Irradiation of skin with visible light induces reactive oxygen species and matrix-degrading enzymes

Daily skin exposure to solar radiation causes cells to produce reactive oxygen species (ROS), which are a primary factor in skin damage. Although the contribution of the UV component to skin damage has been established, few studies have examined the effects of non-UV solar radiation on skin physiology. Solar radiation comprises <10% of UV, and thus the purpose of this study was to examine the physiological response of skin to visible light (400-700 nm). Irradiation of human skin equivalents with visible light induced production of ROS, proinflammatory cytokines, and matrix metalloproteinase (MMP)-1 expression. Commercially available sunscreens were found to have minimal effects on reducing visible light-induced ROS, suggesting that UVA/UVB sunscreens do not protect the skin from visible light-induced responses. Using clinical models to assess the generation of free radicals from oxidative stress, higher levels of free radical activity were found after visible light exposure. Pretreatment with a photostable UVA/UVB sunscreen containing an antioxidant combination significantly reduced the production of ROS, cytokines, and MMP expression in vitro, and decreased oxidative stress in human subjects after visible light irradiation. Taken together, these findings suggest that other portions of the solar spectrum aside from UV, particularly visible light, may also contribute to signs of premature photoaging in skin.     

Synergistic effects of long‐wavelength ultraviolet A1 and visible light on pigmentation and erythema

Ultraviolet (UV) radiations from sunlight that reach the surface of the earth are categorized as UVB (wavelength range 280–320 nm) and UVA (320–400 nm). The UVA is further divided into UVA2 (320–340 nm) and UVA1 (340–400 nm). In the United States and other nations, rules have been set outlining how products that are designed to protect against UVB and UVA should be tested, and there are also strict rules about how these products can be labeled. The SPF (sun protection factor) mainly shows the level of protection against UVB only, and SPF along with “Broad Spectrum” on a label shows protection against both UVB and UVA. The criteria that decide whether or not manufacturers can claim a product gives broad spectrum protection, in the US, primarily focus on protection offered below 370 nm. Visible light (VL), which ranges from 400 nm to 700 nm, is a spectrum of wavelengths that are visible to the human eye. To date, only the UV part of sunlight, which is not visible light, has been considered to cause photodamage (damage caused by sunlight) resulting in skin cancers and photoaging (skin ageing due to the sun). The visible part of the sunlight was considered relatively harmless. This study, from the US, investigated skin responses, in terms of sunburn and tanning, caused by visible light in combination with the tail end of long wavelength UVA1 (referred to as VL+UVA1, 370–700 nm) and compared them to those caused by pure visible light (400–700 nm). The findings of the study show that skin responses, in terms of pigmentation (colouring/tanning) and erythema (redness/sunburn), resulting from VL+UVA1 were stronger than those induced by pure visible light alone. This implies that wavelengths that current broad spectrum sunscreens do not cover can affect pigmentation and erythema. These wavelengths may have a role in conditions aggravated by sun exposure such as melasma and post‐inflammatory hyperpigmentation, especially in patients with skin of color. The development of prodcts that protect against visible light and long wavelength UVA1 will be helpful for these, as well as for the management of certain skin disorders triggered by UVA1 and VL.     

Free radicals induced by sunlight in different spectral regions – in vivo versus ex vivo study

Sunlight represents an exogenous factor stimulating formation of free radicals which can induce cell damage. To assess the effect of the different spectral solar regions on the development of free radicals in skin, in vivo electron paramagnetic resonance (EPR) investigations with human volunteers and ex vivo studies on excised human and porcine skin were carried out. For all skin probes, the ultraviolet (UV) spectral region stimulates the most intensive radical formation, followed by the visible (VIS) and the near infrared (NIR) regions. A comparison between the different skin models shows that for UV light, the fastest and highest production of free radicals could be detected in vivo, followed by excised porcine and human skin. The same distribution pattern was found for the VIS/NIR spectral regions, whereby the differences in radical formation between in vivo and ex vivo were less pronounced. An analysis of lipid composition in vivo before and after exposure to UV light clearly showed modifications in several skin lipid components; a decrease of ceramide subclass [AP2] and an increase of ceramide subclass [NP2], sodium cholesterol sulphate and squalene (SQ) were detectable. In contrast, VIS/NIR irradiation led to an increase of ceramides [AP2] and SCS, and a decrease of SQ. These results, which are largely comparable for the different skin models investigated in vivo and ex vivo, indicate that radiation exposure in different spectral regions strongly influences radical production in skin and also results in changes in skin lipid composition, which is essential for barrier function.     

