| Autor: |
Kissová I; UMR5095 CNRS, Université de Bordeaux 2, 1 Rue Camille Saint-Saëns, F-33077 Bordeaux Cedex, France., Deffieu M, Samokhvalov V, Velours G, Bessoule JJ, Manon S, Camougrand N |
| Jazyk: |
angličtina |
| Zdroj: |
Free radical biology & medicine [Free Radic Biol Med] 2006 Dec 01; Vol. 41 (11), pp. 1655-61. Date of Electronic Publication: 2006 Aug 16. |
| DOI: |
10.1016/j.freeradbiomed.2006.08.012 |
| Abstrakt: |
Autophagy, a process involved in the degradation and the recycling of long-lived proteins and organelles to survive nitrogen starvation, is generally non-selective. However, recent data suggest that selective forms of autophagy exist, that are able to specifically target several organelles, including mitochondria. Conversely, mitochondrial alterations could trigger autophagy. Such a selective form of autophagy might be involved in the elimination of damaged mitochondria. We reported previously that, mitochondria were early targets of rapamycin-induced autophagy. Here we report that rapamycin-induced autophagy is accompanied by the early production of reactive oxygen species and by the early oxidation of mitochondrial lipid. Inhibition of these oxidative effects by resveratrol largely impaired autophagy of both cytosolic proteins and mitochondria, and delayed subsequent cell death. These results support a role of mitochondrial oxidation events in the activation of autophagy. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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