Interaction of imatinib with liposomes: Voltammetric and AFM characterization

The interaction of imatinib with 1,2-dipalmitoyl-sn-glycero-3-phosphocholine (DPPC) and 2-oleoyl-1-stearoyl-sn-glycero-3-phosphocholine (OSPC) liposomes and the adsorption of DPPC and OSPC were studied using atomic force microscopy (AFM) at highly oriented pyrolytic graphite (HOPG) and differential...

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Published in:Bioelectrochemistry (Amsterdam, Netherlands) Netherlands), 2009-02, Vol.74 (2), p.278-288
Main Authors: Diculescu, Victor C., Chiorcea-Paquim, Ana-Maria, Tugulea, Laura, Vivan, Marilene, Oliveira-Brett, Ana-Maria
Format: Article
Language:English
Subjects:
1,2-Dipalmitoylphosphatidylcholine
Benzamides
DPPC
Electrochemistry
Glivec
Graphite
Hydrogen Bonding
Imatinib
Imatinib Mesylate
Lipid Bilayers
Liposomes
Liposomes - chemistry
Microscopy, Atomic Force - methods
OSPC
Phosphatidylcholines
Piperazines - chemistry
Pyrimidines - chemistry
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Summary:The interaction of imatinib with 1,2-dipalmitoyl-sn-glycero-3-phosphocholine (DPPC) and 2-oleoyl-1-stearoyl-sn-glycero-3-phosphocholine (OSPC) liposomes and the adsorption of DPPC and OSPC were studied using atomic force microscopy (AFM) at highly oriented pyrolytic graphite (HOPG) and differential pulse voltammetry at glassy carbon electrode (GCE). The HOPG induces the rupture of the liposomes and allows the lipids to adsorb along one of the three axes of symmetry of the HOPG basal planes, forming well-ordered lamellar structures. After interaction, both DPPC monolayers and DPPC–imatinib complexes are adsorbed onto HOPG. The OSPC–imatinib complexes self-organize only into ordered but larger domains of parallel stripes that maintain the threefold symmetry of the HOPG, due to an easier imatinib penetration into the unsaturated OSPC liposome bilayers. The voltammetric results show that upon interaction, the electrochemical active moiety of imatinib is incorporated into the lipid bilayer becoming unavailable to the GCE surface for oxidation, leading to local structural modifications of the lipid bilayer which were also electrochemically detected. A model is proposed for the liposome–imatinib interaction considering that imatinib interacts primarily by van der Waals and hydrogen bonds with the phosphatidylcholine headgroups, leading to defects in the liposome bilayer and allowing further incorporation of imatinib into the liposome lamellae.
ISSN:1567-5394
1878-562X
DOI:10.1016/j.bioelechem.2008.10.003