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UVA
Terms modified by UVA Selected AbstractsPositive photocontact responses are not elicited to sunscreen ingredients exposed to UVA prior to application onto the skinCONTACT DERMATITIS, Issue 4 2007Shyamal Wahie Photocontact allergic reactions to sunscreen chemicals are investigated by photopatch testing. It has generally been assumed that for photocontact allergy to be shown, the putative pro-allergen must be in the skin at the time of ultraviolet A (UVA) exposure. However, this assumption has not, to our knowledge, been tested. The objective of this study was to determine whether positive photocontact responses can still be elicited when sunscreen chemicals are exposed to UVA prior to application onto the skin. 3 patients known to have positive photocontact reactions to a total of 6 sunscreen chemicals were studied. For conventional photopatch testing, patch test strips were applied onto the back and removed 1 D later, and the area was irradiated with UVA (5 J/cm2). For pre-irradiated testing, patches were exposed to the same dose of UVA immediately before application onto the back and then removed 1 D later. Skin responses were visually assessed by a blinded investigator 1 and 2 D after patch test removal. The same photocontact responses of the same magnitude, as previously documented for each patient, were seen at each of the conventional UVA-exposed patch test sites. However, in no patient was a positive response elicited at any of the sites where pre-irradiated patches had been applied. This study shows that positive photocontact responses to sunscreen chemicals do not occur when the putative pro-allergen is irradiated prior to application onto the skin. This suggests that for a photoallergic reaction to occur, the sunscreen chemical needs to be within the skin when activated by UVA. [source] Water soluble fraction of solar-simulated light-exposed crude oil generates phosphorylation of histone H2AX in human skin cells under UVA exposureENVIRONMENTAL AND MOLECULAR MUTAGENESIS, Issue 6 2007Yuko Ibuki Abstract Crude oil contains compounds, which have toxic and cancer-causing properties to humans. The oil spilled in environments is usually exposed to sunlight; however, the toxicity of sunlight-exposed oil is poorly understood. In this study, we found that the water soluble fraction (WSF) of crude oil irradiated with solar-simulated light (SSL) generated phosphorylation of histone H2AX (,-H2AX) in human skin cells under UVA irradiation, which was due to the formation of DNA double strand breaks (DSBs). Crude oil was exposed to SSL for ,7 days. The WSF obtained from unexposed crude oil showed no toxicity, whereas the WSF obtained from crude oil pre-exposed to SSL induced acute cell death on exposure to UVA irradiation (induction of phototoxicity), which was more remarkable in human skin fibroblasts than human skin keratinocytes. ,-H2AX was detected in both cell lines immediately after treatment with the WSF plus UVA. Interestingly, ,-H2AX was detectable even at low SSL- and UVA-doses, which induced no cytotoxicity. The WSF of crude oil irradiated with SSL, generated DSBs under UVA irradiation, which were detected by biased sinusoidal field gel electrophoresis. This was confirmed using xrs-5 cells isolated from CHO-K1 cells, which are deficient in a repair enzyme for DSBs; the WSF plus UVA induced a more dramatic decrease in survival in xrs-5 cells than CHO-K1 cells. These findings demonstrate that exposure of crude oil to sunlight makes the WSF phototoxic, generating DSBs accompanying the appearance of ,-H2AX in human skin cells. Environ. Mol. Mutagen., 2007. © 2007 Wiley-Liss, Inc. [source] Photocatalytic oxidation of methanol using silica-titania composites in a packed-bed reactorENVIRONMENTAL PROGRESS & SUSTAINABLE ENERGY, Issue 4 2006Jennifer M. Stokke Abstract The processing of forest products into pulp, paper, paperboard, and other wood products results in the generation of volatile organic compounds (VOCs) and hazardous air pollutants (HAPs). This work focused on the development of a photocatalytic packed-bed reactor for the oxidation of methanol, which is the primary constituent in high volume low concentration gases emitted from pulp and paper mills. Bench-scale studies using an annular reactor packed with silica-titania composite (STC) pellets were conducted to maximize methanol removal and minimize the formation of byproducts, such as formaldehyde. Parameters such as STC pore size (ca. 40, 120, and 260 Å) and UV wavelength (UVA and UVC) were varied. In the dark, the STC pellets removed methanol via adsorption and had a finite adsorption capacity dependent on the surface area of the composite. When irradiated with UV light, the STC pellets adsorbed and oxidized methanol simultaneously. At the bench-scale, 40 Å STC pellets irradiated with UVC light achieved the greatest methanol removal (ca. 90%) with minimal byproduct formation (i.e., effluent formaldehyde concentration was <1 ppmv). Based on these results, a 40 acfm pilot reactor was fabricated and achieved methanol removal rates up to 66% ± 7% with <1 ppmv formaldehyde production at steady state. © 2006 American Institute of Chemical Engineers Environ Prog, 2006 [source] Synthesis of para -Amino Benzoic Acid,TiO2 Hybrid Nanostructures of Controlled Functionality by an Aqueous One-Step ProcessEUROPEAN JOURNAL OF INORGANIC CHEMISTRY, Issue 6 2008Raed Rahal Abstract In situ amino acid surface-modified TiO2 nanoparticle syntheses were performed by a simple one-pot hydrolysis of heteroleptic titanium alkoxide [Ti(OiPr)3(O2CC6H4NH2)]m in water with NnBu4Br. This process allowed precise control of the surface grafting rate by varying the amount of precursors and provided highly functionalized nanomaterials. Their compositions and microstructures were determined by C, H and N elemental analyses, TGA-MS, 13C CP-MAS NMR, XRD, TEM, BET, Raleigh diffusion, FTIR, Raman, XPS and UV/Vis experiments. The results indicated that (i) the aggregation rate increased with an increase in the loading of the organic substrate and (ii) the amino acid is chemisorbed as a carboxylate group onto the TiO2 nanoparticles, which leads to a strong interaction between the amino acid and the TiO2 nanoparticle and good stability of these hybrids. Applications of low-aggregated nanomaterials were demonstrated as efficient protection additive against UVA + UVB radiations.