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Ultraviolet light-induced damage to the DNA resulting in double-stranded triggers the DNA Damage Response (DDR). This results in Cell Cycle Arrest (CCA) and Nucleotide Excision and Repair (NER) of the photo-damaged DNA. These processes are regulated by a family of phosphatidylinositol-3-kinase family. Cell cycle arrest is inhibitory to rapid healing of tissues. When damage is severe, apoptosis is induced only after multiple failed attempts at repair. Moreover, the intrinsic repair processes are slow and laborious, and do not return the tissues to pre-injury levels. When large segments of the DNA are damaged, or if the damage involves both strands of the DNA, replication errors occur, producing a potentially premalignant cell. The activation of the DDR pathway is regulated by a family of phosphatidylinositol-3 kinase family, the phosphorylation of which may be enhanced by phosphorylase kinase. It is proposed that by avoiding activation of the DDR pathways through inhibition of phosphorylase kinase, curcumin may induce early apoptosis and avoid sequestration of the healing process in “Cell Cycle Arrest” The advantages of early apoptosis allows not only for removal of damaged cells, but prevents the survival of potentially premalignant cells in burns and premalignant lesions in photo-damaged skin. The replacement of damaged cells by new healthy cells allows for more complete repair process than would otherwise occur. Cells activate distinct signaling pathways, in particular, the DNA damage response (DDR pathway, in response to various types of DNA damage, in particular to double stranded DNA breaks (DSBs). The recognition of these breaks is achieved by the multifunctional sensor complex, MRN [5] (MRE11-RAD50-NBS1) that consists of the structure-specific nuclease (MRE11; meiotic recombination 11 protein complex), the ATPase and adenylate kinase subunit (RAD50; radiation sensitive DNA repair protein 50), and the adaptor protein (NSB1; Nijmegan syndrome breakage 1). MRN complexes can bind to the exposed DNA ends directly and unwind the DNA ends in an ATP-dependent manner. One or the earliest events in DDR is the recruitment of the phosphatidylinositol 3-kinase-like kinase (PI-3KK), ATM kinase, by the MRN sensor complex [5-9]. This leads to the dissociation of the inactive dimer, and activation of ATM kinase, a key early enzyme in the DDR pathway. The presence of double stranded DNA breaks (DSB) following ultraviolet injury triggers the DNA damage response (DDR) signaling pathway (Figure 1), through activation of ATM kinase, resulting in nucleotide excision and repair (NER) through histone (H2A) ubiquitination [5,10]. ATM (ataxia telangiectasia mutated) kinase, a member of the phosphatidylinositol 3-kinase family, is responsible for phosphorylating H2AX at ser193 (γH2AX) in response to DSBs [10]. In chronic ultraviolet injury, the ultraviolet-induced replication stress activates ATR (ataxia telangiectasia rad 3 related) kinase, another member of the phosphatidylinositol 3-kinase family, resulting in the recruitment of ATR kinase by ATR-interacting protein to replication protein A (RPA)-coated single stranded DNA, which occurs at stalled replication forks [11]. Both ultraviolet damage and ultraviolet repIntroduction Ultraviolet light-induced DNA damage results in helix distorting DNA lesions predominantly consisting of cyclobutane pyrimidine dimers (CPDs) and 6-4-photoproducts (6-4PP) [1-4]. The damaged DNA segments are removed by nucleotide excision repair (NER) that eliminates large segments of helix distorting lesions in a multistep “cut and patch” type reaction [5]. The damaged DNA is excised as a 25-30 oligonucleotide DNA fragment followed by gap filling through DNA repair synthesis and restoration of an intact DNA duplex by a final ligation step. CASE REPORT

Curcumin-Induced Apoptosis in the Repair of Photodamaged Skin