PARASKEVI-MARIA NECHALIOTI

Oxidative stress is caused by an imbalance between the production and subsequent accumulation of reactive oxygen species (ROS) in cells and tissues and the capacity of a biological system to eliminate these reactive substances. Systemic oxidative stress biomarkers in plasma, serum, urine, or red blood cells have been found to be elevated in many diseases, including skin cancer. UV radiation (UVR) induces damage to biomolecules that enter the bloodstream, reinforcing systemic oxidative stress. On the other hand, pre-existing systemic oxidative stress does not supply the skin with the adequate micronutrients and antioxidant resources to ameliorate the skin’s antioxidant defense against UVR. In both scenarios, skin cancer patients are exposed to oxidative conditions. In the case of warts, oxidation is linked to chronic inflammation, while impaired cutaneous antioxidant defense could ineffectively deal with possible oxidative stimuli from viral agents, such as HPV. Therefore, the aim of our study is to evaluate the existing data on systemic oxidative stress in skin diseases such as non-melanoma skin cancer (NMSC), basal-cell carcinoma (BCC), squamous-cell carcinoma (SCC), and melanoma as well as benign lesions such as actinic keratosis (AK), sebaceous keratosis (SK), and warts. Previous studies have demonstrated that patients with NMSC, melanoma, AK, and warts (both genital and non-genital) are subjected to severe oxidative stress, indicated by disturbed antioxidant enzyme levels, accumulated oxidized proteins and lipid products, and, to a lesser extent, lower concentrations of micronutrients. Interestingly, medical history of NMSC or melanoma as well as stage of skin cancer and treatment approach were found to affect systemic oxidative stress parameters. In the case of warts (both genital and non-genital), high oxidative stress levels were also detected, and they were found to be aligned with their recalcitrant character.