(© Wiley-VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2008) [source] The role of ultraviolet radiation in melanomagenesisEXPERIMENTAL DERMATOLOGY, Issue 2 2010Anna-Katharina Von Thaler Please cite this paper as: The role of ultraviolet radiation in melanomagenesis. Experimental Dermatology 2010; 19: 81,88. Abstract:, The role of ultraviolet radiation (UV) in the pathogenesis has been discussed controversially for many decades. Studies in mice (SCID, HGF/SF, SV40T) which develop malignant melanoma, show a role of UVB in melanomagenesis. In contrast to this, the role of UVA is less clear. We will review the recent in vitro and in vivo data in support of the hypothesis that UVA is also involved in the development of malignant melanoma. The role of UVA in p53 activation, apoptosis, cell cycle arrest and photoproduct formation is discussed. [source] Specific transcriptional responses induced by 8-methoxypsoralen and UVA in yeastFEMS YEAST RESEARCH, Issue 6 2007Michèle Dardalhon Abstract Treatment of eukaryotic cells with 8-methoxypsoralen plus UVA irradiation (8-MOP/UVA) induces pyrimidine monoadducts and interstrand crosslinks and initiates a cascade of events leading to cytotoxic, mutagenic and carcinogenic responses. Transcriptional activation plays an important part in these responses. Our previous study in Saccharomyces cerevisiae showed that the repair of these lesions involves the transient formation of DNA double-strand breaks and the enhanced expression of landmark DNA damage response genes such as RAD51, RNR2 and DUN1, as well as the Mec1/Rad53 kinase signaling cascade. We have now used DNA microarrays to examine genome-wide transcriptional changes produced after induction of 8-MOP/UVA photolesions. We found that 128 genes were strongly induced and 29 genes strongly repressed. Modifications in gene expression concern numerous biological processes. Compared to other genotoxic treatments, c. 42% of the response genes were specific to 8-MOP/UVA treatment. In addition to common DNA damage response genes and genes induced by environmental stresses, a large fraction of 8-MOP/UVA response genes correspond to membrane-related functions. [source] Modulation of the bacterial response to spectral solar radiation by algae and limiting nutrientsFRESHWATER BIOLOGY, Issue 11 2002J. M. Medina-Sánchez SUMMARY 1. The response of bacterial production (measured as [3H]TdR incorporation rate) to spectral solar radiation was quantified experimentally in an oligotrophic high-mountain lake over 2 years. Bacterial responses were consistent: ultraviolet-B (UVB) was harmful, whereas ultraviolet-A (UVA) + photosynthetically active radiation (PAR) and PAR enhanced bacterial activity. Full sunlight exerted a net stimulatory effect on bacterial activity in mid-summer but a net inhibitory effect towards the end of the ice-free period. 2. Experiments were undertaken to examine whether the bacterial response pattern depended on the presence of algae and/or was modulated by the availability of a limiting inorganic nutrient (phosphorus, P). In the absence of algae, [3H]TdR incorporation rates were significantly lower than when algae were present under all light treatments, and the consistent bacterial response was lost. This suggests that the bacterial response to spectral solar radiation depends on fresh-C released from algae, which determines the net stimulatory outcome of damage and repair in mid-summer. 3. In the absence of algae, UVB radiation inhibited bacteria when they were strongly P-deficient (mean values of N : P ratio: 46.1), whereas it exerted no direct effect on bacterial activity when they were not P-limited. 4. P-enrichment of lake water markedly altered the response of bacteria to spectral solar radiation at the end of ice-free period, when bacteria were strongly P-deficient. Phosphorus enrichment suppressed the inhibitory effect of full sunlight that was observed in October, both in whole lake water (i.e. including algae) and in the absence of algae. This indicates that the bacterial P-deficiency, measured as the cellular N : P ratio, was partly responsible for the net inhibitory effect of full sunlight, implying a high bacterial vulnerability to UVB. [source] Fading of artificial hair colour and its prevention by photofiltersINTERNATIONAL JOURNAL OF COSMETIC SCIENCE, Issue 3 2006B. Locke Fading of artificial hair colour has been investigated by simulating actual usage conditions through exposure to artificial radiation in a weatherometer, with 0.35 mW (m2nm),1 at 340 nm, for 16,48 h, and by periodical washing. Hair colour was produced by using commercial two-part, permanent hair dyes with light auburn, medium auburn and dark auburn shades. Formulations based on red couplers, such as 4-amino-2-hydroxytoluene and 1-naphthol, as well as primary intermediates, such as 1-hydroxyethyl-4,5-diamino pyrazole sulphate, were employed. Results indicate that the extent of fading, as measured by the total colour change parameter, dE, is greatest for coloured hair subjected to both irradiation and shampooing, and significantly smaller for hair undergoing only irradiation or washing. Colour loss has been also found to be dependent upon the hair type employed, with coloured natural white and bleached hair undergoing much greater change than coloured brown hair. It has been also shown that hair colour based on pyrazole intermediates displayed the deepest fading as a result of shampooing (dE 4,6 after 10 shampooings) and irradiation per shampooing (dE 14,16 after 32 h of light exposure and four shampooings). The contribution of UV light (UVB + UVA) to the artificial hair-colour loss was found experimentally to be dependent upon the irradiation dose and varied from 63% at 16 h of irradiation time to 27% at 48 h of light exposure. The theoretical extent of photoprotection by a formulation was assessed by calculating the percentage of UV light it attenuates in the wavelength range from 290 to 400 nm. The results indicate that UVB photofilters, such as octyl methoxy cinnamate, absorb <25% of the total UV irradiation at concentrations as high as 30 mg (g hair),1. UVA absorbers were found to be more effective, with benzophenone-3 and benzophenone-4 absorbing about 40% of UV at the same concentration. Corresponding experimental data were in reasonable agreement with the theoretical predictions. The data are also presented for colour protection with treatments containing two photo-absorbers: benzophenone-3,ZnO; benzophenone-4,ZnO; octyl methoxy cinnamate,ZnO; and dimethylpabaimidopropyl laurdimonium tosylate-benzophenone-3. [source] Relationship between UVA protection and skin response to UV light: proposal for labelling UVA protectionINTERNATIONAL JOURNAL OF COSMETIC SCIENCE, Issue 4 2004M. Jean-Louis Refrégier Synopsis Definition and validation of a most relevant method to assess ultravoilet A (UVA) protection is a major concern for industry, authorities and consumers. However, due to the lack of knowledge about all the biological phenomena involved, the level of UVA protection needed, the ways to assess and label it, remain controversial. In order to overcome this situation, the paper deals with the outcomes of a mathematical model to calculate the distribution between ultravoilet B (UVB) and UVA components of skin responses to UV light. Mathematical calculations of UVB and UVA erythemal