Key result
5-Fluorouracil and capecitabine induced cytotoxicity in rat cardiomyocytes via oxidative stress and mitochondrial dysfunction leading to caspase-3 activation, with 5-FU being more potent.
Population
Freshly isolated rat cardiomyocytes
Design
Preclinical
Authors
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No immediate clinical implications; hypothesis-generating for oxidative stress-targeted cardioprotection in fluoropyrimidine therapy.
5-FU and capecitabine induce cardiotoxicity through oxidative stress and mitochondrial dysfunction, with 5-FU exhibiting more potent cytotoxic effects including lysosomal membrane leakiness.
Eskandari et al. (2014) studied Cardiotoxicity. 5-Fluorouracil and capecitabine was evaluated on Cytotoxic mechanisms including ROS formation, lipid peroxidation, glutathione depletion, and mitochondrial dysfunction. 5-Fluorouracil and capecitabine induced cytotoxicity in rat cardiomyocytes via oxidative stress and mitochondrial dysfunction leading to caspase-3 activation, with 5-FU being more potent.
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