Key result
In vitro exposure to 5-fluorouracil induced dose- and time-dependent irreversible changes in erythrocyte morphology, ionic balance, and membrane fluidity, potentially explaining its cardiotoxicity.
5-fluorouracil induces irreversible changes in erythrocyte morphology and function in vitro, suggesting a potential mechanism for its cardiotoxicity via impaired oxygen delivery to the heart.
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May implicate erythrocyte dysfunction in 5-FU cardiotoxicity; hypothesis-generating and requires in vivo validation.
In the present study, we showed that the antineoplastic drug 5-fluorouracil (5-FU) induces in vitro exposure-time/dose-dependent changes on the level of an erythrocyte's morphology, ionic balance, and membrane fluidity. These changes are partially or fully irreversible, and we suggest that they are provoked by an irreversible depletion of ATP. Because of these changes that could also occur in vivo during 5-FU infusion, a certain amount of erythrocytes with echinocytic shape and diminished ability to deliver oxygen is present in blood for longer periods of time. This renders oxygen transport and delivery more difficult, leaving the heart with an insufficient supply of oxygen, thus leading to cardiotoxicity.
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Spasojević et al. (2005) studied this question. 5-fluorouracil (5-FU) was evaluated on Erythrocyte morphology, ionic balance, and membrane fluidity. In vitro exposure to 5-fluorouracil induced dose- and time-dependent irreversible changes in erythrocyte morphology, ionic balance, and membrane fluidity, potentially explaining its cardiotoxicity.
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