References of "Willet, K"
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See detailProtective effect of EGB 761 against oxidative phosphorylation damages of brain mitochondria after Anoxia/reoxygenation in vivo and in vitro
Du, G.; Willet, K.; Jarmuszkiewicz, W. et al

in Toxicology Mechanisms and Methods (2004), 14

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See detailTransplantation pulmonaire et fonction mitochondriale
Detry, Olivier ULiege; Willet, K.; Meurisse, Michel ULiege et al

in Bulletin et Mémoires de l'Académie Royale de Médecine de Belgique (2001), 156(6, Pt 2), 355-9

The mechanisms of cellular lesions induced by lung ischemia and reperfusion are not fully understood and, in particular, the consequences of pulmonary ischemia and reperfusion injury on mitochondrial ... [more ▼]

The mechanisms of cellular lesions induced by lung ischemia and reperfusion are not fully understood and, in particular, the consequences of pulmonary ischemia and reperfusion injury on mitochondrial function have not been previously investigated. Therefore, we studied the respiratory function of isolated pulmonary mitochondria in a swine model of lung ischemia and reperfusion. We demonstrated that prolonged hypothermic (4 degrees C) ischemia induces significant lesions of the mitochondrial respiratory chain, particularly if ischemia is followed by normothermic reperfusion. These results should be integrated in the cellular alterations induced by the ischemia-reperfusion injury. In another swine model mimicking controlled non-heart beating donors, we demonstrated that thirty minutes of cardiac arrest do not promote significant alteration of the mitochondrial respiratory function. In contrast, forty-five minutes of cardiac arrest, induced significant mitochondrial lesions. This pulmonary tolerance to normothermic cardiac arrest might be explained by the presence of air in the lung airways, allowing some aerobic metabolism after circulatory arrest. These results suggested that lung grafts might be harvested from non-heart beating donors after thirty minutes of cardiac arrest, significantly increasing the pulmonary graft pool. [less ▲]

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See detailResistance of Isolated Pulmonary Mitochondria During in Vitro Anoxia/Reoxygenation
Willet, K.; Detry, Olivier ULiege; Sluse, Francis ULiege

in Biochimica et Biophysica Acta (2000), 1460(2-3), 346-52

The aim of the study was to investigate the effect of in vitro anoxia/reoxygenation on the oxidative phosphorylation of isolated lung mitochondria. Mitochondria were isolated after harvesting from fresh ... [more ▼]

The aim of the study was to investigate the effect of in vitro anoxia/reoxygenation on the oxidative phosphorylation of isolated lung mitochondria. Mitochondria were isolated after harvesting from fresh pig lungs flushed with Euro-Collins solution. Mitochondrial respiratory parameters were determined in isolated mitochondria before anoxia (control), after 5-45 min anoxia followed by 5 min reoxygenation, and after 25 or 40 min of in vitro incubation in order to follow the in vitro aging of mitochondria during respiratory assays. Respiratory parameters measured after anoxia/reoxygenation did not show any oxidative phosphorylation dysfunction, indicating a high resistance of pulmonary mitochondria to in vitro anoxia/reoxygenation (up to 45 min anoxia). These results indicate that mitochondria are not directly responsible of their oxidative phosphorylation damage observed after in vivo ischemia (K. Willet et al., Transplantation 69 (2000) 582) but are a target of others cellular injuries leading to mitochondrial dysfunction in vivo. [less ▲]

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See detailEGb 761 protects liver mitochondria against injury induced by in vitro anoxia/reoxygenation.
Du, G.; Willet, K.; Mouithys-Mickalad, Ange ULiege et al

in Free Radical Biology and Medicine (1999), 27

The present study investigated the protective effects of Ginkgo biloba extract (EGb 761) on rat liver mitochondrial damage induced by in vitro anoxia/reoxygenation. Anoxia/reoxygenation was known to ... [more ▼]

The present study investigated the protective effects of Ginkgo biloba extract (EGb 761) on rat liver mitochondrial damage induced by in vitro anoxia/reoxygenation. Anoxia/reoxygenation was known to impair respiratory activities and mitochondrial oxidative phosphorylation efficiency. ADP/O (2.57 +/- 0.11) decreased after anoxia/reoxygenation (1.75 +/- 0.09, p < .01), as well as state 3 and uncoupled respiration (-20%, p < .01), but state 4 respiration increased (p < .01). EGb 761 (50-200 microg/ml) had no effect on mitochondrial functions before anoxia, but had a specific dose-dependent protective effect after anoxia/reoxygenation. When mitochondria were incubated with 200 microg/ml EGb 761, they showed an increase in ADP/O (2.09 +/- 0.14, p < .05) and a decrease in state 4 respiration (-22%) after anoxia/reoxygenation. In EPR spin-trapping measurement, EGb 761 decreased the EPR signal of superoxide anion produced during reoxygenation. In conclusion, EGb 761 specially protects mitochondrial ATP synthesis against anoxia/reoxygenation injury by scavenging the superoxide anion generated by mitochondria [less ▲]