Atmospheric skin aging—Contributors and inhibitors

Cutaneous aging is a complex biological process consisting of 2 elements: intrinsic aging, which is primarily determined by genetics, and extrinsic aging, which is largely caused by atmospheric factors, such as exposure to sunlight and air pollution, and lifestyle choices, such as diet and smoking. The role of the solar spectrum, comprised of ultraviolet light, specifically UVB (290‐320 nm) and UVA (320‐400) in causing skin damage, including skin cancers, has been well documented. In recent years, the contribution of visible light (400‐700 nm) and infrared radiation (above 800 nm) in causing skin damage, similar to the photodamage caused by UV light, is also being elucidated. In addition, other atmospheric factors such as air pollution (smog, ozone, particulate matter, etc.) have been implicated in premature skin aging. The skin damage caused by environmental exposure is largely attributable to a complex cascade of reactions inside the skin initiated by the generation of reactive oxygen species (ROS), which causes oxidative damage to cellular components such as proteins, lipids, and nucleic acids. These damaged skin cells initiate inflammatory responses leading to the eventual damage manifested in chronically exposed skin. Novel therapeutic strategies to combat ROS species generation are being developed to prevent the skin damage caused by atmospheric factors. In addition to protecting skin from solar radiation using sunscreens, other approaches using topically applied ingredients, particularly antioxidants that penetrate the skin and protect the skin from within, have also been well documented. This review summarizes current knowledge of atmospheric aggressors, including UVA, UVB, visible light, infrared radiation (IR), and ozone on skin damage, and proposes new avenues for future research in the prevention and treatment of premature skin aging caused by such atmospheric factors. New therapeutic modalities currently being developed are also discussed.     

Do different ethnic groups need different sun protection?

Background: In the present study, the transmission of sunlight trough the human skin barrier into the living tissue was investigated in the spectral region between 280 and 700 nm.
Methods: The experiments were performed with a fiber-based spectrometer on sliced skin obtained from volunteers with different skin types. One fiber was positioned directly on the skin surface and the second one underneath the skin samples. The distribution of the sunlight under the epidermis was determined.
Results: Significant differences were found in the absorption properties of the different skin types, which were mainly determined by the variations in melanin concentration and distribution. It was found that sunscreens for specific ethnic groups need different combinations of UV filters, if a balanced relation between ultraviolet B (UVB) and ultraviolet A (UVA) protection is to be obtained. On the other hand, it could be demonstrated that the human skin is also well protected against visible and near-infrared light by melanin.
Conclusions: The higher the skin type category, the better the protection in the visible part of the spectrum of the sun. This stimulates the hot discussion at the present time, as to whether sunscreens should also contain protection compounds in the visible and near-infrared parts of the spectrum.     

Spectral characteristics of visible light‐induced pigmentation and visible light protection factor

Solar radiation is a major contributor to the development of skin cancer. Recent studies have shown that visible light (VL), a major portion of solar spectrum, induces biologic effects on the skin. Ultraviolet filters in currently available broad‐spectrum sunscreens do not offer protection against VL. This study was designed to identify the spectral characteristics of the skin responses induced by VL, which can be utilized for time efficient in vivo VL testing. Thirty‐one subjects were irradiated with a light source emitting visible light with less than 0.5% long wavelength UVA1 (VL + UVA1, 370‐700 nm), and 41 subjects were irradiated with pure visible light (pure VL, 400‐700 nm). Assessments including clinical photography, investigator's global assessment of pigmentation and erythema, and diffuse reflectance spectroscopy (DRS) performed immediately and seven days after irradiation. Clinical and spectroscopic data showed that VL + UVA1 spectral output induced significantly darker and persistent skin responses as compared to those induced by pure VL. Spectroscopic signatures of skin responses induced by both radiation sources were identified. The signatures were found to be specific to the radiation source and time of collection. A method to evaluate VL protection factor, using quantitative information from the spectral signatures obtained, was proposed.     

