UVB Exposure (uvb + exposure)

Distribution by Scientific Domains

Selected Abstracts

Effect of Cloud Cover on UVB Exposure Under Tree Canopies: Will Climate Change Affect UVB Exposure?

Richard H. Grant
ABSTRACT The effect of cloud cover on the amount of solar UV radiation that reaches pedestrians under tree cover was evaluated with a three-dimensional canopy radiation transport model. The spatial distribution of UVB irradiance at the base of a regular array of spherical tree crowns was modeled under the full range of sky conditions. The spatial mean relative irradiance (I), and erythemal irradiance of the entire below-canopy domain and the spatial mean relative irradiance and erythemal irradiance in the shaded regions of the domain were determined for solar zenith angles from 15 to 60. The erythemal UV irradiance under skies with 50% or less cloud cover was not remarkably different from that under clear skies. In the shade, the actual irradiance was greater under partly cloudy than under clear skies. The mean ultraviolet protection factor for tree canopies under skies with 50% or less cloud cover was nearly equivalent to that for clear sky days. Regression equations of spatially averaged Ir. as a function of cloud cover fraction, solar zenith angle and canopy cover were used to predict the variation in erythemal irradiance in different land uses across Baltimore, MD. [source]

In vivo UVB irradiation induces clustering of Fas (CD95) on human epidermal cells

Bo Bang
Abstract:,In vitro studies with human cell lines have demonstrated that the death receptor Fas plays a role in ultraviolet (UV)-induced apoptosis. The purpose of the present study was to investigate the relation between Fas expression and apoptosis as well as clustering of Fas in human epidermis after a single dose of UVB irradiation. Normal healthy individuals were irradiated with three minimal erythema doses (MED) of UVB on forearm or buttock skin. Suction blisters from unirradiated and irradiated skin were raised, and Fas, FasL, and apoptosis of epidermal cells were quantified by flow cytometry. Clustering of Fas was demonstrated by confocal laser scanning microscopy on cryostat sections from skin biopsies. Soluble FasL in suction blister fluid was quantified by ELISA. Flow cytometric analysis demonstrated increased expression intensity of Fas after irradiation, with 1.6-, 2.2- and 2.7-fold increased median expression at 24, 48 and 72 h after irradiation, respectively (n = 4). Apoptosis was demonstrated by the TUNEL reaction, and the maximum of apoptotic cells was detected at 48 h after irradiation. Double-staining for Fas and TUNEL showed that apoptosis was restricted to the Fas-positive epidermal subpopulation, but there was no correlation between the intensities of Fas expression and TUNEL reaction. Median expression intensity of FasL-positive cells transiently decreased to 0.9- and 0.8-fold of the preirradiation respective level after 24 h and 48 h, respectively, and returned to the respective preirradiation level at 72 h after irradiation (n = 4). Concentrations of soluble FasL in suction blister fluid from UVB-irradiated skin did not differ from those in unirradiated skin (n = 5). Confocal laser scanning microscopy showed a rapid clustering of Fas within 30 min after irradiation. A simultaneous clustering of the adapter signalling protein FADD suggested that Fas clustering has a functional significance. Our results are in accordance with previous findings from in vitro studies, and suggest that Fas is activated in vivo in human epidermis after UVB exposure. [source]

Responses of plants in polar regions to UVB exposure: a meta-analysis

Abstract We report a meta-analysis of data from 34 field studies into the effects of ultraviolet B (UVB) radiation on Arctic and Antarctic bryophytes and angiosperms. The studies measured plant responses to decreases in UVB radiation under screens, natural fluctuations in UVB irradiance or increases in UVB radiation applied from fluorescent UV lamps. Exposure to UVB radiation was found to increase the concentrations of UVB absorbing compounds in leaves or thalli by 7% and 25% (expressed on a mass or area basis, respectively). UVB exposure also reduced aboveground biomass and plant height by 15% and 10%, respectively, and increased DNA damage by 90%. No effects of UVB exposure were found on carotenoid or chlorophyll concentrations, net photosynthesis, Fv/Fm or ,PSII, belowground or total biomass, leaf mass, leaf area or specific leaf area (SLA). The methodology adopted influenced the concentration of UVB absorbing compounds, with screens and natural fluctuations promoting significant changes in the concentrations of these pigments, but lamps failing to elicit a response. Greater reductions in leaf area and SLA, and greater increases in concentrations of carotenoids, were found in experiments based in Antarctica than in those in the Arctic. Bryophytes typically responded in the same way as angiosperms to UVB exposure. Regression analyses indicated that the percentage difference in UVB dose between treatment and control plots was positively associated with concentrations of UVB absorbing compounds and carotenoids, and negatively so with aboveground biomass and leaf area. We conclude that, despite being dominated by bryophytes, the vegetation of polar regions responds to UVB exposure in a similar way to higher plant-dominated vegetation at lower latitudes. In broad terms, the exposure of plants in these regions to UVB radiation elicits the synthesis of UVB absorbing compounds, reduces aboveground biomass and height, and increases DNA damage. [source]