components of skin response to sunlight are developed from the well-known determination procedure to calculate the sunburn protection factor (SPF) of sunscreens. The model establishes the relationship between the UVA component of skin erythemal response to overall UV radiation received from sunlight and the ratio SPF/PFAe (erythemal protection factor) where SPF is the product and PFAe is related to the UVA part of the sunlight. Depending on the efficacy profile of sunscreens, the skin erythemal response may be mainly promoted by UVB rays as it normally occurs in unprotected skin or on contrary by UVA rays. Therefore, the efficacy profile of sunscreens defines the deepness where biological events induced by sunlight take place. This new relationship pinpoints the tremendous importance of the protection afforded by sunscreen products in the UVA range when erythema is taken as biological response. By extrapolation of the model to any other biological skin response it becomes possible to predict how to improve the efficiency of sunscreen products in the future. UVA protection afforded by sunscreens should be improved until reaching the same level as the SPF protection factor so that all UV-induced biological responses could be prevented or lowered at the same extend. To enforce this improvement, a proposal to classify sunscreen products in relation with their UVA protection is made. Résumé Bien que les méfaits du rayonnement UVA soient à présent reconnus et l'importance de s'en protéger au même titre que ceux du rayonnement UVB totalement admise, l'obtention d'un consensus au niveau international, sur les méthodes pour mesurer l'efficacité des produits solaires vis-à-vis des UVA et sur les niveaux d'efficacité souhaitables, semble impossible à atteindre. Afin de tenter de surmonter les obstacles actuels, nous présentons un modèle mathématique qui permet d'établir la relation qui dèfinit le poids relatif des rayonnements UVB et UVA dans l'initiation des phénomènes biologiques engendrés par le rayonnement solaire, en fonction des caractéristiques du produit solaire utilisé et en particulier de son efficacité protectrice vis-à-vis des UVA. Dans le cas de l'érythème nous établissons ainsi que la proportion des effets engendrés par le rayonnement UVA est définie par le rapport SPF/PFAe: le SPF étant le facteur de protection contre l'érythème vis-à-vis de l,ensemble du rayonnement UV, c'est l'indice de protection affiché sur les produits; et, PFAe étant le facteur de protection du produit vis-à-vis du seul rayonnement UVA. L'extrapolation possible de ce modèle à l'ensemble des phénomènes biologiques met en évidence que le facteur de proportionnalité entre la protection globale et celle apportée vis-à-vis des UVA (SPF/PFAe) permet d'établir une classification de la qualité des systèmes filtrants en fonction de leur aptitude à prèvenir l'ensemble des méfaits du rayonnement solaire. Ce modèle démontre l'importance d'évaluer l,efficacité protectrice des produits solaires vis-à-vis du rayonnement UVA et son enseignement plus pertinent que celle de seulement évaluer l'allure des spectres d'absorption. Nous jugeons que l'application directe de ce modèle, au même titre que les méthodes d'évaluation de l,allure des spectres d'absorption, n'est aujourd'hui pas souhaitable en raison des connaissances et donc de la validation insuffisantes des méthodes in vitro en particulier pour évaluer les produits non parfaitement photostables. En conséquence, nous proposons de mettre en place une qualification qui repose sur l'évaluation de la protection UVA par les mèthodes in vivo dûment étudiées et validées telles que les méthodes PPD ou PFA. La mise en place du système proposé de qualification des produits solaires, permettrait d'apporter rapidement aux consommateurs une meilleure information sur la qualité des produits et permettrait de créer une dynamique d'amélioration de la qualité de l'ensemble des produits commercialisés. [source] In vitro testing to assess the UVA protection performance of sun care productsINTERNATIONAL JOURNAL OF COSMETIC SCIENCE, Issue 1 2001Applied Cosmetics) Task Force, Members of the DGK (German Society for Scientific, Sun Protection'. Synopsis The UVA protection delivered by sunscreens is an issue of increasing importance due to the increasing knowledge about UVA-induced skin damage. In Europe there is no officially accepted method available to determine the degree of UVA protection. Therefore, the objective of the present study was to design a protocol combining the merits of an in vitro model, which are simple and reproducible, with aspects known to be relevant from in vivo studies. The principle is: an UV-transparent support to which the test product is applied, a (pre)irradiation and a transmission measurement. Transpore® tape (standard support for SPF determinations) was found to be incompatible with many preparations on prolonged contact times. Roughened quartz was adopted as a suitable alternative. Transmission measurements on this support are not reliable with a layer of 2 mg cm,2 (standard for SPF) due to detection limitations of spectrophotometers, hence a reduced layer of 0.75 mg cm,2 was adopted. Overall, it is very difficult to apply products in a reproducible thin layer on appropriate substrates. As a consequence, absolute parameters derived from the transmission profile show relatively large dispersion, whereas relative parameters, such as critical wavelength ,c[1] or UVA/UVB ratio are much less sensitive to unavoidable variations in layer thickness. An increase in deviations was observed when the samples were irradiated before measurement. It is crucial to control the output carefully (spectral distribution and even more importantly, irradiance and dose delivered) of the light source. By doing so and also taking into account the previous learning steps, a protocol was drafted and tested in a ringtest (four samples in six laboratories). The results are encouraging and show that if relative parameters (e.g. ,c, UVA/UVB ratio) are considered, the intra- as well as interlaboratory reproducibility is clearly better than can be obtained in vivo. In general, we describe a suitable method, which can be considered in any future official discussions about the methodology to determine UVA protection. Résumé La protection contre les UVA apportée par les écrans solaires est un sujet d'importance croissante en raison de la progression des connaissances concernant les dommages à la peau causés par les UVA. En Europe il n'existe pas de méthode disponible officiellement reconnue pour déterminer le degré de protection contre les UVA. Par conséquent, l'objectif de la présente étude est de concevoir un protocole associant les avantages d'un modèle in vitro, qui est simple et reproductible, avec des aspects connus comme appartenant aux études in vivo. Le principe est le suivant: un support transparent aux UV auquel