Key result
Doxorubicin-transferrin and free doxorubicin induce ROS and leukemia cell death that vitamin C diminishes.
Why the study?
Does doxorubicin-transferrin conjugate induce ROS production and programmed cell death in human leukemia cell lines compared to free doxorubicin?
Does doxorubicin-transferrin conjugate induce ROS production and programmed cell death in human leukemia cell lines compared to free doxorubicin?
Doxorubicin-transferrin conjugate induces cell death in leukemia cell lines via ROS production, an effect that can be attenuated by the antioxidant vitamin C.
Vitamin C may blunt doxorubicin activity in leukemia models; leaves open clinical relevance pending patient studies.
In this study we focused on evaluation of the pro-oxidant properties of doxorubicin-transferrin (DOX-TRF) conjugate and its potency to damage macromolecules which are components of cellular compartments. Our experiments were performed on two human leukemia cell lines: K562 (chronic erythromyeloblastoid leukemia) and CCRF-CEM (acute lymphoblastic leukemia). We determined the reactive oxygen species (ROS) production and programmed cell death (PCD) induction by free DOX and its conjugate. Besides this, the lipid peroxidation and protein damage which can be provoked by DOX alone and DOX-TRF conjugate were assessed. ROS were produced in leukemia cells incubated with free DOX and DOX-TRF conjugate and the extent of apoptosis and necrosis was strongly dependent on the cell line, sensitivity to drug and time of incubation with the investigated compounds. The role of ROS in DOX-TRF conjugate-induced cell death was confirmed by the diminution effects of the antioxidant vitamin C.
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Szwed et al. (2014) studied Leukemia (in vitro cell lines K562 and CCRF-CEM). Doxorubicin-transferrin (DOX-TRF) conjugate vs. Free doxorubicin (DOX) was evaluated on Reactive oxygen species (ROS) production and programmed cell death (PCD) induction. Doxorubicin-transferrin conjugate and free doxorubicin induced reactive oxygen species production and cell death in leukemia cell lines, which was diminished by vitamin C.
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