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Biomedical Engineering and Bioengineering Commons

Open Access. Powered by Scholars. Published by Universities.®

2013

Marquette University

Free radicals

Articles 1 - 2 of 2

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 Dec 2013

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 ...


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 Mar 2013

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 giving either ...