le produit testé est appliqué, une (pré)irradiation et une mesure de transmission. Le ruban Transpore® (support standard pour la détermination des SPF) se révèle incompatible avec de nombreuses préparations lors de temps de contact prolongés. Le quartz rugueux est adopté comme alternative appropriée. Les mesures de transmission sur ce support ne sont pas fiables avec une couche de 2 mg/cm2 (norme pour les SPF) en raison des limites de détection des spectrophotomètres, et on adopte donc une couche réduite de 0,75 mg/cm2. Il est surtout très difficile d'appliquer des produits en une couche fine reproductible sur des substrats appropriés. En conséquence, les paramètres absolus tirés du profil de transmission montrent une assez grande dispersion, tandis que les paramètres relatifs, tels que la longueur d'onde critique ,c[l] ou le rapport UVA/UVB sont beaucoup moins sensibles aux variations inévitables de l'épaisseur de la couche. On observe une augmentation des écarts lorsque les échantillons sont irradiés avant la mesure. Il est crucial de contrôler soigneusement la sortie (distribution spectrale et encore plus important, irradiation et dose délivrée) de la source lumineuse. Dans ces conditions, et en tenant aussi compte des enseignements des étapes précédentes, un protocole a étéébauché et testé lors d'un essai tournant (quatre échantillons dans six laboratoires). Les résultats sont encourageants et montrent que si on considère les paramètres relatifs (par exemple ,c, rapport UVA/UVB), la reproductibilité intra et interlaboratoires est clairement meilleures que ce qu'on peut obtenir in vivo. D'une façon générale, nous décrivons une méthode appropriée, qui peut être considérée dans tout échange officiel futur concernant la méthodologie pour déterminer la protection contre les UVA. [source] UVB phototherapy and skin cancer risk: a review of the literatureINTERNATIONAL JOURNAL OF DERMATOLOGY, Issue 5 2005Ernest Lee MD Background, UVB phototherapy is a common treatment modality for psoriasis and other skin diseases. Although UVB has been in use for many decades, many clinicians are hesitant to use this type of phototherapy because of concern over increasing the skin cancer risk. Over the past 20 years, numerous studies have been published examining this issue, but a consensus or analysis of the skin cancer risk is required for the dermatologist to make an educated risk,benefit analysis. Objective, To assess the risk of skin cancer associated with UVB phototherapy. Methods, All prospective or retrospective studies were identified in MEDLINE from 1966 to June 2002. Bibliographies were searched to identify any additional studies examining this issue. All studies that attempted to quantify or qualify any additional skin cancer risk from UVB phototherapy were included. Study selection was performed by two independent reviewers. Results, Eleven studies (10 of which concerned psoriasis patients), involving approximately 3400 participants, were included. Of note, three of the studies involved the same cohort: members of the 16-center US Psoralen plus UVA (PUVA) Follow-up Study. Other than the most recent Finnish study, all studies eventually showed no increased skin cancer risk with UVB phototherapy. One of the PUVA cohort studies examined genital skin cancers, and found an increased rate of genital tumors associated with UVB phototherapy, although this study has not been duplicated. Conclusion, The evidence suggests that UVB phototherapy remains a very safe treatment modality. [source] Protective effects of quercetin on ultraviolet A light-induced oxidative stress in the blood of ratJOURNAL OF APPLIED TOXICOLOGY, Issue 5 2002Ahmet Kahraman Abstract The oxidative effects of ultraviolet A (UVA) light (320,400 nm) and the antioxidant effects of quercetin were examined in rat blood. For this purpose, rats were divided into three groups: control, ultraviolet (UV) and ultraviolet + quercetin (UV + Q). The UV and UV + Q groups were irradiated for 4 h a day with UVA light (1.25 mW cm2) during periods of 3, 6 and 9 days. Quercetin (50 mg kg,1 body wt.) was administered intraperitoneally in the UV + Q group rats before irradiation periods. Blood was taken 3, 6 and 9 days post-treatment. Plasma malondialdehyde (MDA) levels significantly increased after 9 days of daily exposure to UVA. Whole blood glutathione (GSH) levels significantly declined after 3,9 days of irradiation. Glutathione peroxidase activity on days 6 and 9 and glutathione reductase activities on days 3, 6 and 9 post-irradiation were diminished significantly. Superoxide dismutase and catalase activities decreased significantly 3,9 days post-irradiation. The administration of quercetin before the 9-day period of irradiation significantly reduced the increase in plasma MDA value. Whole blood GSH levels significantly decreased with the administration of quercetin on all days. Quercetin significantly increased antioxidant enzymes diminished by UVA irradiation. Exposure of rats to UVA light leads to oxidative stress, reflected by increased MDA and reduced antioxidant enzyme levels. The administration of quercetin appears to be a useful approach to reduce the damage produced by UVA radiation. Copyright © 2002 John Wiley & Sons, Ltd. [source] IMPACTS OF SOLAR UV RADIATION ON THE PHOTOSYNTHESIS, GROWTH, AND UV-ABSORBING COMPOUNDS IN GRACILARIA LEMANEIFORMIS (RHODOPHYTA) GROWN AT DIFFERENT NITRATE CONCENTRATIONS,JOURNAL OF PHYCOLOGY, Issue 2 2009Yangqiao Zheng Solar ultraviolet radiation (UVR, 280,400 nm) is known to affect macroalgal physiology negatively, while nutrient availability may affect UV-absorbing compounds (UVACs) and sensitivity to UVR. However, little is known about the interactive effects of UVR and nitrate availability on macroalgal growth and photosynthesis. We investigated the growth and photosynthesis of the red alga Gracilaria lemaneiformis (Bory) Grev. at different levels of nitrate (natural or enriched nitrate levels of 41 or 300 and 600 ,M) under different solar radiation treatments with or without UVR. Nitrate-enrichment enhanced the growth, resulted in higher concentrations of UVACs, and led to negligible photoinhibition of photosynthesis even at noon in the presence of UVR. Net photosynthesis during the noon period was severely inhibited by both ultraviolet-A radiation (UVA) and ultraviolet-B radiation (UVB) in the thalli grown in seawater without enriched nitrate. The absorptivity of UVACs changed in response to changes in the PAR dose when the thalli were shifted back and forth from solar radiation to indoor low light, and exposure to UVR significantly induced the synthesis of UVACs. The thalli exposed to PAR alone exhibited higher growth rates than those that received PAR + UVA or PAR + UVA + UVB at the ambient or enriched nitrate concentrations. UVR inhibited growth approximately five times as much as it inhibited photosynthesis within a range of 60,120 ,g UVACs · g,1 (fwt) when the thalli were grown under nitrate-enriched conditions. Such differential inhibition implies that other metabolic processes are more sensitive to solar UVR than photosynthesis. [source] Photoprotection of bacterial-derived melanin against ultraviolet A,induced cell death and its potential application as an active sunscreenJOURNAL OF THE EUROPEAN ACADEMY OF DERMATOLOGY & VENEREOLOGY, Issue 7 2008J Geng Abstract Background, The increase in the incidence of non-melanoma skin tumours, photoaging, and immunosuppression demand for more effective sunscreen on ultraviolet A (UVA) irradiation. Objectives, The aim of the study is to evaluate the photoprotective effects of a bacterial-derived melanin against UVA-induced damages in vitro and in vivo. Methods, Human fibroblasts were used to assess the role of the bacterial-derived melanin on cell viability against UVA. