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Biomedical Engineering and Bioengineering Commons™
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Articles 1 - 3 of 3
Full-Text Articles in Biomedical Engineering and Bioengineering
Depleted Energy Charge And Increased Pulmonary Endothelial Permeability Induced By Mitochondrial Complex I Inhibition Are Mitigated By Coenzyme Q1 In The Isolated Perfused Rat Lung, Robert D. Bongard, Ke Yan, Raymond G. Hoffmann, Said H. Audi, Xiao Zhang, Brian J. Lindemer, Mary I. Townsley, Marilyn P. Merker
Depleted Energy Charge And Increased Pulmonary Endothelial Permeability Induced By Mitochondrial Complex I Inhibition Are Mitigated By Coenzyme Q1 In The Isolated Perfused Rat Lung, Robert D. Bongard, Ke Yan, Raymond G. Hoffmann, Said H. Audi, Xiao Zhang, Brian J. Lindemer, Mary I. Townsley, Marilyn P. Merker
Biomedical Engineering Faculty Research and Publications
Mitochondrial dysfunction is associated with various forms of lung injury and disease that also involve alterations in pulmonary endothelial permeability, but the relationship, if any, between the two is not well understood. This question was addressed by perfusing isolated intact rat lung with a buffered physiological saline solution in the absence or presence of the mitochondrial complex I inhibitor rotenone (20 μM). Compared to control, rotenone depressed whole lung tissue ATP from 5.66±0.46 (SEM) to 2.34±0.15 µmol·g−1 dry lung, with concomitant increases in the ADP:ATP and AMP:ATP ratios. Rotenone also increased lung perfusate lactate (from 12.36±1.64 to 38.62±3.14 µmol·15 …
Mitochondrial Handling Of Excess Ca2+ Is Substrate-Dependent With Implications For Reactive Oxygen Species Generation, Mohammed Aldakkak, David F. Stowe, Ranjan K. Dash, Amadou K.S. Camara
Mitochondrial Handling Of Excess Ca2+ Is Substrate-Dependent With Implications For Reactive Oxygen Species Generation, Mohammed Aldakkak, David F. Stowe, Ranjan K. Dash, Amadou K.S. Camara
Biomedical Engineering Faculty Research and Publications
The mitochondrial electron transport chain is the major source of reactive oxygen species (ROS) during cardiac ischemia. Several mechanisms modulate ROS production; one is mitochondrial Ca2+ uptake. Here we sought to elucidate the effects of extramitochondrial Ca2+ (e[Ca2+]) on ROS production (measured as H2O2 release) from complexes I and III. Mitochondria isolated from guinea pig hearts were preincubated with increasing concentrations of CaCl2 and then energized with the complex I substrate Na+ pyruvate or the complex II substrate Na+ succinate. Mitochondrial H2O2 release rates were assessed after …
Enhanced Na+/H+ Exchange During Ischemia And Reperfusion Impairs Mitochondrial Bioenergetics And Myocardial Function, Mohammed Aldakkak, David F. Stowe, James S. Heisner, Marisha Spence, Amadou K.S. Camara
Enhanced Na+/H+ Exchange During Ischemia And Reperfusion Impairs Mitochondrial Bioenergetics And Myocardial Function, Mohammed Aldakkak, David F. Stowe, James S. Heisner, Marisha Spence, Amadou K.S. Camara
Biomedical Engineering Faculty Research and Publications
Inhibition of Na+/H+ exchange (NHE) during ischemia reduces cardiac injury due to reduced reverse mode Na+/Ca2+ exchange. We hypothesized that activating NHE-1 at buffer pH 8 during ischemia increases mitochondrial oxidation, Ca2+ overload, and reactive O2 species (ROS) levels and worsens functional recovery in isolated hearts and that NHE inhibition reverses these effects. Guinea pig hearts were perfused with buffer at pH 7.4 (control) or pH 8 +/- NHE inhibitor eniporide for 10 minutes before and for 10 minutes after 35- minute ischemia and then for 110 minutes with pH 7.4 buffer alone. Mitochondrial NADH and FAD, [Ca2+], and superoxide …