Abstract
Proton cancer therapy (PCT) utilizes high-energy proton projectiles to obliterate cancerous tumors with low damage to healthy tissues and without the side effects of X-ray therapy. The healing action of the protons results from their damage on cancerous cell DNA. Despite established clinical use, the chemical mechanisms of PCT reactions at the molecular level remain elusive. This situation prevents a rational design of PCT that can maximize its therapeutic power and minimize its side effects. The incomplete characterization of PCT reactions is partially due to the health risks associated with experimental/clinical techniques applied to human subjects. To overcome this situation, we are conducting time-dependent and non-adiabatic computer simulations of PCT reactions with the electron nuclear dynamics (END) method. Herein, we present a review of our previous and new END research on three fundamental types of PCT reactions: water radiolysis reactions, proton-induced DNA damage and electron-induced DNA damage. These studies are performed on the computational prototypes: proton + H2O clusters, proton + DNA/RNA bases and + cytosine nucleotide, and electron + cytosine nucleotide + H2O. These simulations provide chemical mechanisms and dynamical properties of the selected PCT reactions in comparison with available experimental and alternative computational results.
Highlights
Proton cancer therapy (PCT) employs high-energy H+ projectiles to obliterate cancerous tumors [1,2,3,4,5,6]
Water radiolysis reactions were simulated with the computational prototypes H+ + (H2 O)1–6
Proton-induced DNA damage was simulated with the computational prototypes H+ + cytosine nucleotide and H+ + DNA/RNA bases
Summary
Proton cancer therapy (PCT) employs high-energy H+ projectiles to obliterate cancerous tumors [1,2,3,4,5,6]. The therapeutic effect of PCT results from the H+ radiation damage on the DNA of cancerous cells [1,2,3,4,5,6]. That type of accumulated and unrepaired DNA damage leads to several anomalies in the cancerous cells that provoke their apoptosis [1,2,3,4,5,6]. The applied H+ radiation enters the patient’s body as collimated beams of H+ projectiles with an initial kinetic energy of. The H+ projectiles travelling through the body progressively lose their energy to the tissues; the degree of cell damage is directly proportional to the amount of energy deposited.
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