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PBL 3 – Jack and his Spots FQ – Effect of UV exposure on the Skin

PBL 3 – Jack and his Spots FQ – Effect of UV exposure on the Skin. Rick Allen. Skin interaction with UV. Chromophore – molecule with differing light absorbance capability Skin chromophores = DNA, urocanic acid, aromatic amino acids

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PBL 3 – Jack and his Spots FQ – Effect of UV exposure on the Skin

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  1. PBL 3 – Jack and his SpotsFQ – Effect of UV exposure on the Skin Rick Allen

  2. Skin interaction with UV • Chromophore – molecule with differing light absorbance capability • Skin chromophores = DNA, urocanic acid, aromatic amino acids • Chromophores take photon. Use energy to form new molecule (photoproduct), often covalent bonds w. neighbouring molecules. • Vit D production • Properties of UVR

  3. Molecular Level Damage • Absorbed energy to covalent bonds • CT or CCTT are UVB signature mutations • Not speedily fixed, stays as a lesion. • The four-membered ring ring is called a cyclobutanepyrimidinedimer (CPD) or (6-4)

  4. Macroscopic level damage • Sunburn • Inflammation signs based on exposure dose, not duration (few hours) • Afferent nerves release neuropeptidesitch, pain, inflammation, immunomodulation. • UVR causes melanocytes, keratinocytes and endothelial cells to release neutrophins and hormones  vasodilation, mast cell degranulation, and other cytokine release attracting inflam. mediators. • Mast cell products ~1hr, neutrophil and T cell at 3hrs w. max at 48hrs • Mitochondrial damage, keratinocyte and fibroblast enzymes  ROS  activation and death.

  5. Macroscopic Damage • Skin aging • ROS  cell surface receptor activation  AP-1 activation  ↓ collagen production. • UV  nuclear factor  MMP-1 (collagenase) • Neutrophils  MMP – 8 (collagenase) • Half dead collagen accumulates, ↓ integrity, ↓ elasticticity and inhibits new collagen.

  6. Immunosuppression • CPD are made within APC (Langerhan’s)  ↓ antigen- presenting capacity. Damage persists for days, unable to repair, migrate to lymph node. ROS may be involved. • UVB internalises some cell surface receptors • Membrane lipids oxidised  will bind to PAF receptors  cytokine synthesis (IL – 10) • UVB hits keratinocytes  IL-10 and TNF-α • IL-10 from Th2 suppresses Th1 cytokines, promotes Th2 activation over Th1 and causes Th1 anergy • This induces T suppressor cells which shut down activated T cells. NK T cells observed with reg. powers.

  7. Adaptive Responses • Hyperplasia of dermis and stratum corneum. • UVR triggered, protective • Antioxidant defences • Tanning • DNA photodamage/repair  melanogenesis • Tyrosinaseactivivty↑ w. UV exposure • UV damage ↑ cell surface receptors for keratinocyte-derived melanogenic factors • UVA  immediate skin darkening • UVB  ↑ activity and # of melanocytes • Melanocyte dendrites elongate and branch.

  8. References • http://www.accessmedicine.com/content.aspx?aID=2868631&searchStr=ultraviolet+rays#2868631 • http://www.accessmedicine.com/content.aspx?aID=2966157 • http://www.accessmedicine.com/content.aspx?aID=2987235

  9. Questions • Describe how DNA is damaged/mutated by UV rays. • Explain the mechanism behind photodamage resulting in premature aging.

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