Abstract

Photodynamic therapy (PDT) involves the use of photochemical reactions mediated through the interaction of photosensitizing agents, light and oxygen to destroy abnormal tissue. The transfer of energy from the activated photosensitizer to available oxygen results in the formation of toxic reactive oxygen species, such as singlet oxygen and free radicals, which can damage proteins, lipids, nucleic acids, and other cellular components. PDT is now commonly used in ophthalmology, dermatology and oncology however the therapeutic response to PDT exhibits variability, ranging from highly sensitive to extremely resistant. Over the last 10 years it has been suggested that nitric oxide (NO) may play a role in PDT, with evidence that NO is produced by both tumour and normal cells in addition to controlling important functions in tumour progression. NO may also influence the outcome of cancer therapies, such as PDT. PDT induces oxidative stress, vascular-mediated damage and leukocyte recruitment, processes all sensitive to NO. This review outlines the role of nitric oxide in PDT primarily focusing on vascular damage and how this may be modulated to improve therapeutic outcome.

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