Mitochondrial‐targeted H 2 S Donor (AP39) Ameliorates Doxorubicin‐Induced Cardiomyopathy

Although doxorubicin cardiomyopathy is a lethal disease, currently there are no effective treatments available. Doxorubicin is a potent inducer of mitochondrial reactive oxygen species (ROS), thus leading to mitochondrial damage and dysfunction. Hydrogen sulfide, a gaseous signaling molecule, is actively produced in mitochondria and impacts its function especially during stress states. Here, we tested if mitochondrial‐targeted H 2 S donors can ameliorate the myocardial mitochondrial dysfunction induced by the oncological drug. We used three‐months‐old C57 mice (n=8) to induce doxorubicin cardiomyopathy and treated them with different doses of AP39 compound (an H 2 S donor). We have characterized the histological, gravimetric and molecular changes after the treatments in the myocardium. The results suggested that the mitochondrial‐targeted H 2 S donor has the potential for ameliorating myocardial mitochondrial dysfunction and doxorubicin cardiomyopathy. Support or Funding Information American Heart Association‐17SDG33670578 to Dr. Veeranki and HL074185 . This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .