Photochemistry and photobiology of actinic erythema: defensive and reparative cutaneous mechanisms
A.C. Tedesco1, L. Martínez2 and S. González2
1Departamento de Química, Faculdade de Filosofia, Ciências e Letras, Universidade de São Paulo, 14040-901 Ribeirão Preto, SP, Brasil
2Wellman Laboratories of Photomedicine, Department of Dermatology, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA
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 (1O2), superoxide (O2.-) and hydroxyl radicals (.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.
Key words: sunburn, antioxidant, DNA photodamage, reactive oxygen species, UV radiation
Braz J Med Biol Res, May 1997, Volume 30(5) 561-575. Open Access.
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The sun emits electromagnetic radiation over a wide range of wavelengths that include the ultraviolet (200-400 nm), visible (400-760 nm) and the near- and far-infrared regions (>800 nm) (1). The damage to the ozone layer, an effective barrier against the penetration of ultraviolet radiation to the earth, has had a tremendous impact on interest in the study of the potentially damaging effects of UV light on different organisms, man among them (2,3). Single or multiple exposures to solar radiation without appropriate protection can produce a variety of unwanted effects that are of interest to the physician, especially the dermatologist. These effects are the result of acute and chronic photobiological responses that are in turn a consequence of photochemical reactions such as those listed in Table 1 (4,5).
The basic cutaneous response resulting from exposure to solar radiation is the actinic erythema or "sunburn" which appears 3 to 4 h after exposure and can last 5 to 6 days depending on the intensity (6). Other signs and symptoms include skin sensitivity to touch, as well as edema, discomfort and pain. Delayed pigmentation or tanning begins after the second or third day and, finally, after a period of 6 to 10 days peeling can occur (7,8).
The photobiological effects of ultraviolet radiation show that the UVB components (290-320 nm) in particular are erythematogenic and carcinogenic, and induce photoaging and direct damage to DNA, RNA, proteins and other cell constituents. Nonetheless, UVA radiation (320-400 nm) also plays an important role in the induction of erythema by the photosensitized generation of reactive oxygen species (ROS), such as singlet oxygen (1O2) or the superoxide (O2. -) and hydroxyl radicals (.OH) that damage DNA and cell membranes, and promote carcinogenesis and the changes associated with photoaging (9). Therefore, both the UVA and UVB components trigger this acute inflammatory response which appears in the form of erythema.
The characteristics associated with the erythema induced by exposure to radiation under laboratory conditions depend on both the intensity and dose of the wavelength used (10-12). UVC (200-290 nm)-induced erythema is the least intense and disappears after a couple of hours, but the erythema induced by UVB and UVA radiation can persist for days since these components penetrate deeper into the skin (13-15). It should be emphasized that even though UVB radiation is more erythematogenic than UVA (the minimal dose required at 297 nm for the erythema response is 1250 times higher than at 365 nm) (16,17) more photons in the UVA region reach the earth's surface (10-100-fold higher for UVA than UVB). Table 2 lists the major reactions induced by the different wavelength ranges of solar radiation.
The histological changes occurring in the skin after exposure also depend on the wavelength of the radiation. These changes may be preceded by the appearance of diskeratotic cells and a reduction in the number of Langerhans cells in the case of UVB exposure (González S, Malallah YH and Johnson B, unpublished data). For UVA radiation, the histopathological changes are fundamentally restricted to the dermis and depend largely on the presence of photosensitizers (Table 3). However, recent studies by Lavker et al. (18) in humans have shown that chronic exposure to UV radiation at sub-erythematogenic doses may also induce the appearance of diskeratotic cells and a reduction in the number of Langerhans cells.
In this review we will focus on erythema as an inflammatory response after exposure to ultraviolet radiation, when the absorption of photons by chromophores in the skin promotes a series of photochemical reactions responsible for this response. First, we will discuss the nature of these reactions, i.e., the production of free radicals and ROS. Several processes will be described, such as lipid peroxidation and its possible role as an initiating mechanism in the photoinduced damage. Also, the antioxidant systems present in the organism as means of protection will be discussed. Finally, we will discuss the biochemical alterations describing the different mediators implicated such as products of arachidonic acid, histamine, cytokines and neuropeptides. These mediators released by keratinocytes and other cutaneous cells, along with the expression of adhesion molecules on their surface, are of fundamental importance for leukocyte adhesion and the onset of the inflammatory response.
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