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and nuclear morphology were employed to evaluate the photoprotection at the cellular level. Fluorometric assays were performed to detect the formation of reactive oxygen species (ROS) in the cells. Evaluations of the bacterial-derived melanin as a sunscreen were measured by transmission test and persistent pigment darkening on human skin. Results, Bacterial-derived melanin efficiently scavenged ROS in the fibroblasts after UVA irradiation. The cell viability of xeroderma pigmentosum (XP) fibroblast treated with varied doses of melanin increased dramatically in comparison with untreated control and the treated XP fibroblasts became more resistant to UVA-induced apoptosis than normal fibroblasts. Although the relative transmission didn't change too much with different concentration of bacterial-derived melanin, this melanin could keep UVA-irradiated skin from pigment darkening and act as an active sunscreen on skin. Conclusions, The bacterial-derived melanin provided significant protection to fibroblast cell and human skin against the UVA radiation. It has the potential to be developed as an active sunscreen for the patients with photosensitivity skin to sun exposure. [source] Measurement of protection afforded by ultraviolet-absorbing window film using an in vitro model of photodamageLASERS IN SURGERY AND MEDICINE, Issue 4 2006Eric F. Bernstein MD Abstract Background and Objectives The effects of chronic sun damage including telangiectasias, solar lentigos, rhytides, enlarged pores, sagging skin, and pre-cancerous and cancerous growths are among the most common presenting complaints in a dermatologist's office. These changes are often worse on the driver's side of the face, emphasizing the role of UVA exposure received while driving in producing these changes. This study was undertaken to measure the ability of car window glass alone and in combination with ultraviolet (UV)-absorbing film to reduce UV-damage as measured using an established in vitro model of photoprotection. Study Design Materials and Methods Using the 3T3 neutral red uptake photoprotection assay with solar simulating radiation (SSR) administered by a xenon arc solar simulator, we measured the photoprotection ability of auto glass, window film that filters UV radiation, and the combination of window film and auto glass. Results As measured by the 3T3 neutral red uptake photoprotection assay, auto glass reduced cell death from SSR by 29%, while window film reduced it 90%, and the combination of auto glass and film reduced cell death by 93%, when compared to unfiltered SSR. Conclusions Window film that filters UV radiation results in dramatic reductions in cytotoxicity when measured by the neutral red uptake photoprotection assay. Widespread use of window film provides an ever-present barrier to ultraviolet A (UVA) exposure and could potentially reduce the detrimental effects of UVA, including photoaging, skin cancer, and ocular damage, such as cataracts. In addition, such film is essential for patients suffering from conditions sensitive to UV radiation, such as lupus erythematosis. Lasers Surg. Med. 38:337,342, 2006. © 2006 Wiley-Liss, Inc. [source] UV stabilising synergies between carbon black and hindered light stabilisers in linear low density polyethylene filmsMACROMOLECULAR SYMPOSIA, Issue 1 2003A. Richard Horrocks Abstract The combined effects of selected carbon black pigments and hindered light stabilisers (HALS) on the UV stabilities of linear low density polyethylene film have been studied under UVA and UVB fluorescent radiation sources. While the presence of HALS do not change the chemistry of film photodegradation, whether they are low or high molecular variants, their presence significantly extends film lifetime relative to the sum of the effects of carbon black and HALS individually. These lifetime extensions may be defined in terms of a synergy factor defined with respect to film time to lose a specific percentage of a tensile property, namely t20, the time to lose 20% of initial elongation-at-break, or the carbonyl index associated with this condition. It is proposed that possible causes of this synergy are a result of the UV screening effect of the carbon black particles which provide lower concentrations of polymer radicals for the HALS component to interact with and/or an accompanying thermal stabilising effect by the latter as a consequence of the higher polymer local temperature during irradiation of pigmented films. [source] INK4a-ARF mutations in skin carcinomas from UV irradiated hairless miceMOLECULAR CARCINOGENESIS, Issue 4 2004N. Soufir Abstract To characterize further the role of the INK4a-ARF locus in the multistep process of skin carcinogenesis, we performed a mutational analysis of this locus in skin lesions from hairless mice either irradiated with UVB alone or with a solar simulator delivering UVA,+,B. INK4a-ARF mutations were present in five of 57 squamous cell carcinomas (9%), but no mutation was detected in precancerous lesions. All mutations were C:G,>,T:A transitions located at dipyrimidic sites, the hallmark of UVB mutagenesis. Three mutations affected only the p19ARF reading frame, whereas two mutations affected only the p16INK4a transcript. This study demonstrates for the first time UV-induced mutations of INK4a-ARF that occur in a small percentage in late stages skin tumors. © 2004 Wiley-Liss, Inc. [source] Effect of UVA or UVB Irradiation on Cutaneous Lipids in Films or in SolutionPHOTOCHEMISTRY & PHOTOBIOLOGY, Issue 3 2010Chloé Merle The barrier function of the skin is largely due to the stratum corneum which is essentially composed of lipids. Different external factors, such as UV irradiation, affect this skin layer and are responsible for a destabilization of the supramolecular organization of its constituted lipids. In this work, mass spectrometry and infrared spectroscopy are combined to study the correlation between the formation of oxidative compounds by