DOXORUBICIN REMEDY OR HARM? CARDIOTOXICITY AND NOT ONLY

B. PALA, M. PECORARO, M.C. DI MARCANTONIO, L. CENTURIONE, M.C. BUDANI, G.M. TIBONI, R. MURARO, A. PINTO, A. POPOLO, G. MINCIONE

Article ID: 6407
Vol 32, Issue 4S1, 2018
DOI: https://doi.org/10.54517/jbrha6407
Received: 8 September 2018; Accepted: 8 September 2018; Available online: 8 September 2018; Issue release: 8 September 2018

Abstract

Doxorubicin (Doxo) is a chemotherapeutic agent whose clinical use is hampered by the serious dosedependentcardiotoxicity. The accumulation of Reactive Oxygen Species (ROS) is widely accepted asa key factor of cardiotoxic effects. Mitochondrial Connexin 43 (Cx43) conferred cardioprotection byreducing cytosolic and mitochondrial ROS production. Topic of this work was the identification ofantioxidant enzymes and molecules involved in Doxo-induced damage, in absence and in presence ofRadicicol (Rad), an inhibitor of Cx43 translocation to mitochondria. Due to increasing numbers of youngcancer survivors and the raising concerns for their fertility state, elucidating the biological mechanismsof chemotherapy risk is highly relevant. Moreover, it is known that Doxo-induced ovarian toxicity isassociated with apoptosis of mouse granulosa cells.



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