bcl(2) was downregulated. We could record the apoptotic signals and ROS generation in PC12 cells receiving 4-HNE exposure for such a short period of time. Induction in the expression and activity of caspase 3 has also indicated the mitochondrial mediation in the apoptosis induction.
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Apoptosis
/
Aldehídos
/
Mitocondrias
Límite:
Animals
Idioma:
En
Revista:
Hum Exp Toxicol
Asunto de la revista:
TOXICOLOGIA
Año:
2012
Tipo del documento:
Article
País de afiliación:
Arabia Saudita
Pais de publicación:
Reino Unido