UV irradiation and the lipid organization. Experiments were carried out on unsaturated lipids in film or solution form, exposed to UVA or UVB irradiation. UV exposure leads to the formation of oxygenated entities in the case of lipids with an unsaturated fatty acid moiety, resulting in a decrease in their packing which is greater when the lipids are in solution. The packing decrease is even greater following UVB irradiation. [source] Requirement for Metalloproteinase-dependent ERK and AKT Activation in UVB-induced G1-S Cell Cycle Progression of Human KeratinocytesPHOTOCHEMISTRY & PHOTOBIOLOGY, Issue 4 2009Weinong Han UVB (280,315 nm) in natural sunlight represents a major environmental challenge to the skin and is clearly associated with human skin cancer. Here we demonstrate that low doses of UVB induce keratinocyte proliferation and cell cycle progression of human HaCaT keratinocytes. Different from UVA, UVB irradiation induced extracellular signal-regulated kinase (ERK) and AKT activation and their activation are both required for UVB-induced cell cycle progression. Activation of epidermal growth factor receptor (EGFR) was observed after UVB exposure and is upstream of ERK/AKT/cyclin D1 pathway activation and cell cycle progression following UVB radiation. Furthermore, metalloproteinase (MP) inhibitor GM6001 blocked UVB-induced ERK and AKT activation, cell cycle progression, and decreased the EGFR phosphorylation, demonstrating that MPs mediate the EGFR/ERK/AKT/cyclin D1 pathways and cell cycle progression induced by UVB radiation. In addition, ERK or AKT activation is essential for EGFR activation because ERK or AKT inhibitor blocks EGFR activation following UVB radiation, indicating that EGFR/AKT/ERK pathways form a regulatory loop and converge into cell cycle progression following UVB radiation. Identification of these signaling pathways in UVB-induced cell cycle progression of quiescent keratinocytes as a process mimicking tumor promotion in vivo will facilitate the development of efficient and safe chemopreventive and therapeutic strategies for skin cancer. [source] Ultraviolet-A and -B Differentially Modify the Tyrosine-Kinase Profile of Human Keratinocytes and Induce the Expression of Arg,PHOTOCHEMISTRY & PHOTOBIOLOGY, Issue 2 2008Gabriele Klosner To investigate the expression profile of protein tyrosine kinases (PTKs) in normal human epidermal keratinocytes (NHEK) in response to UVA and UVB we employed a reversed transcriptase polymerase chain reaction (PCR) approach using degenerate primers derived from the conserved catalytic domain of PTKs. Quantitative real-time PCR with specific primers was used to confirm the influence of UV on the expression of the identified PTKs. Arg (Abelson-related gene, Abl2) was the PTK with the highest prevalence (30% of all PTKs) and UVA led to a further induction of Arg expression reaching nine-fold mRNA baseline expression at 17 h after irradiation. UVB was followed by an initial downregulation and a subsequent increase in Arg mRNA reaching five-fold baseline levels after 24 h. We conclude that UVA and UVB differentially modify the expression of PTKs in NHEK, and that Arg appears to have a major role in the response of keratinocytes to UV. These results provide a basis for further studies of PTK in UV-induced signaling that regulates protective responses, cell growth and carcinogenesis in the skin. [source] Photodynamic Action of Benzo[a]pyrene in K562 CellsPHOTOCHEMISTRY & PHOTOBIOLOGY, Issue 6 2007Daza De Moraes Vaz Batista Filgueira Benzo[a]pyrene (BaP) is ubiquitously distributed in the environment, being considered the most phototoxic element among polycyclic aromatic hydrocarbon (PAHs). In presence of oxygen, PAHs can act as a photosensitizer by means of promoting photo-oxidation of biological molecules (photodynamic action, PDA). Thus, the present study analyzed the photodynamic action of BaP under UVA irradiation (BaP + UVA) and its oxidative effects on K562 cells. The evaluation of BaP kinetics showed that the highest intracellular concentration occurred after 18 h of incubation. Cell viability, reactive oxygen species (ROS) generation, lipid peroxidation, DNA damage (breaks and DNA,protein cross-link [DNAPC]) were assessed after exposure to BaP, UVA and BaP plus UVA irradiation (BaP + UVA). Cell viability was decreased just after exposure to BaP + UVA. Lipid peroxidation and DNA breaks increased after BaP + UVA exposure, while the DNAPC increased after BaP, UVA and BaP + UVA exposure, suggesting that BaP + UVA effects were a consequence of both type II (producing mainly singlet oxygen) and type I (producing others ROS) mechanisms of PDA. [source] Photoperiod at conception predicts C677T-MTHFR genotype: A novel gene-environment interactionAMERICAN JOURNAL OF HUMAN BIOLOGY, Issue 4 2010Mark Lucock Data is presented, which suggest that the day length a woman experiences during the periconceptional period predicts the C677T-MTHFR genotype of her child. Logistic regression analysis involving 375 neonates born in the same geographical location within a three year period demonstrated that photoperiod (minutes) at conception predicts both genotype (P = 0.0139) and mutant allele carriage (P = 0.0161); the trend clearly showing that the 677T-MTHFR allele frequency increases as photoperiod increases. We propose a number of explanations, including a hypothesis in which a long photoperiod around conception decreases maternal systemic folate because of UVA induced dermal oxidative degradation of 5-methyl-H4folate, leading to a lower cellular 5,10-methylene-H4folate status. In this scenario, 5,10-methylene-H4folate would be more efficiently used for dTMP and DNA synthesis by 677T-MTHFR embryos than wildtype embryos giving the 677T-MTHFR embryos increased viability, and hence increasing mutant T-allele frequency. Alternate hypotheses include: increased seasonal availability of folate rich foods that genetically buffer any negative effect of 677T-MTHFR in embryos; seasonal oxidative stress lowering embryo-toxic homocysteine; an undefined hormonal effect of photoperiod on the neuroendocrine axis, which mediates genotype/embryo selection. The effect of photoperiod on genotype seems clear, but the speculative molecular mechanism underpinning the effect needs careful examination. Am. J. Hum. Biol., 2010. © 2010 Wiley-Liss, Inc. [source] Evaluation of a High Exposure Solar UV Dosimeter for Underwater UsePHOTOCHEMISTRY & PHOTOBIOLOGY, Issue 4 2007Peter W. Schouten ABSTRACT Solar ultraviolet radiation (UV) is known to have a significant effect upon the marine ecosystem. This has been documented by many previous studies using a variety of measurement methods in aquatic environments such as oceans, streams and lakes. Evidence gathered from these investigations has shown that UVB radiation (280,320 nm) can negatively affect numerous aquatic life forms, while UVA radiation (320,400 