A clinical evaluation of the efficacy and tolerability of a novel topical antioxidant formulation featuring vitamin C,astaxanthin, and fermented turmeric

Background

Ultraviolet light, visible light, infrared light, and pollution are a few examples of environmental factors that exacerbate the formation of reactive oxygen species (ROS) that cause damage to skin cells' DNA, proteins, and lipids. By supplementing the skin with antioxidants, we can help neutralize ROS formed by these extrinsic factors before they can damage the skin.

Aims

This prospective open-label study explores the safety and efficacy of this novel topical formulation of antioxidants (vitamin C, astaxanthin, fermented turmeric, and vitamin E) designed to fight free radical damage and improve overall skin quality, as well as the appearance of fine lines, wrinkles, radiance, and hyperpigmentation of the skin.

Patients/Methods

This single-center clinical study evaluated the efficacy of twice-daily application of the test article (Asta C™ Vitamin C Age Defense Serum, Dr. Whitney Bowe Beauty) in 32 subjects for 12 weeks. Healthy female subjects aged 35–60 with mild to moderate fine lines, wrinkles, and hyperpigmentation/uneven skin tone were enrolled in this study. Fitzpatrick skin types I–VI, all skin types (dry, normal, combination, oily), and subjects with sensitive skin were included.

Results

All subjects demonstrated improvement in overall skin quality (face, neck, and chest) by the end of the 12-week study period. One hundred percent of subjects demonstrated improvement in the appearance of fine lines at Week 12.

Conclusions

Overall, the current clinical study demonstrates that Asta C™ is safe, well-tolerated, and effective in improving overall skin quality, as well as the appearance of fine lines, wrinkles, radiance, and hyperpigmentation of the skin.     

A case of porphyria cutanea tarda with experimental light urticaria

Photobiological tests were carried out on a 32-year-old man who suffered from porphyria cutanea tarda (PCT). The patient developed an immediate type of skin reaction with erythema and whealing following monochromatic irradiation at 400 nm, but did not have any abnormal immediate skin reaction after exposure to natural sunlight. Pre- or simultaneous irradiation with visible light, wavelength greater than 650 nm, suppressed the development of urticaria induced by 400 nm monochromatic radiation. On the basis of these findings and our previous observation of an inhibitory spectrum in two cases of solar urticaria, we suggest that there is also an inhibitory spectrum in PCT. This could explain the extremely low incidence of immediate erythematous or urticarial reactions in sun-exposed skin in these patients.     

Evaluation of carotenoids and reactive oxygen species in human skin after UV irradiation: a critical comparison between in vivo and ex vivo investigations

UV irradiation is one of the most harmful exogenous factors for the human skin. In addition to the development of erythema, free radicals, that is reactive oxygen species (ROS), are induced under its influence and promote the development of oxidative stress in the skin. Several techniques are available for determining the effect of UV irradiation. Resonance Raman spectroscopy (RRS) measures the reduction of the carotenoid concentration, while electron paramagnetic resonance (EPR) spectroscopy enables the analysis of the production of free radicals. Depending on the method, the skin parameters are analysed in vivo or ex vivo. This study provides a critical comparison between in vivo and ex vivo investigations on the ROS formation and carotenoid depletion caused by UV irradiation in human skin. The oxygen content of tissue was also determined. It was shown that the antioxidant status measured in the skin samples in vivo and ex vivo was different. The depletion in the carotenoid concentration in vivo exceeded the value determined ex vivo by a factor of about 1.5, and the radical formation after UV irradiation was significantly greater in vivo by a factor of 3.5 than that measured in excised human skin, which can be explained by the lack of oxygen ex vivo.     