Cooler temperatures increase sensitivity to ultraviolet B radiation in embryos and larvae of the frog Limnodynastes peronii

Abstract Recent studies suggest that complex interacting processes are driving global amphibian declines. Increased ultraviolet B (UVB) radiation in the solar spectrum associated with ozone depletion has been implicated in declines, and evidence suggests that the effects of UVB radiation on amphibians may be greater at cooler temperatures. We tested the thermal sensitivity of UVB effects on amphibians in a controlled factorial experiment using the striped marsh frog, Limnodynastes peronii as a model species. We compared survival, growth and locomotor performance of embryonic and larval L. peronii reared under low and high UVB exposures at both 20 and 30 C. Embryonic and larval L. peronii proved extremely sensitive to UVB damage and exhibited greater sensitivity at 20 C compared with 30 C. Embryonic survival to Gosner stage 25 was unaffected by UVB exposure at 30 C, but at 20 C survival was reduced to 52% under high UVB. Larval survival exhibited a similar trend. At 20 C, all tadpoles survived under low UVB, whereas under high UVB there was 100% mortality after 15 days of exposure. At 30 C, 86% survived under low UVB, but only 46% survived under high UVB. Sublethal effects such as, embryonic malformation, retarded larval growth and reduced larval swimming performance were also greater at 20 C compared with 30 C. Our results strongly indicate that UVB damage in amphibians is markedly increased at cooler temperatures. Thus, populations of UVB sensitive species occurring at cold climates may be at greater risk of declines due to increased solar UVB radiation. [source]

Cyclooxygenase-2 deficiency increases epidermal apoptosis and impairs recovery following acute UVB exposure

Jacqueline K. Akunda
Abstract The cyclooxygenases, COX-1 and COX-2, are involved in cutaneous responses to both acute and chronic UV exposure. In the present study, wild-type (WT), COX-1,/, and COX-2,/, mice were used to determine the influence of the individual isoform on mouse skin responses to acute UVB treatment. Immunohistochemistry and Western analysis indicated that COX-2, and not COX-1, was induced by UVB (2.5 or 5.0 kJ/m2), but that COX-1 remained the major source of prostaglandin E2 production. UVB exposure significantly increased epidermal apoptosis in all genotypes compared to untreated mice. However, while the number of apoptotic cells in WT and COX-1,/, mice were about equal, the number of apoptotic cells was 2.5-fold greater in COX-2,/, mice. Apoptosis in WT and COX-2,/, mice peaked at 24 h post-exposure. The increased apoptosis and reduced proliferation in COX-2,/, mice resulted in about a 50% decrease in epidermal thickness at 24,48 h post-exposure compared to about a 50% increase in epidermal thickness in WT mice. UVB-induced cell replication, as measured by BrdU labeling, was reduced in COX-2,/, compared to WT mice at 24,96 h. However, by 96 h post-exposure, both WT and COX-2,/, mice showed epidermal hyperplasia. The data indicate that COX-2 induction initially protects against the acute sunburn effects of UVB, but that continuous induction of COX-2 may contribute to skin cancer in chronic UVB exposure. 2007 Wiley-Liss, Inc. [source]

Protective effect of vitamin E on ultraviolet B light,induced damage in keratinocytes

Samar Maalouf
Abstract Ultraviolet (UV) B radiation is the most common environmental factor in the pathogenesis of skin cancer. Exposure of human skin to UVB radiation leads to the depletion of cutaneous antioxidants, the activation of nuclear factor kappa B (NF-,B), and programmed cell death (apoptosis). Although antioxidant supplementation has been shown to prevent UVB-induced photooxidative damage, its effect on components of cell signaling pathways leading to gene expression has not been clearly established. In the present study, the effect of the antioxidant vitamin, ,-tocopherol (,-T), and its acetate analog, ,-tocopherol acetate (,-TAc), on UVB-induced damage in primary and neoplastic mouse keratinocytes was investigated. The ability of both vitamins to modulate UVB-induced apoptosis and activation of the transcription factor NF-,B were studied. Treatment of normal and neoplastic mouse epidermal keratinocytes (308 cells) with 30,60 mJ/cm2 UVB markedly decreased viable cell number and was accompanied by DNA fragmentation. When both vitamins were applied to cells at times before and after UVB radiation, a significant increase in the percentage of viable cells and concomitant decrease in the number of apoptotic cells was noted, with vitamin pretreatment providing a better protection than posttreatment. Simultaneous posttreatment of irradiated cells with ,-TAc abolished the cytotoxic effects of UVB and restored cell viability to control levels. In addition, simultaneous posttreatment of irradiated cells with ,-T reduced the number of apoptotic cells by half, indicating a synergistic effect of two such treatments compared with any single one. Flow cytometry analysis indicated that vitamin treatment suppressed both an increase in pre-G0 cells and a decrease in cycling cells by UVB exposure. In addition, NF-,B activation was detected 2 h after UV exposure and was maintained for up to 8 h. Pretreatment with vitamins significantly inhibited NF-,B activation at 4 and 8 h. These results indicate that vitamin E and its acetate analog can modulate the cellular response to UVB partly through their action on NF-,B activation. Thus, these antioxidant vitamins are potential drugs for the protection from or the reduction of UVB-associated epidermal damage. 2002 Wiley-Liss, Inc. [source]

