**2. Basic principles**

Photosensitized oxidations have been of interest to chemists and biologists since Raab's discovery that microorganisms are killed by light in the presence of oxygen and sensitizing dyes [1].

The mechanism of action of photosensitizers is divide in two different types and generally involves direct oxidation by hydrogen peroxide (H2O2), superoxide anion radical (O2 ∙) and hydroxyl radical (∙OH) (Type I reaction) of biological targets (membranes, proteins, and DNA), as well as oxidation mediated by singlet oxygen (1 O2) that is mainly formed through energy transfer from triplet states to molecular oxygen (Type II reaction) [8-10].

The generation of Reactive Oxygen Species (ROS), in both types I or II, are dependent on the uptake of a photosensitizing dye, often a haematoporphyrin derivative, by the tumor or other abnormal target tissue, the subsequent irradiation of the tumor with visible light of an appropriate wavelength, and the presence of molecular oxygen [10]. An adequate concentra‐ tion of molecular oxygen is also needed for tissue damage. If any one of these components is absent, there is no photodynamic response, and the overall effectiveness therefore requires careful planning of both tissue photosensitization and light dosimetry.

PDT response is induced by more than one cellular mechanism. A photosensitiser can directly target the tumor cells, inducing necrosis or apoptosis (Figure 1) [11]. Alternatively, tumor necrosis can be induced by damaging its vasculature [12].

**Figure 1.** Treatment procedure for topical PDT. A) Skin cancer lesion; B) Cream application (MAL or ALA); C) Occlusion of the lesion; D) Illumination; E) Inflammation and tecidual necrosis; F) Curative
