Reactive oxygen species . skin damage

The main cause of non-melanoma skin cancers are mutations due to formation of cyclo-pyrimidine dimers in the DNA, which occur after absorption of UVB by the DNA, as the absorption spectrum of DNA shows some overlap with the UVB range. Apart from this direct interaction, UVB and UVA can indirectly induce damage to the DNA via formation of radicals and reactive oxygen species (Fig. 3). 

Anthocyanins are able to prevent oxidative damage to DNA, proteins, lipids, and other macromolecules caused by reactive oxygen species (ROS). Anthocyanins have a systemic action, since they are absorbed and circulate in the blood, and it is in this circulating form that they act upon different target tissues in the human body. Anthocyanins may also act locally, in the gut, if they are not absorbed by intestinal mucosa. Finally, they may also act as topical agents, for example, by protecting the skin from UV radiation. 

The first step in XJVR-induced skin cancer is UVR-initiated DNA mutation, which causes the transformation of the normal cells to malignant cells. For UVR to initiate a biological reaction, it has to be absorbed by endogenous molecules (chromophores). UVB is absorbed directly by the DNA, and therefore can directly induce DNA mutation (224), in the form of thymine dimer formation (289). Some protein components may also ad as chromophores for UVB (224). UVA is absorbed by the reduced forms of the co-enzymes nicotinamide adenine dinucleotide (NADH) and nicotinamide adenine dinucleotide phosphate (NADPH), tryptophan, riboflavin, and melanin (224,290). UVA-induced DNA damage is believed to be mediated by oxygen reactive species that are released after the absorption of UVA by those endogenous chromophores and results in photooxidation of selected bases... 

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