Mitochondrial accumulation of doxorubicin in cardiac and diaphragm muscle following exercise preconditioning. Academic Article

abstract

• Doxorubicin (DOX) is a highly effective anthracycline antibiotic. Unfortunately, the clinical use of DOX is limited by the risk of deleterious effects to cardiac and respiratory (i.e. diaphragm) muscle, resulting from mitochondrial reactive oxygen species (ROS) production. In this regard, exercise is demonstrated to protect against DOX-induced myotoxicity and prevent mitochondrial dysfunction. However, the protective mechanisms are currently unclear. We hypothesized that exercise may induce protection by increasing the expression of mitochondria-specific ATP-binding cassette (ABC) transporters and reducing mitochondrial DOX accumulation. Our results confirm this finding and demonstrate that two weeks of exercise preconditioning is sufficient to prevent cardiorespiratory dysfunction.

authors

• Morton, Aaron

published proceedings

• Mitochondrion

altmetric score

• 4.75

author list (cited authors)

• Morton, A. B., Mor Huertas, A., Hinkley, J. M., Ichinoseki-Sekine, N., Christou, D. D., & Smuder, A. J.

citation count

• 40

complete list of authors

• Morton, Aaron B||Mor Huertas, Andres||Hinkley, J Matthew||Ichinoseki-Sekine, Noriko||Christou, Demetra D||Smuder, Ashley J

publication date

• March 2019

publisher

• Elsevier  Publisher

published in

• Mitochondrion  Journal

keywords

• Animals
• Anthracycline
• Antibiotics, Antineoplastic
• Atp-binding Cassette Transporter
• Diaphragm
• Doxorubicin
• Female
• Heart
• Mitochondria
• Myocardium
• Physical Conditioning, Animal
• Rats, Sprague-Dawley

PubMed Central ID

• 29474837

Digital Object Identifier (DOI)

• 10.1016/j.mito.2018.02.005

start page

• 52

end page

• 62

volume

• 45

URL

• http://dx.doi.org/10.1016/j.mito.2018.02.005