PL101 Vitamin D and Photoprotection
and/or necrotic cell death) and secondary effects (i.e., damage to PL101 the vasculature and inflammatory reaction ending in the systemic Vitamin D and photoprotection: progress to date immunity). In recent times, more and more efforts are addressed Katie Marie Dixon to recognize the better PS employing in cancer PDT. Rose Department of Anatomy and Histology, Bosch Institute, Bengal Acetate (RBAc), administrated for 60 minutes at 10-5M University of Sydney, Sydney, NSW, Australia 2 and activated with 1,6 J/cm green light, is a powerful PS. It is Vitamin D compounds are produced in the skin following able to initiate in HeLa cells several signaling processes leading exposure to ultraviolet radiation (UVR). We previously reported to rapid, independent, successive, long-lasting and time-related that vitamin D compounds protect against UVR-induced cell onset of apoptosis and autophagic cell death by signals death and DNA damage (cyclobutane pyrimidine dimers; CPD originating from or converging on almost all intracellular and 8-oxoguanine) in cultured human skin cells. We have further organelles, i.e. mitochondria, lysosomes, Golgi apparatus and evidence that these photoprotective effects are mediated by the ER, despite RBAc primary perinuclear localization. Particularly, non-genomic pathway for vitamin D. We used an in vivo model apoptosis occurs as early as 1h after PDT via activation of to investigate the photoprotective effects of topical 1,25- intrinsic pathway, followed by activation of extrinsic, caspase- dihydroxyvitamin D3 (1,25D) and low calcemic analogs 12-dependent and caspase-independent pathways. The clearance (including a non-genomic agonist) in Skh:hr-1 mice exposed to 3 of RBAc photokilled HeLa cells, in terms of recruitment, MED of UVR, showing significant reductions in apoptotic recognition and removal, is very efficient both in vitro and in sunburn cells (SBCs) and CPDs.
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