DNA damage initiates photobiologic reactions in the skin.

Ultraviolet (UV) radiation can induce acute and chronic photobiologic reactions in the absence of exogenous chromophores. Nuclear DNA is a major chromophore to initiate UV-induced physiologic reactions. The XPA-gene deficient mouse, an animal model of xeroderma pigmentosum, develops increased photobiologic reactions including acute inflammation, immunosuppression and skin cancers, because of the defect in the excision repair of UV-induced DNA lesions.