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Oxidative Medicine and Cellular Longevity
Volume 2013 (2013), Article ID 285825, 11 pages
Review Article

Plasma Lipoproteins as Mediators of the Oxidative Stress Induced by UV Light in Human Skin: A Review of Biochemical and Biophysical Studies on Mechanisms of Apolipoprotein Alteration, Lipid Peroxidation, and Associated Skin Cell Responses

1Faculdade de Medicina de Lisboa, Hospital de Santa Maria, Clínica Dermatologica Universitaria, Avenida Professor Egas Moniz, 1699 Lisboa Codex, Portugal
2INSERM, U1088, UFR de Pharmacie, 3 rue des Louvels, 80036 Amiens, France
3CHU Amiens, Pôle Biologie, Pharmacie et Santé des Populations, Centre de Biologie Humaine, Laboratoire de Biochimie, Avenue René Laennec, Salouël, 80054 Amiens, France
4UFR de Médecine et de Pharmacie, Université de Picardie Jules Verne, 3 rue des Louvels, 80036 Amiens, France
5Radiation Laboratory, University of Notre Dame, Notre Dame, IN 46556, USA
6Département RDDM, Muséum National d'Histoire Naturelle, 43 rue Cuvier, 75231 Paris, France

Received 10 January 2013; Accepted 21 March 2013

Academic Editor: Kota V. Ramana

Copyright © 2013 Paulo Filipe et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


There are numerous studies concerning the effect of UVB light on skin cells but fewer on other skin components such as the interstitial fluid. This review highlights high-density lipoprotein (HDL) and low-density lipoprotein (LDL) as important targets of UVB in interstitial fluid. Tryptophan residues are the sole apolipoprotein residues absorbing solar UVB. The UVB-induced one-electron oxidation of Trp produces Trp and radicals which trigger lipid peroxidation. Immunoblots from buffered solutions or suction blister fluid reveal that propagation of photooxidative damage to other residues such as Tyr or disulfide bonds produces intra- and intermolecular bonds in apolipoproteins A-I, A-II, and B100. Partial repair of phenoxyl tyrosyl radicals (TyrO) by a-tocopherol is observed with LDL and HDL on millisecond or second time scales, whereas limited repair of a-tocopherol by carotenoids occurs in only HDL. More effective repair of Tyr and a-tocopherol is observed with the flavonoid, quercetin, bound to serum albumin, but quercetin is less potent than new synthetic polyphenols in inhibiting LDL lipid peroxidation or restoring a-tocopherol. The systemic consequences of HDL and LDL oxidation and the activation and/or inhibition of signalling pathways by oxidized LDL and their ability to enhance transcription factor DNA binding activity are also reviewed.