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Oxidative stress

Reoxygenation after hypoxia and glucose depletion causes reactive oxygen species production by mitochondria in HUVEC

¹Laboratoire d'Etude de la Microcirculation, Equipe d’accueil 3509, Faculté de Médecine Lariboisière St. Louis, 75010 Paris; and ²Equipe d’accueil 3540, Laboratoire d'Anesthésie, Hôpital de Bicêtre, 94270 Kremlin Bicêtre, France

Submitted 22 January 2004 ; accepted in final form 10 June 2004

In hemorrhagic shock, local hypoxia is present and followed by reoxygenation during the therapeutic process. In endothelium, reactive oxygen species (ROS) have been identified as a cause of inflammatory reactions and tissular lesions in ischemic territory during reoxygenation. This study was designed to identify the enzymatic mechanisms of ROS formation during reoxygenation after hypoxia. Because severe shock, in vivo, can affect both O₂ and nutriments, we combined hypoxia at a level close to that found in terminal vessels during shock, with glucose depletion, which induces a relevant additional stress. Human umbilical vein endothelial cells (HUVEC) underwent 2 h of hypoxia (PO₂ 20 mmHg) without glucose and 1 h of reoxygenation (PO₂ 120 mmHg) with glucose. ROS production was measured by the fluorescent marker 2',7'-dichlorodihydrofluorescein diacetate, and cell death by propidium iodide. After 1 h of reoxygenation, fluorescence had risen by 143 ± 17%. Cell death was equal to 8.6 ± 2.4%. Antimycin A and stigmatellin, which inhibits the type III mitochondrial respiratory chain complex, reduced ROS production to values of 61 ± 10 and 59 ± 7%, respectively, but inhibitors of other chain complexes did not affect it. In addition, the increase in fluorescence was not affected by inhibition of NADPH oxidase, xanthine oxidase, NOS, cyclooxygenase, cytochrome P-450 monooxygenase, or monoamine oxidase. We did not observe any increase in cell death. These results show that, in HUVEC, mitochondria are responsible for ROS production after hypoxia and reoxygenation and suggest that a ROS release site is activated in the cytochrome b of the type III respiratory chain complex.

endothelium; hydrogen peroxide; cytochrome b; human umbilical vein endothelial cells

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