Age-dependent generation of reactive oxygen species in the skin of live hairless rats exposed to UVA light

Aging proceeds by highly complicated biochemical processes, in which the involvement of the reactive oxygen species (ROS) and free radicals has been implicated. Although the relationship between UV-induced photoaging and ROS generation has been proposed, it has been difficult to establish direct proof of the generation of ROS in the skin under UV exposure. Recently, we reported finding endogenously generated ROS in the skin of live mice after UVA light exposure by a method of in vivo chemiluminescent detection, in which superoxide anion radical (*O2-) and singlet oxygen species (1O2) are contributed. In light of the results, we tried to understand the age-dependent changes in ROS generation in the skin of hairless rats under UVA exposure. Chemiluminescent levels due to ROS in the untreated and UVA-exposed skin decreased age dependently, and the signal intensities in old rats were significantly lower than those in young rats. However, the ratios of chemiluminescent intensities in the UVA-exposed skin to those in the untreated skin were significantly enhanced in an age-dependent manner. These results suggest that the antioxidative ability against ROS generation in the skin, possessed by antioxidant enzymes and low molecular weight antioxidants, is lowered age dependently.     

Involvement of active oxygen in lipid peroxide radical reaction of epidermal homogenate following ultraviolet light exposure.

To elucidate the radical mechanism of lipid peroxidation induced by ultraviolet light (UV) irradiation, an electron spin resonance (ESR) study was made on epidermal homogenate prepared from albino rat skin. The exposure of the homogenate to UV light resulted in an increase in lipid peroxide content, which was proportional to the time of UV exposure. Using ESR spin trapping (dimethyl-1-pyrroline-N-oxide, DMPO), the DMPO spin adduct spectrum of lipid radicals (L.) was measured following UV exposure (DMPO-L.:aN = 15.5 G, aH = 22.7 G), as was the spectrum of DMPO-hydroxyl radical (DMPO-OH, aN = aH = 15.5 G). In the presence of superoxide dismutase, the DMPO spin adduct spectrum of lipid radicals was found to be reduced remarkably. Therefore, it was shown that the generation of the lipid radicals partially involves superoxide anion radicals, in addition to hydroxyl radicals. In the ESR free-radical experiment, an ESR signal appeared at g = 2.0064 when the ESR tube filled with homogenate was exposed to UV light at -150 degrees C. The temperature-dependent change in the ESR free radical signal of homogenate exposed to UV light was observed at temperatures varying from -150 degrees C to room temperature. By using degassed samples, it was confirmed that oxygen is involved in the formation of the lipid peroxide radicals (LOO.) from the lipid radicals (L.).     

Infrared plus visible light and heat from natural sunlight participate in the expression of MMPs and type I procollagen as well as infiltration of inflammatory cell in human skin in vivo

BACKGROUND: Compared with the detailed characterization of the ultraviolet (UV) response in human skin, the effects of infrared (IR) and other regions of the sunlight are scarce. OBJECTIVES: To determine the participation of IR/visible light and heat components of the sunlight on matrix metalloproteinases (MMPs) and type I procollagen expression, and inflammatory cell infiltration in human skin in vivo. METHODS: The buttocks of 16 healthy volunteers (aged 24-43 years, 10 male and 6 female) were irradiated with a 1.1-3 minimal erythema dose (MED) of natural sunlight. To determine the differential effects of UV, IR/visible rays and solar heat alone, the exposed sites were covered with either a UV filter or black cloth, respectively, during irradiation. Skin samples were taken 24h later. RESULTS: IR/visible light spectrum of sunlight significantly increased MMP-1 and MMP-9 expression and decreased type I procollagen expression. Solar heat also contributed to the increased MMP-1 expression. Only the UV region recruited neutrophils into the dermis, while UV, IR/visible light and heat contributed to macrophage infiltration. CONCLUSIONS: IR/visible light and heat of natural sunlight, in addition to UV, play a role in modulating the expressions of MMPs and procollagen, and inflammatory cell infiltration in human skin.     

