Cellfood improves respiratory metabolism of endothelial cells and inhibits hypoxia-induced reactive oxygen species (ROS) generation

• Autorzy: Ferrero E. , Fulgenzi A. , Belloni D. , Foglieni C. , Ferrero M.E.
• Języki publikacji: EN

Abstrakty

EN

Endothelial mitochondria, the major site of ATP generation, modulate the intracellular dynamics of reactive oxygen species (ROS), which, in turn, control endothelial function. Adequate oxygen (O2) supply is required by endothelial cells (EC). Both hypoxia and hyperoxia may favor the overproduction of ROS leading to oxidative stress, mitochondrial damage and endothelial dysfunction. We investigated the capability and mechanisms of CellfoodTM (CF), an antioxidant compound, to modulate O2 availability and mitochondrial respiratory metabolism and to regulate ROS generated by hypoxia in EC in vitro. Human umbilical vein endothelial cells (HUVEC) and ECV-304 were evaluated for the O2 consumption using a Clark's electrode. The O2 consumption rate rose, during the first minutes after CF addition and was associated with increase in mitochondrial oxidative capacity and good cell viability. Similar behaviours were observed when EC were exposed to CF for up to 8 days. The O2 consumption increased and was accompanied by both intracellular rise of ATP and maintainment of LDH concentration. Hypoxia-induced ROS generation was significantly inhibited by CF, through the up-regulated expression of MnSOD, an anti-oxidant responsible for mitochondrial function preservation. The EC hypoxic response is mediated by the hypoxia master regulator HIF-1alpha whose activation was attenuated by CF, in concomitance with MnSOD up-regulation. Our results suggest a role for CF in improoving respiratory metabolism and in activating anti-oxidant mechanisms in EC, thus preserving endothelial function.

Słowa kluczowe

EN

endothelial cell; endothelial dysfunction; human umbilical vein endothelial cell; hyperoxia; hypoxia; hypoxia inducible factor-1alpha; mitochondrial activity; oxidative stress; reactive oxygen species; respiratory metabolism; superoxide dismutase

• Wydawca: -
• Czasopismo: Journal of Physiology and Pharmacology
• Rocznik: 2011
• Tom: 62
• Numer: 3
• Opis fizyczny: p.287-293,fig.,ref.

Twórcy

autor

Ferrero E.

• Dipartimento di Morfologia Umana e Scienze Biomediche - Citta Studi, "Universita degli Studi di Milano", via Mangiagalli 31, 20133 Milan, Italy

autor

Fulgenzi A.

autor

Belloni D.

autor

Foglieni C.

autor

Ferrero M.E.