Brianna Scacchi, Brian Costello, Joseph Ceccoli and Paul Lawrence, Ph.D. | Biocogent, LLC
Skin aging can be accelerated by a variety of extrinsic factors including physical damage from the external environment. As is well-known, one of the major assaults on skin is promulgated by ultraviolet (UV) radiation emanating from the sun. UV light is a non-ionizing form of radiation that can be divided into three types based on their respective wavelength ranges: UV-A, UV-B and UV-C.
Each type inflicts damage to a varying degree on the DNA genetic code in the nuclei of skin cells—presenting in the form of mutations known as thymidine dimers or cyclopyrimidine dimers (CPDs) and 6,4-photoproducts (6,4-PPs). The cumulative damage incurred from this radiation is the driving force behind the phenomenon known as photoaging.
Skin cells are equipped with pathways to repair DNA damage. One such pathway, the nucleotide excision repair pathway (NER), targets the genomic damage incurred from exposure to UV light. This pathway is primarily responsible for the careful removal of so-called bulky adducts, CPDs and 6,4-PPs, which impede the progression of DNA replication and messenger ribonucleic acid (mRNA) transcription complexes along the DNA double helix.
The repair process follows four successive steps: 1) recognition of the genetic damage, usually by the presence of stalled transcription complex; 2) incision into the particular DNA strand possessing the damaged nucleotides; 3) the removal of the damaged portion of DNA; and 4) final repair by the synthesis of new DNA and its ligation into the strand to replace the excised portion. This repair mechanism has the capacity to replace oligonucleotide lengths of approximately 20-30 nucleotides.
In relation, the capability of a unique class of polyphenolic molecules known as phlorotannins (1,3,5-trihydroxybenzene) to resist and repair UV-induced DNA damage has been identified in brown algae. These polymers of the compound phloroglucinol are exclusive to marine seaweeds and have reported photoprotective effects, as they absorb UV light. Many species of brown algae have been explored and show a demonstrable correlation between phlorotannin content and the suppression of DNA damage.
Furthermore, there is evidence from other phlorotannin-containing brown algae species that UV exposure induces the cellular production of phlorotannin molecules. These compounds are usually found distributed along the periphery of cells, particularly concentrated in the cell wall, which suggests their presence may be offsetting the UV light irradiation these seaweeds experience from sunlight and its reflection off the water surface.
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