Photochemistry and photobiology of actinic erythema: defensive and reparative cutaneous mechanisms

Abstract

Sunlight is part of our everyday life and most people accept it as beneficial to our health. With the advance of our knowledge in cutaneous photochemistry, photobiology and photomedicine over the past four decades, the terrestrial solar radiation has become a concern of dermatologists and is considered to be a major damaging environmental factor for our skin. Most photobiological effects (e.g., sunburn, suntanning, local and systemic immunosuppression, photoaging or dermatoheliosis, skin cancer and precancer, etc.) are attributed to ultraviolet radiation (UVR) and more particularly to UVB radiation (290-320 nm). UVA radiation (320-400 nm) also plays an important role in the induction of erythema by the photosensitized generation of reactive oxygen species (singlet oxygen OH)) that damage DNA and cellular membranes, and promote carcinogenesis and the changes associated with photoaging. Therefore, research efforts have been directed at a better photochemical and photobiological understanding of the so-called sunburn reaction, actinic or solar erythema. To survive the insults of actinic damage, the skin appears to have different intrinsic defensive mechanisms, among which antioxidants (enzymatic and non-enzymatic systems) play a pivotal role. In this paper, we will review the basic aspects of the action of UVR on the skin: a) photochemical reactions resulting from photon absorption by endogenous chromophores; b) the lipid peroxidation phenomenon, and c) intrinsic defensive cutaneous mechanisms (antioxidant systems). The last section will cover the inflammatory response including mediator release after cutaneous UVR exposure and adhesion molecule expression.Correspondence

Activation of p70 Ribosomal Protein S6 Kinase Is an Essential Step in the DNA Damage-dependent Signaling Pathway Responsible for the Ultraviolet B-mediated Increase in Interstitial Collagenase (MMP-1) and Stromelysin-1 (MMP-3) Protein Levels in Human Dermal Fibroblasts

“…Apart from independent evidence that interstitial collagenase (MMP-1) and stromelysin-1 (MMP-3) play a major role in multistage processes of carcinogenesis and cutaneous photoaging (16,21,24,(65)(66)(67) and that UVB-mediated DNA damage is an essential prerequisite for the development of skin cancer (67,68) and premature aging (67,69), pyrimidine dimers in transcriptionally active DNA have previously been shown to transduce signals, finally resulting in transactivation of UV-responsive genes like interstitial collagenase (29,30). However, little is known about DNA damage-dependent signaling components being activated upstream from these genes of interest.…”

The antioxidant action of Polypodium leucotomos extract and kojic acid: reactions with reactive oxygen species

“…), but many others need to be added exogenously to the system. The energy of the triplet excited state for the sensitizers is then transferred to an adjacent triplet oxygen molecule, transforming molecular oxygen to the singlet oxygen (1).…”

“…, hydroxyl radical · OH, singlet oxygen 1 O 2 , and hydrogen peroxide H 2 O 2 ) have been considered to be important agents of aging and various human diseases (1,2), such as cancer, heart diseases, multiple sclerosis, Parkinson's disease, autoimmune disease, stroke, and others. Among the various radicals, the hydroxyl radical is presumed to play a central role due to its strong activity (3).…”

Ultraviolet Action Spectrum and Effect of EPC-K1 on Ultraviolet Radiation-induced Injury in Cultured Normal Human Epidermal Keratinocytes

“…UV radiation-induced cell injury results from DNA damage and/or photochemicalinduced oxidative stress 25,26 . Various chromophores contained in human skin could act as endogenous UV sensitizers of photo-oxidative stress 7,27 , by generating ROS that damage DNA and cellular membranes, and promote carcinogenesis [4][5][6][7]28 . UV energy is absorbed by sensitizers following initial formation of an excited state and their subsequent interaction with substrate molecules type I photochemical reaction or molecular oxygen type II photochemical reaction by energy and/or electron transfer 29 ; both resulting in ROS production.…”