Evaluation of ex vivo melanogenic response to UVB,UVA, and visible light in facial melasma and unaffected adjacent skin

BackgroundThe independent role of solar radiation in the differential melanogenesis between melasma and adjacent skin is unknown.ObjectivesTo assess the melanogenic responses of skin with facial melasma and of the adjacent skin to UVB, UVA, and visible light, in an ex vivo model.MethodsThis was a quasi-experimental study involving 22 patients with melasma. Facial melasma and adjacent skin samples were collected and stored in DMEM medium, at room temperature. One fragment was placed under the protection from light, while another was exposed to UVB, UVA, and visible light (blue-violet component): 166 mJ/cm², 1.524 J/cm², and 40 J/cm², respectively. Subsequently, all samples were kept for 72 hours in a dark environment and stained by Fontana-Masson to assess basal layer pigmentation, dendrites, and melanin granulation.ResultsEffective melanogenesis was observed in the basal layer in melasma and in the normal adjacent skin after all irradiations (p < 0.01), with the following median increment: UVB (4.7% vs. 8.5%), UVA (9.5% vs. 9.9%), and visible light (6.8% vs. 11.7%), with no significant difference between anatomical sites. An increase in melanin granulation (coarser melanosomes) was observed only after irradiation with UVA and only in the skin with melasma (p = 0.05). An increase in the melanocyte dendrite count induced by UVB radiation was observed in both anatomical sites (p ≤ 0.05).Study limitationsUse of an ex vivo model, with independent irradiation regimes for UVB, UVA, and visible light.ConclusionsMelanogenesis induced by UVB, UVA, and visible light was observed both in melasma and in the adjacent skin. The morphological patterns suggest that different irradiations promote individualized responses on the skin with melasma.     

Visualizing nuclei in skin cryosections: viable options to 4'6-diamidino-2-phenylindol for confocal laser microscopy

Background: Visualization of nuclei in skin (cryo‐) sections is essential for both, rapid overview and reliable orientation within skin samples. Therefore, nuclear staining is a very common counterstain for immunohistochemical studies of human skin as this nuclear staining precisely depicts the cellular distribution within the epidermis. Moreover, it clearly shows the epidermal–dermal border as well as the transition zone between the living and the cornified layers of the epidermis. For standard epifluorescence microscopy, 4′6‐diamidino‐2‐phenylindol (DAPI) is commonly used. For confocal laser scanning microscopy (CLSM), however, DAPI is often not suitable because its excitation maximum is in the ultraviolet (UV) range (Ex_max 359 nm) when bound to DNA, and UV lasers and the corresponding optics are not part of CLSM standard configuration. Methods: In order to find an adequate DAPI substitute that is excitable with standard visible light lasers, the following nuclear stains were tested: LOLO^?‐1 iodide (Ex_max 565 nm), TOTO^®‐3 iodide (Ex_max 642 nm), LO‐PRO^?‐1 iodide (Ex_max 567 nm), SYTO^® 84 (Ex_max 567 nm), SYTO^® 85 (Ex_max 567 nm), SYTOX^® Green (Ex_max 488 nm) and SYTOX^® Orange (Ex_max 547 nm), Propidium iodide (Ex_max 535 nm). Besides optimal concentration and incubation time, following criteria were also evaluated: photobleaching, background, e.g. cytoplasmic staining of RNA, and sensitivity to different fixation conditions (unfixed, IEM fixation, PLP fixation and PFA fixation). Results: According to these criteria Sytox^® Green showed the best overall staining score and can be used for variously fixed skin samples and shows a distinct and stable green nuclear fluorescence.     