Requirement for Metalloproteinase-dependent ERK and AKT Activation in UVB-induced G1-S Cell Cycle Progression of Human Keratinocytes

Weinong 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]

Decrease in Langerhans Cells and Increase in Lymph Node Dendritic Cells Following Chronic Exposure of Mice to Suberythemal Doses of Solar Simulated Radiation

Pauline McLoone
ABSTRACT Exposure of certain strains of mice to ultraviolet radiation (UVR) causes suppression of some innate and adaptive immune responses. One such consequence of acute UVB exposure is a reduction in the number of Langerhans cells (LC) in the epidermis and an increase in dendritic cells (DC) in lymph nodes draining the irradiated skin sites. Exposure to chronic UVB irradiation also has effects on the immune system, but it is unknown what effects are caused by repeated doses of solar simulated radiation (SSR). Consequently, the main aims of the present study were to determine whether repeated exposure to low doses of SSR would lead to similar changes in these cell populations and whether chronic doses of SSR activate a protective photoadaptation mechanism. Groups of C3H/HeN mice were irradiated daily with 3.7 J/cm2 SSR from Cleo Natural lamps for 2, 10, 20, 30 or 60 days. Further groups of mice received an additional dose of 7.4 J/cm2 SSR on days 2, 10, 30 or 60 to test for photoadaptation. The numbers of LC in the epidermis and DC in the lymph nodes draining irradiated skin sites were counted 24 h after the final irradiation. With the exception of mice irradiated for only 2 days, LC were significantly reduced throughout the chronic irradiation protocol, and no recovery occurred. DC numbers were significantly increased in the draining lymph nodes of mice irradiated for 20 days and 60 days. [source]

UVB Irradiation of Normal Human Skin Favors the Development of Type-2 T-cells In Vivo and in Primary Dermal Cell Cultures,

Sergio Di Nuzzo
ABSTRACT To determine the effect of UVB exposure on the balance of type-1 or type-2 T-cells in skin, we examined the expression of key markers interferon (IFN)-, and interleukin (IL)-4 in cryostat sections. IFN-, mRNA was clearly detectable in nonirradiated control skin, and IFN-, protein was found in 2% of the dermal CD3pos T-cells, whereas IL-4 mRNA was hardly detectable, and no IL-4 protein was found. In contrast, IL-4 mRNA expression increased upon irradiation, and IL-4 was found in 2% of the T-cells at day 2 after UVB-exposure. Concomitantly, IFN-, mRNA expression decreased, and IFN-, protein became absent. We also analyzed T-cells present in primary dermal cell cultures, which were used as an in vitro equivalent of the in vivo situation. As compared with T-cells from control skin, T-cells in dermal cell cultures from UVB-exposed skin displayed an increased IL-4 and decreased IFN-, expression. No such skewing occurred when the T-cells from irradiated skin were cloned in the absence of a dermal microenvironment. Except for an occasional positive T-cell, type-1,associated cell-surface markers (CCR5, CXCR3) or type-2 markers (CCR3, CD30, CRTH2) were undetectable in situ. But these markers were expressed on cultured dermal T-cells from UVB-exposed and control skin at a comparable level, but did not correlate with the IFN-, and IL-4 production. Altogether, UVB-induced changes of the dermal microenvironment favor the development of type-2 T-cells. [source]

Cyclooxygenase-2 Expression in Murine and Human Nonmelanoma Skin Cancers: Implications for Therapeutic Approaches,

