Evaluation of the biological effect in dna damage repair of a high broad spectrum containing nicotinamide and panthenol in actinic keratoses and field cancerization

Nicotinamide is the precursor of NAD (nicotinamide adenine dinucleotide), an essential coenzyme in the production of ATP (adenosine triphosphate), the main source of cellular energy. Previous studies in mice showed that oral consumption or topical application of nicotinamide prevents immunosuppression and reduces the number of tumors induced by UV radiation. In humans, topical application of 5% Nicotinamide prevents immunosuppression caused by solar UV radiation, butnot burns. Furthermore, oral Nicotinamide reduces thediagnosis rate of new non-melanoma skin cancers and actinic keratoses in high-risk patients. It has been suggested that one of the mechanisms by which Nicotinamide may protect against photodamage is by increasing ATP production which enhances DNA repair. Additionally, nicotinamide acts as a PARP1 inhibitor. Extensive DNA damage leads to overactivation of PARP1 which can lead to NAD depletion. Thus, cells are unable to enter apoptosis, since the process requires a large amount of energy.Using a high broad spectrum UVB-UVA sunscreen containing Nicotinamide and Panthenol can help reverse chronic sundamage to the DNA of skin cells.