Date of Award
2013
Degree Type
Thesis
Degree Name
Master of Science (MS)
First Advisor
Lindon Young, PhD
Second Advisor
Robert Barsotti, PhD
Third Advisor
Ruth Borghaei, PhD
Fourth Advisor
Marcus G Bell, PhD
Abstract
Reactive oxygen species (ROS) generated during myocardial I/R contribute to post-reperfused cardiac contractile dysfunction. Damaged cardiomyocyte mitochondria are major sites of excess ROS generation during reperfusion. We hypothesized that reducing mitochondrial ROS formation should attenuate myocardial I/R injury and thereby improve function of isolated perfused rat hearts subjected to I(30min)/R(45min) compared to untreated I/R hearts. Mitoquinone (MitoQ, MW=579g/mol; complexed with cyclodextrin (MW=1135g/mol) to improve water solubility, total MW=1714g/mol), a coenzyme Q derivative, and SS-31 (Szeto-Schiller) peptide ((D-Arg)-Dmt-Lys-Phe-Amide, MW=639g/mol, Genemed Synthesis, Inc., San Antonio, TX), an alternating cationic-aromatic peptide, are selective mitochondrial ROS inhibitors which significantly improved post-reperfused cardiac function compared to untreated I/R controls in this study (p
Recommended Citation
Ondrasik, Regina, "Cardioprotective Effects of Mitochondrial-Targeted Antioxidants in Myocardial Ischemia/Reperfusion (I/R) Injury" (2013). PCOM Biomedical Studies Student Scholarship. 87.
https://digitalcommons.pcom.edu/biomed/87