Abstract

Photodynamic therapy (PDT) is a less-invasive treatment of cancer and precancerous lesions. Porphyrin derivatives have been used and studied as the photosensitizers for PDT. In general, the biomacromolecules oxidation by singlet oxygen, which is produced through energy transfer from the photoexcited photosensitizers to oxygen molecules, is an important mechanism of PDT. However, the traditional PDT effect may be restricted, because tumors are in a hypoxic condition and in certain cases, PDT enhances hypoxia via vascular damage. To solve this problem, the electron transfer-mediated oxidation of biomolecules has been proposed as the PDT mechanism. Specifically, porphyrin phosphorus(V) complexes demonstrate relatively strong photooxidative activity in protein damage through electron transfer. Furthermore, other photosensitizers, e.g., cationic free-base porphyrins, can oxidize biomolecules through electron transfer. The electron transfer-supported PDT may play the important roles in hypoxia cancer therapy. Furthermore, the electron transfer-supported mechanism may contribute to antimicrobial PDT. In this chapter, recent topics about the biomolecules photooxidation by electron transfer-supported mechanism are reviewed.

Highlights

  • Photodynamic therapy (PDT) is a less-invasive treatment of cancer and other nonmalignant conditions [1–3]

  • This chapter reviewed the several topics about the photosensitizers, which play electron transfer-supported mechanism. 1O2 is the important reactive species in PDT and antimicrobial photodynamic therapy (aPDT)

  • In the study of PDT photosensitizer for cancer, phosphorus(V) porphyrins showed the selectivity for cancer cell and relatively strong PDT effects

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Summary

Introduction

Photodynamic therapy (PDT) is a less-invasive treatment of cancer and other nonmalignant conditions [1–3]. In the case of cancer treatment, less-toxic PDT reagents, photosensitizers, cause oxidative damage to biomolecules, including protein, nucleic acids, and/or other compounds, under visible-light irradiation. This photosensitized reaction results in necrosis or apoptosis of cancer cells [1–3]. In certain cases, PDT itself enhances hypoxia [23] via vascular damage [24] This “hypoxia problem” of tumor is very important to improve the PDT effect. Electron extraction from biomolecules to photoexcited photosensitizer is the mechanism of oxidative biomolecule damage. This electron transfer oxidation may be an important mechanism to resolve the “hypoxia problem” and to develop the effective PDT photosensitizers. The initial process of electron transfer-mediated biomolecule oxidation is an electron extraction from the targeting biomolecule, such as protein, to the photoexcited photosensitizer

Driving force dependence of electron transfer
Excitation energy and electron transfer
Kinetics of electron transfer
Photosensitized protein damage by phosphorus(V) porphyrin through electron transfer
Cancer selective photodynamic action of phosphorus(V) porphyrin photosensitizers
Photosensitized oxidation of folic acid by phosphorus(V) porphyrin through electron transfer
Protein photooxidation through electron transfer by cationic porphyrins
Activity control based on the electron transfer
Electron transfer mechanism and antimicrobial photodynamic therapy
Photosensitized DNA damage through electron transfer
Conclusions
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