[In vitro protection of cerebral mitochondrial function by E-resveratrol in anoxia followed by re-oxygenation].
Using an experimental model of anoxia-reoxygenation applied to suspensions of mitochondria isolated from rat cortex, we have searched the effects of resveratrol added to the suspension or previously injected to rats from which mitochondria were extracted. With this model, we observe that resveratrol counteracts decoupling effects induced by anoxia-reoxygenation. It also fully inhibits intermembrane cytochrome c release, initial step of mitochondrial apoptosis and blocks ATP generation which achieves it. These effects are concentration-dependent and take place at low concentrations. It is concluded that resveratrol limits or suppresses the mitochondrial deleterious effects promoted by anoxia followed by reoxygenation.
Tillement
J P
JP
Service hospitalo-universitaire de Pharmacologie, UFR de Médecine de Paris XII, 8 rue du Général Sarrail-94010 Créteil. tillement@univ-paris12.fr
D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D017209:Apoptosis; D002540:Cerebral Cortex / Q000473:pathology / Q000502:physiology*; D003574:Cytochrome c Group / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D002534:Hypoxia, Brain / Q000503:physiopathology / Q000517:prevention & control*; D008928:Mitochondria / Q000187:drug effects* / Q000502:physiology*; D051381:Rats; D000077185:Resveratrol; D013267:Stilbenes / Q000494:pharmacology*
D000975:Antioxidants; D003574:Cytochrome c Group; D013267:Stilbenes; D000255:Adenosine Triphosphate; D000077185:Resveratrol