Journal article
An impaired mitochondrial electron transport chain increases retention of the hypoxia imaging agent diacetylbis(4-methylthiosemicarbazonato)copper II
PS Donnelly, JR Liddell, SC Lim, BM Paterson, MA Cater, MS Savva, AI Mot, JL James, IA Trounce, AR White, PJ Crouch
Proceedings of the National Academy of Sciences of the United States of America | Published : 2012
Abstract
Radiolabeled diacetylbis(4-methylthiosemicarbazonato)copper II[Cu II(atsm)] is an effective positron-emission tomography imaging agent for myocardial ischemia, hypoxic tumors, and brain disorders with regionalized oxidative stress, such as mitochondrial myopathy, encephalopathy, and lactic acidosis with stroke-like episodes (MELAS) and Parkinson's disease. An excessively elevated reductive state is common to these conditions and has been proposed as an important mechanism affecting cellular retention of Cu from Cu II(atsm). However, data from whole-cell models to demonstrate this mechanism have not yet been provided. The present study used a unique cell culture model, mitochondrial xenocybri..
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Funding Acknowledgements
The metal-responsive element-luciferase and Renillaluciferase constructs were kindly provided by Dr. Leo Klomp, Department of Metabolic and Endocrine Diseases, University Medical Center Utrecht, The Netherlands. The research was supported by funds from the Australian National Health and Medical Research Council and the Australian Research Council.