Abstract

ABSTRACTWe report total electron-impact ionisation cross sections (EICSs) of cisplatin, its hydrolysis products and transplatin in the energy range from threshold to 10 keV using the binary-encounter-Bethe (BEB) and its relativistic variant (RBEB), and the Deutsch-Märk (DM) methods. We find reasonable agreement between all three methods, and we also note that the RBEB and the BEB methods yield very similar (almost identical) results in the considered energy range. For cisplatin, the resulting EICSs yield cross section maxima of 22.09 × 10−20 m2 at 55.4 eV for the DM method and 18.67 × 10−20 m2 at 79.2 eV for the (R)BEB method(s). The EICSs of monoaquated cisplatin yield maxima of 12.54 × 10−20 m2 at 82.8 eV for the DM method and of 9.74 × 10−20 m2 at 106 eV for the (R)BEB method(s), diaquated cisplatin yields maxima of 7.56 × 10−20 m2 at 118.5 eV for the DM method and of 5.77 × 10−20 m2 at 136 eV for the (R)BEB method(s). Molecular geometry does not affect the resulting EICS significantly, which is also reflected in very similar EICSs of the cis- and trans-isomer. Limitations of the work as well as desirable future directions in the research area are discussed.

Highlights

  • Having been discovered as early as 1845, cis-diamminedichloridoplatinum(II), cis-Pt(NH3)2Cl2, in short, cisplatin, see Figure 1(a), is up to now one of the most leading drugs used in anticancer chemotherapy

  • We report calculated electronimpact ionisation cross sections (EICSs) for cisplatin and its hydrolysis products as well as for transplatin from threshold to 10 keV

  • We depict the results reported earlier by Żywicka and Możejko [21] and by Mahato et al [22]. We find that both methods, i.e. DM and BEB, are in reasonable agreement with each other, deviating by about 15–20% from each other

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Summary

Introduction

Having been discovered as early as 1845, cis-diamminedichloridoplatinum(II), cis-Pt(NH3)2Cl2, in short, cisplatin, see Figure 1(a), is up to now one of the most leading drugs used in anticancer chemotherapy. To the administration of the drug and its transfer into cells, the Pt-Cl bonds are hydrolised [1,2,3], i.e. the chloride ligands are replaced by water molecules. Replacement of one ligand results in monoaquated cisplatin, i.e. cis-[Pt(NH3)2(OH2)Cl]+, replacement of both ligands results in diaquated cisplatin, i.e. cis[Pt(NH3)2(OH2)2]2+ see Figure 1(b,c), respectively. The hydrolysed products bind to DNA, forming intrastrand cross-links between nucleobases. This inhibits the cell replication process, which is the primary mode of action of the drug’s anticancer activity [1,2,3,4].

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