Abstract
Ultraviolet radiation is one of the most pervasive environmental interactions with humans. Chronic ultraviolet irradiation increases the danger of skin carcinogenesis. Probably, oxidative stress is the most important mechanism by which ultraviolet radiation implements its damaging effects on normal cells. However, notwithstanding the data referring to the negative effects exerted by light radiation and oxidative stress on carcinogenesis, both factors are used in the treatment of skin cancer. Photodynamic therapy (PDT) consists of the administration of a photosensitiser, which undergoes excitation after suitable irradiation emitted from a light source and generates reactive oxygen species. Oxidative stress causes a condition in which cellular components, including DNA, proteins, and lipids, are oxidised and injured. Antitumor effects result from the combination of direct tumour cell photodamage, the destruction of tumour vasculature and the activation of an immune response. In this review, we report the data present in literature dealing with the main signalling molecular pathways modified by oxidative stress after photodynamic therapy to target skin cancer cells. Moreover, we describe the progress made in the design of anti-skin cancer photosensitisers, and the new possibilities of increasing the efficacy of PDT via the use of molecules capable of developing a synergistic antineoplastic action.
Highlights
The cancer tissue concentrations of TNF-α and MDA were considerably greater in treated cancers than in controls, and these results were related to the histological modifications
These data propose that Photodynamic therapy (PDT) stimulates the innate immune system and that this action is due to Reactive oxygen species (ROS) production [85]
Intracellular ROS and the mitochondrial membrane potential (∆Ψmt ) were evaluated, employing a DCFH-DA probe and DiOC6 dye. Their results revealed that the therapy of basal cell carcinoma (BCC) cells with 1j-ultraviolet A (UVA) provoked augmented ROS production and the loss of mmp (∆Ψmt ) [108]
Summary
Ultraviolet radiation (UVR) is one of the most pervasive environmental interactions with humans. Cellular injury resulting from excessive ROS generation represents a consequence of interference with three major cellular components: cellular membranes, proteins and DNA In this regard, oxidative stress damages cellular components with the consequent alteration of overall biological activities [20]. Oxidative stress damages cellular components with the consequent alteration of overall biological activities [20] Both the superoxide anion and hydroxyl radical species can cause the oxidative degradation of cellular membranes in a process known as lipid peroxidation. Excessive concentrations of ROS promote an altered cell growth, DNA damage and epigenetic modifications, and cause the onset of several diseases including tumours [23,24]. The stimulation of NF-E2-related factor 2 (NRF2), a transcription element that activates antioxidant systems, reduces ROS concentrations and prevents ROS-caused DNA alterations after UV exposure, blocking the process of skin carcinogenesis [28]. This report proposes that, as opposed to ROS-caused oncogenic signalling, oxidative stress in melanoma cells blocks metastasis [38]
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