Mitigating long-term cardiac adverse effects of radiation exposure: emerging opportunities in protein oxidation and autophagy modulation

Monday, September 22, 2014 — Poster Session II
4:00 p.m. – 6:00 p.m.	FAES Academic Center	FDA/CBER	MOLBIO-16

Authors

• E.T. Rosen
• Y. Gonzalez
• B. Aryal
• L. Chehab
• J. Dickey
• A.V. Rao

Abstract

Radiation-induced heart disease (RIHD) presents a significant challenge in the event of an accidental radiation exposure of a population to ionizing radiation. Likewise, in the oncology setting, patients who receive acute doses of irradiation to the thoracic cavity for Hodgkin’s Lymphoma and breast cancer are subject to an elevated risk of RIHD. The ability to mitigate the long-term cardiac effects of radiation exposure in these populations by modulating protein oxidation and the process of autophagy in the heart has the potential to lead to improved health outcomes. We utilized the spontaneously hypertensive rat (SHR), which has proven a good model for drug-induced cardiotoxicity, to evaluate radiation-induced heart disease. A marked difference in both heart and whole body mass was observed in the high dose group after one year. Anemic conditions were noted by low red blood cell counts observed in both males and females in animals receiving the highest dose of irradiation. Elevated cardiac troponin T levels revealed cardiotoxicity at earlier time points. Echocardiography revealed left ventricular volume at diastole was increased and left ventricular mass decreased following high irradiation exposures. We are currently exploring the oxidative stress-mediated molecular mechanisms behind the radiation-induced cardiac damage.

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