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See detailComparative Effects of University of Wisconsin and Euro-Collins Solutions on Pulmonary Mitochondrial Function after Ischemia and Reperfusion
Detry, Olivier ULiege; Willet, K.; Lambermont, Bernard ULiege et al

in Transplantation (1998), 65(2), 161-6

BACKGROUND: The aim of this study was to compare the effects of Euro-Collins and University of Wisconsin solutions on pulmonary mitochondrial function after cold ischemia and subsequent warm reperfusion ... [more ▼]

BACKGROUND: The aim of this study was to compare the effects of Euro-Collins and University of Wisconsin solutions on pulmonary mitochondrial function after cold ischemia and subsequent warm reperfusion. METHODS: Seventeen pigs underwent lung harvesting after classical lung flush with either University of Wisconsin or Euro-Collins solutions. The mitochondria were isolated from fresh swine lungs, from swine lungs subjected to 24 hr of cold ischemia, and from swine lungs subjected to 24 hr of ischemia followed by 30 min of subsequent ex vivo reperfusion at 37 degrees C with Krebs-Henseleit buffer solution and air ventilation. Mitochondrial oxidative phosphorylation parameters were determined in isolated mitochondria by in vitro measurement of oxygen consumption rates. During reperfusion, the lung function was assessed by the pulmonary aerodynamic parameters and the pulmonary vascular resistance. RESULTS: Relative to controls, mitochondria submitted to cold ischemia showed an alteration in the oxidoreductase activities of the respiratory chain. However, the yield of oxidative phosphorylation was conserved. After reperfusion, pulmonary mitochondria underwent a significant worsening in the oxidoreductase activities of the respiratory chain, and a decrease in the respiratory control and the efficiency of oxidative phosphorylation. Meanwhile, the reperfused lungs showed evidence of early dysfunction, assessed by the aerodynamic parameters and pulmonary vascular resistance. In this model, there was no advantage of University of Wisconsin solution over Euro-Collins solution. CONCLUSIONS: The mild mitochondrial alterations after cold ischemia were not sufficient to explain the limited tolerance of lung to ischemia. After reperfusion, the mitochondrial damage was more severe and could be involved in the posttransplant lung dysfunction. [less ▲]

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See detailProtective effect of Ginkgo biloba extract (Egb 761) on functional impairments of mitochondria induced by anoxia-reoxygenation in situ and in vitro
Sluse, Francis ULiege; DU, G.-H.; Willet, K. et al

in Packer, L.; Christen, Y. (Eds.) Gingko biloba extract (EGb 761) : lessons from cell biology (1998)

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See detailConsequences of Cold and Warm Ischemia on Pulmonary Mitochondrial Respiratory Function
Detry, Olivier ULiege; Willet, K.; Lambermont, Bernard ULiege et al

in Transplantation Proceedings (1997), 29(5), 2338-9

IN RECENT years, pulmonary transplantation has become the treatment of choice for several end-stage lung diseases, but remains limited by the scarcity of suitable donors and the lack of reliable prolonged ... [more ▼]

IN RECENT years, pulmonary transplantation has become the treatment of choice for several end-stage lung diseases, but remains limited by the scarcity of suitable donors and the lack of reliable prolonged method of lung preservation.1 Transplantation of lung 6 hours postharvest leads to an increased incidence of primary graft dysfunction, due in part to ischemic damage of pulmonary cell structure and metabolism, and to acute reperfusion injury. However, very little is known about the real mechanisms of pulmonary cell injuries before, during, and after lung transplantation. <br /> <br />During ischemia, the cytosolic and mitochondrial adenine nucleotide content falls,2,3 phospholipids are degraded, membrane permeabilities are increased, and the cytosolic levels of Na+, Ca2+ and phosphate are raised.4 Thus, cold and warm ischemia may induce cell dysfunctions and irreversible injuries responsible for necrosis. As mitochondia are believed to be the site of the determinants of irreversibility,5 the study of permanent oxidative phosphorylation damage after ischemia should be of great interest. <br /> <br />The aim of this present study was to investigate the consequences of warm and cold ischemia on the oxidative phosphorylation of isolated lung mitochondria [less ▲]

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See detailEffects of ischemia and reperfusion on the mitochondrial function of pig lungs
WILLET, K; DETRY, Olivier ULiege; DEGOTTE, M et al

Conference (1996)

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See detailMitochondrial function impairing after lung ischemia
DETRY, Olivier ULiege; WILLET, K; LAMBERMONT, Bernard ULiege et al

Conference (1996)

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See detailComparative effects of ischemia and reperfusion on the mitochondrial function in kidney and lung
WILLET, K; DETRY, Olivier ULiege; DEGOTTE, M et al

Conference (1996)

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See detailMitochondrial oxidative phosphorylation : in vitro and in situ effect of EGb 761
Willet, K.; DETRY, Olivier ULiege; Evens, A. et al

in Packer, L.; Trabet, Maret G; Xin, Wenjuan (Eds.) Proceedings of the international symposium on natural antioxidants molecular mechanisms and health effects (1996)

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See detailMitochondrial oxidative phosphorylation injuries occurring in situ and in vitro.
Willet, K.; Vaz de Macedo, D.; DETRY, Olivier ULiege et al

in Transplantation Proceedings (1995), 27

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