Inhibition of ultraviolet-induced formation of reactive oxygen species,lipid peroxidation,erythema and skin photosensitization by Polypodium leucotomos

González S, Pathak MA. Inhibition of ultraviolet-induced formation of reactive oxygen species, lipid peroxidation, erythema and skin photosensitization by Polypodium leucotomos. Photodermatol Photoimmunol Photomed 1996: 12: 45–56. © Munksgaard, 1996 The acute reactions of human skin to solar ultraviolet radiation (290–400 nm) are recognized as a form of inflammation reactions that are mediated by several possible mechanisms including (a) direct action of photons on DNA, (b) generation of reactive free radicals and reactive oxygen species involving the formation of O₂*?, ¹O₂, H₂O₂, *OH, etc., (c) generation of prostaglandins (PGD₂, PGE₂, etc.), histamine, leucotrienes, and other inflammatory mediators. It is conceivable that UV-induced reactions represent oxidative stress mediated by the formation of free radicals, reactive oxygen, lipid peroxidation, liberation of membrane phospholipids, and subsequent formation of prostaglandins by cyclo-oxygenase pathway. In this study, we examined the role of reactive oxygen species and lipid peroxidation in in vitro reactions as well as in vivo skin inflammation reactions induced by (a) UVB radiation (290–320 nm), and (b) skin photosensitization reaction by PUVA treatment involving 8-methoxypsoralen and UVA (320–400 nm) radiation and presented data for the generation of superoxide anion (O₂*-) and lipid peroxides. We have also evaluated, both in vitro as well as in vivo systems, the quenching or the inhibition of O₂*- by a plant extract known as Polypodium leucotomos. The P. leucotomos extract was found to exhibit interesting antioxidant and anti-inflammatory as well as photoprotective properties against photo-oxidative stress involving the generation of reactive oxygen, lipid peroxidation under in vitro reactions as well as in vivo experimental conditions. Significant inhibition of UVB-induced erythemal response, and 8-methoxypsoralen plus UVA-induced phototoxic reaction after topical application or oral administration of the photosensitizer could be demonstrated in guinea pig skin and human skin following the topical application of P. leucotomos extract. The photoprotective mechanism of P. leucotomos involving interaction with reactive oxygen species or free radicals appears to have potential clinical usefulness in preventing sunburn and inhibiting phototoxic reaction.     

In vivo oxygen radical generation in the skin of the protoporphyria model mouse with visible light exposure: an L-band ESR study

Although oxygen radicals are thought to play a key role in the skin injury that is caused by protoporphyria, there is no direct evidence of generation of these radicals in vivo. This study measured the generation of oxygen radicals caused by visible light non-invasively in the skin of griseofulvin-induced protoporphyria model mice, using an in vivo electron spin resonance spectrometer equipped with a surface-coil-type resonator that could detect radicals within about 0.5 mm of the skin surface. A durable nitroxyl radical was administered intravenously as a probe. Light irradiation enhanced the decay of the nitroxyl signal in griseofulvin-treated mice, whereas light irradiation did not enhance the signal decay in control mice. The enhanced signal decay was completely suppressed by intravenous administration of hydroxyl radical scavengers, superoxide dismutase or catalase, or the intraperitoneal administration of desferrioxamine. The enhanced signal decay with illumination was reversible, and quickly responded to turning the light on and off. These observations suggest that the hydroxyl radical is generated via an iron-catalyzed reaction in the skin. This paper demonstrates, for the first time, the specific generation of oxygen radicals in response to light irradiation of the skin of protoporphyria model mice.     

Visualization and characterization of UVB-induced reactive oxygen species in a human skin equivalent model

Reactive oxygen species (ROS) play important roles in the process of ultraviolet-induced skin damage or photoaging. Although many enzymatic and chemical methods have been developed for evaluating ROS, evaluation methods for ROS generation in living systems are quite limited. Here we propose a unique system to visualize UVB-induced ROS and investigate the biological impact of ROS. In brief, a human skin equivalent model (HSEM) was exposed to UVB. Emitted luminescence from the HSEM was visualized and semi-quantified by using a chemiluminescent probe (CLA) and an ultra low-light imaging apparatus. The effects of anti-oxidative compounds such as ascorbate, β-carotene, superoxide dismutase (SOD), and yeast ferment filtrate (YFF) on the HSEM were evaluated by semi-quantification of emitted chemiluminescence (CL) intensities, MTT assay and 8-hydroxy-2′-deoxyguanosine (8-OHdG) staining. Visualization of time- and space-dependent dynamics of ROS generation in the HSEM was successfully achieved by utilizing a sensitive two-dimensional ultra-low light luminograph. Treatments with β-carotene and SOD effectively suppressed CL intensity, indicating the generation of ¹O₂ and O₂ ^{· ?} in the HSEM under UVB exposure. Tested anti-oxidative compounds also attenuated UVB-induced CL and ameliorated the induced skin damages in terms of 8-OHdG formation and cell death. As a conclusion, this model is useful for not only visualizing the production of UVB-induced ROS in real-time but also evaluating the efficacy of topically applied anti-oxidative compounds to suppress ROS generation and attenuate sequential chemical and biological responses.     