nm) can both damage and possibly even repair certain types of underwater life. Chemical dosimeters such as polysulphone have been tested to record underwater UV exposures and in turn quantify the relationship between water column depth and dissolved organic carbon levels to the distribution of biologically damaging UV underwater. However, these studies have only been able to intercept UV exposures over relatively short time intervals. This paper reports on the evaluation of a high exposure UV dosimeter for underwater use. The UV dosimeter was fabricated from poly 2,6-dimethyl-1,4-phenylene oxide (PPO) film. This paper presents the dose response, cosine response, exposure additivity and watermarking effect relating to the PPO dosimeter as measured in a controlled underwater environment and will also detail the overnight dark reaction and UVA and visible radiation response of the PPO dosimeter, which can be used for error correction to improve the reliability of the UV data measured by the PPO dosimeters. These results show that this dosimeter has the potential for long-term underwater UV exposure measurements. [source] Photochemistry and Photocytotoxicity of Alkaloids from Goldenseal (Hydrastis canadensis L.) 3: Effect on Human Lens and Retinal Pigment Epithelial CellsPHOTOCHEMISTRY & PHOTOBIOLOGY, Issue 4 2007Colin F. Chignell ABSTRACT The dried root or rhizome of Goldenseal (Hydrastis canadensis L.) contains several alkaloids including berberine, hydrastine, palmatine and lesser amounts of canadine and hydrastinine. Preparations derived from Goldenseal have been used to treat skin and eye ailments. Berberine, the major alkaloid in Goldenseal root powder, has been used in eye drops to treat trachoma, a disease characterized by keratoconjunctivitis. Berberine and palmatine are also present in extracts from Berberis amurensis Ruprecht (Berberidaceae) which are used to treat ocular disorders. We have previously shown that Goldenseal alkaloids are phototoxic to keratinocytes (Chem Res Toxicol. 14, 1529, 2001; ibid 19, 739, 2006) and now report their effect on human lens and retinal pigment epithelial cells. Human lens epithelial cells (HLE-B3) were severely damaged when incubated with berberine (25 ,M) and exposed to UVA (5 J cm,2). Under the same conditions, palmatine was less phototoxic and hydrastine, canadine and hydrastinine were inactive. Moderate protection against berberine phototoxicity was afforded by the antioxidants ascorbate (2 mM) and N -acetylcysteine (5 mM). When exposed to UVA (5 J cm,2) both berberine (10 ,M) and palmatine (10 ,M) caused mild DNA damage as determined by the alkaline comet assay which measures single strand breaks. Berberine and palmatine are the only Goldenseal alkaloids with appreciable absorption above 400 nm. Because light at wavelengths below 400 nm is cut off by the anterior portion of the adult human eye only berberine and palmatine were tested for phototoxicity to human retinal pigment epithelial (hRPE) cells. Although berberine did damage hRPE cells when irradiated with visible light (, > 400 nm) approximately 10 times higher concentrations were required to produce the same amount of damage as seen in lens cells. Palmatine was not phototoxic to hRPE cells. Neither berberine nor palmatine photodamaged DNA in hRPE. Infusions of Goldenseal are estimated to contain ,1 mM berberine, while in tinctures the alkaloid concentration may be more than 10 times higher. Our findings show that eyewashes and lotions derived from Goldenseal or containing berberine must be used with caution when the eyes are exposed to bright sunlight but that oral preparations are not likely to cause ocular phototoxicity. [source] Determination of Wavelength-Specific UV Protection Factors of Sunscreens in Intact Skin by EPR Measurement of UV-Induced Reactive Melanin RadicalPHOTOCHEMISTRY & PHOTOBIOLOGY, Issue 4 2007Leslie Lund ABSTRACT There remains an unmet need for skin tissue-based assays for the measurement of the UVA protection and efficacy of sunscreens. Here we describe development of a novel electron paramagnetic resonance assay that uses the photogeneration of reactive melanin radical as a measure of UV light penetration to melanocytes in situ in skin. We have used areas of focal melanocytic hyperplasia in the skin of Monodelphis domestica to model the human nevus. We show that we are able to use this assay to determine the monochromatic protection factors (mPF) of research and commercial sunscreens at specific narrow wavebands of UVB, UVA and blue visible light. Both commercial sunscreens, a sun protection factor (SPF) 4 and an SPF 30 product, had mPFs in the UVB range that correlated well with their claimed SPF. However, their mPF in the UVA ranges were only about one-third of claimed SPF. This technique can be used to design and assay sunscreens with optimally balanced UVA and UVB protection. [source] Photosensitized DNA Damage and its Protection via a Novel Mechanism,PHOTOCHEMISTRY & PHOTOBIOLOGY, Issue 1 2007Yusuke Hiraku UVA, which accounts for approximately 95% of solar UV radiation, can cause mutations and skin cancer. Based mainly on the results of our study, this paper summarizes the mechanisms of UVA-induced DNA damage in the presence of various photosensitizers, and also proposes a new mechanism for its chemoprevention. UVA radiation induces DNA damage at the 5,-G of 5,-GG-3, sequence in double-stranded DNA through Type I mechanism, which involves electron transfer from guanine to activated photosensitizers. Endogenous sensitizers such as riboflavin and pterin derivatives and an exogenous sensitizer nalidixic acid mediate DNA photodamage via this mechanism. The major Type II mechanism involves the generation of singlet oxygen from photoactivated sensitizers, including hematoporphyrin and a fluoroquinolone antibacterial lomefloxacin, resulting in damage to guanines without preference for consecutive guanines. UVA also produces superoxide anion radical by an electron transfer from photoexcited sensitizers to oxygen (minor Type II mechanism), and DNA damage is induced by reactive species generated through the interaction of hydrogen peroxide with metal ions. The involvement of these mechanisms in UVA carcinogenesis is discussed. In addition, we found that xanthone derivatives inhibited DNA damage caused by photoexcited riboflavin via the quenching of its excited triplet state. It is thus considered that naturally occurring quenchers including xanthone derivatives may act as novel chemopreventive agents against photocarcinogenesis. [source] Radiation Sources Providing Increased UVNUVB Ratios Induce Photoprotection Dependent on the UVA Dose in Hairless MicePHOTOCHEMISTRY & PHOTOBIOLOGY, Issue 2 2006Vivienne E. Reeve ABSTRACT In studies involving mice in which doses of UVA (320,400 nm) and UVB (290,320 nm) radiation were administered alone or combined sequentially, we observed a protective