Nine out of 10 sunbeds in England emit ultraviolet radiation levels that exceed current safety limits

Background Exposure to ultraviolet (UV) radiation from sunlight is recognized as the principal cause of skin cancer. Moreover, sunbeds have been classified as carcinogenic by the International Agency for Research on Cancer. Despite this, there is a shortage of objective data on UV exposure levels in sunbeds in England. Objectives We set out to measure UV emission levels in sunbeds at sites around England, and to compare these levels with both current standards and natural sunlight. Methods Between October 2010 and February 2011, UV spectra were measured on site from a total of 402 artificial tanning units in England. Measurement instrumentation was calibrated, traceable to the National Physical Laboratory. Compliance with the relevant British and European standard was determined, and a skin‐cancer weighting factor was used to compare the carcinogenic potential of sunbeds with that of sunlight. Results For compliance with the European standard, erythemal‐effective irradiance should not exceed 0·3 W m^?2. The values that we measured ranged between 0·10 and 1·32 W m^?2 with a mean of 0·56 ± 0·21 W m^?2. Only 10% of sunbeds surveyed were within the recommended limit. Application of the skin‐cancer weighting factor produced values that varied from 0·17 to 2·52 W m^?2 with a mean of 0·99 ± 0·41 W m^?2. The comparable value for Mediterranean noonday sun was 0·43 W m^?2. Conclusions Nine out of 10 sunbeds surveyed throughout England emitted levels of UV radiation that exceed the maximum levels contained within the European standard. Moreover, the skin cancer risk for comparable times of exposure was up to six times higher than that for Mediterranean sunlight. This situation is unacceptable and stricter control measures must be put in place.     

Role of oxidative stress and the antioxidant network in cutaneous carcinogenesis

Melanoma and nonmelanoma skin cancers are among the most prevalent cancers in the human population. Solar ultraviolet radiation is considered a major etiological factor but the relationship between dose, timing, and nature of exposure to tumor development is still unclear. Free radicals are generated by normal physiologic processes, including aerobic metabolism and inflammatory response, but may inflict cellular damage when generation is increased and antioxidant defense mechanisms are overwhelmed. Important findings supporting the free radical hypothesis in skin carcinogenesis are: (1) Reactive oxygen species (ROS) are generated in UVA- and UVB-irradiated skin in excessive doses, (2) the natural cutaneous antioxidant defense is impaired upon UV-exposure, (3) free radicals are involved in all steps of carcinogenesis, (4) supplementation with antioxidants can inhibit skin carcinogenesis, and (5) conditions that increase ROS generation enhance photocarcinogenesis. These findings provide a promising rationale for the development of powerful new antioxidant strategies in the prevention and therapy of skin cancer.     

Photodynamic therapy in dermatology

Photodynamic therapy (PDT) is a modern therapy modality, based upon the application of a photosensitizing agent like aminolevulinic acid, a physiological precursor of porphyrins, onto the tissue followed by illumination with light of the visible wavelength spectrum. During this oxygen‐dependent reaction, reactive oxygen species (ROS) are generated that have immunomodulatory or cytotoxic effects. PDT shows excellent cosmetic results especially for its key indication in dermatology – the treatment of non‐melanoma skin cancer. The associated pain and the low tissue penetration are the most frequent limiting factors of PDT. We review basic principles and recent developments in photosensitizers and light sources. Key oncological and non‐oncological indications are presented as well.