effect of UVA against UVB-induced erythemdedema and systemic suppression of contact hypersensitivity. The UVA immunoprotection was mediated by the induction of the stress enzyme heme oxygenase-1 (HO-1) in the skin, protection of the cutaneous Th1 cytokines interferon-gM (IFN-,) and IL-12 and inhibition of the UVB-induced expression of the Th2 cytokine IL-10. In this study, we seek evidence for an immunological waveband interaction when UVA and UVB are administered concurrently to hairless mice as occurs during sunlight exposure in humans. A series of spectra providing varying ratios of UVA/UVB were developed, with the UVA ratio increased to approximately 3.5 times the UVA component in solar simulated UV (SSUV). We report that progressively increasing the UVA component of the radiation while maintaining a constant UVB dose resulted in a reduction of both the erythemdedema reaction and the degree of systemic immunosuppression, as measured as contact hypersensitivity. The UVA-enhanced immunoprotection was abrogated in mice treated with a specific HO enzyme inhibitor. UVA-enhanced radiation also upregulated the expression of cutaneous IFN-, and IL-12 and inhibited expression of both IL-6 and IL-10, compared with the activity of SSUV. The results were consistent with the previously characterized mechanisms of photoprotection by the UVA waveband alone and suggest that the UVA component of solar UV may have beneficial properties for humans. [source] Impairment of Eye Lens Cell Physiology and Optics by Broadband Ultraviolet A,Ultraviolet B Radiation,PHOTOCHEMISTRY & PHOTOBIOLOGY, Issue 3 2002O. M. Oriowo ABSTRACT The phototoxicity of ultraviolet A (UVA) alone and UVA plus ultraviolet B (UVB) combined on cultured porcine lenses was investigated by analyzing cellular function as measured with a fluorescence bioassay approach and optical integrity, in terms of sharpness of the lens focus as measured with a scanning laser system. The bioassay consisted of carboxyfluorescein diacetate-acetoxymethyl ester and alamarBlue fluorescent dyes. Aseptically dissected porcine lenses were maintained in modified medium 199 without phenol red supplemented with 1% penicillin,streptomycin and 4% porcine serum. At 1 week of preincubation, baseline measurements were obtained. Then the lenses were treated with single exposures of different UVA and UVB energy levels. The lenses treated with 86 J/cm2 UVA alone showed a significant (P < 0.05) decrease in cellular and optical integrity at 48 h after exposure, whereas those treated with 43 J/cm2 UVA alone did not show significant phototoxic effect. Lenses treated with 15.63 J/cm2 UVA plus 0.019 J/cm2 UVB combined showed significant adverse effects beginning from 48 h after exposure. Also, there was no recovery. These findings show that a high UVA dose alone and relatively low UVA in combination with low UVB radiant exposure can impair lens cellular and optical functions, respectively. [source] UV Erythema Reducing Capacity of Mizolastine Compared to Acetyl-salicylic Acid or both Combined in Comparison to Indomethacin,,PHOTOCHEMISTRY & PHOTOBIOLOGY, Issue 4 2001Jens-Uwe Grundmann ABSTRACT UV light exerts hazardous effects such as induction of skin cancer and premature skin aging. In this study we evaluated an assumptive anti-inflammatory effect of the nonsedative histamine H1-receptor antagonist, mizolastine, on UV-induced acute sunburn reaction. Therefore, a clinical, randomized, double-blind, four-arm, crossover study was conducted in healthy young female volunteers (skin type II) comparing the UV sensitivity under mizolastine, acetyl-salicylic acid (ASA), indomethacin or a mizolastine/ASA combination. Moreover, HaCaT keratinocytes were incubated with mizolastine under various UV treatment modalities in vitro to study its effect on the release of inflammatory cytokines, i.e. interleukin (IL)-1,, IL-6 and tumor necrosis factor , (TNF-,). All three drugs were effective in suppressing the UVB-, UVA- and combined UVA/UVB-erythema. However, the strongest effects were observed using the combined treatment with both 250 mg ASA and 10 mg mizolastine. An inhibitory effect in vitro of 10 nM mizolastine upon UV-induced cytokine release from HaCaT keratinocytes was observed for IL-1, at 24 h after 10 J/cm2 UVA1, for IL-6 at 48 h after 10 J/cm2 UVA1 and 30 mJ/cm2 UVB, and also for TNF-, at 4 h after 10 J/cm2 UVA, 10 J/cm2 UVA1 and 30 mJ/cm2 UVB, respectively. The combination of mizolastine and ASA can be strongly recommended as a protective measure against UV erythema development with a lower unwanted side effect profile than that of the hitherto treatment modality, i.e. indomethacin. [source] High Mutation Frequency at Ha-ras Exons 1,4 in Squamous Cell Carcinomas from PUVA-treated Psoriasis Patients,PHOTOCHEMISTRY & PHOTOBIOLOGY, Issue 2 2001Heidemarie Kreimer-Erlacher ABSTRACT Clinical follow-up studies have revealed that PUVA-treated patients are at increased risk of skin cancer, particularly squamous cell carcinoma (SCC). However, since psoralen and UVA (PUVA) is not only a potent mutagen and carcinogen but also an immunosuppressor, and since other (co)carcinogenic factors often exist in psoriasis patients, the exact causes and mechanisms of PUVA-associated SCC are still not completely understood. In order to fill this gap the tools of molecular epidemiology are being used to study the SCC mutational spectra of p53 and Ha-ras, two of the most commonly mutated genes in human cancers. A previous mutation analysis revealed that SCC in PUVA-treated patients often carried mutated p53 genes and that many of the mutations had the UV fingerprint (i.e. C,T or CC,TT transitions at dipyrimidine sites). In the present study DNA-sequencing analysis revealed a total of 18 Ha-ras missense or nonsense mutations at exons 1,4 in 13 of 17 SCC (76%) from 8 of 11 (73%) PUVA-treated psoriasis patients. Six of the 18 mutations (33%) were of UV-fingerprint type (C,T transitions), five (28%) were at 5,-TpG sites (i.e. potential psoralen-binding sites and thus potentially caused by PUVA) and seven were of other type (39%), including six G:C,T:A transversions at hotspot codon 12. In addition, in the case of 6 of the 11 subjects (55%) both tumor and normal skin samples contained a T:A,C:G base change at codon 27 (a 5,-ATT site), a change previously hypothesized to be a possible silent Ha-ras polymorphism at one allele. When we compared the present Ha-ras mutation spectrum with the p53 mutation spectrum from a previous study of the samples, we found that approximately half of the tumors harbored mutations in both Ha-ras and p53. Together, our results indicate that Ha-ras mutations are present in a large proportion of PUVA-associated SCC and that UVB, PUVA and other agents may induce Ha-ras mutations and act together with p53 in the formation of SCC in psoriasis patients. 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