Kathy P. An
ABSTRACT Inflammatory stimuli result in the production of cutaneous eicosanoids, which are known to contribute to the process of tumor promotion. Cyclooxygenase (COX), the rate-limiting enzyme for the production of prostaglandins (PG) from arachidonic acid, exists in at least two isoforms, COX-1 and COX-2. COX-1 is constitutively expressed in most tissues and plays various physiological roles, whereas increased COX-2 expression is known to occur in several types of epithelial neoplasms. Enhanced PG synthesis is a potential contributing factor in UVB-induced nonmelanoma skin cancers (NMSC). Increased COX-2 staining occurs in murine skin neoplasms after chronic exposure to carcinogenic doses of UVB. In this study, immunohistochemical and Western blot analyses were employed to assess longitudinally COX-2 expression in a standard mouse UVB complete carcinogenesis protocol and in human basal cell carcinomas (BCC) and squamous cell carcinomas (SCC). During UVB irradiation of mice, COX-2 expression consistently increased in the hyperplastic skin, the benign papillomas and the SCC. COX-2 expression was also increased in human actinic keratoses, SCC and BCC as well as in murine SCC and BCC. The pattern of COX-2 expression was quite variable, occurring in a patchy distribution in some lesions with staining confined mainly to suprabasal cell layers. In general, COX-2 expression progressively became more extensive in benign papillomas and well-differentiated murine SCC. The staining was predominantly cytoplasmic and perinuclear in some focal areas in tissue stroma around both murine and human tumors. Western blot analysis confirmed negative COX-2 expression in normal skin, whereas acute UVB exposure resulted in increased enzyme expression, which continued to increase in developing papillomas and SCC. Because of the evidence indicating a pathogenic role for eicosanoids in murine and human skin neoplasms, we performed studies to assess the anti-inflammatory and anticarcinogenic effects of green tea extracts, which are potent antioxidants. Acute exposure of the human skin to UVB (minimum erythema dose 4) caused a transient enhancement of the COX-2 expression, which reverted to baseline within hours; however, in murine skin the expression persisted for several days. Pretreatment with the topically applied green tea extract (1 mg/cm2) largely abrogated the acute COX-2 response to UVB in mice or humans. In summary, enhanced COX-2 expression serves as a marker of epidermal UVB exposure for murine and human NMSC. These results suggest that COX-2 inhibitors could have potent anticarcinogenic effects in UVB-induced skin cancer. [source]

Melanin Offers Protection Against Induction of Cyclobutane Pyrimidine Dimers and 6,4 Photoproducts by UVB in Cultured Human Melanocytes,

Nico P. M. Smit
ABSTRACT The goal of this investigation was to correlate the melanin content in human pigmentary cells with the generation of UVB-induced photoproducts and to examine the relationship between the melanin content and the removal of the photoproducts. Cultured melanocytes from light-skinned individuals synthesized less melanin and produced more cyclobutane pyrimidine dimers and 6,4 photoproducts upon UVB exposure than did melanocytes from black skin. Tyrosine-stimulated melanogenesis provided protection against DNA damage in both cell types. In another set of pigmented cell lines a ratio between eumelanin and pheomelanin was determined. The assessment of association between DNA damage induction and the quantity and quality of melanin revealed that eumelanin concentration correlated better with DNA protection than pheomelanin. Skin type,I and skin type,VI melanocytes, congenital nevus (CN)-derived cells and skin type,II melanocytes from a multiple-melanoma patient were grown in media with low or high l -tyrosine concentration. The cells were irradiated with 200 J/m2 UVB, and the levels of the photoproducts were determined immediately and after 6 and 24 h. Once again the induction of the photoproducts was mitigated by increased melanogenesis, and it was inversely correlated with the skin type. No significant differences were found for the removal of photoproducts in the cultures of skin types I and VI and CN cells. No indications of a delay in the removal of photoproducts in the melanocytes from the multiple-melanoma patient were found either. [source]

The effect of ultraviolet B-induced vitamin D levels on host resistance to Mycobacterium tuberculosis: a pilot study in immigrant Asian adults living in the United Kingdom

Paul Devakar Yesudian
Summary Asian immigrants to the United Kingdom demonstrate much higher tuberculosis rates than the indigenous population. This is postulated to be because of their low vitamin D levels, consequent upon a combination of diet and their reduced ultraviolet (UV) exposure in the United Kingdom, because vitamin D enhances antimycobacterial activity in in vitro systems. The aim of this study was to examine the relationship between UVB exposure, vitamin D levels and tuberculo-immunity in Asian immigrants in the United Kingdom. Suberythemal UVB treatments were given to eight subjects on 3 consecutive days, using broadband UVB fluorescent lamps. Blood was sampled for 25-hydroxyvitamin D (25-OH D) and whole blood functional assays were performed for antimycobacterial immunity. The mean 25-OH D level increased from a baseline of 11.23 ng/ml (95% CI 6.7,20.39) to 20.39 ng/ml (95% CI 16.6,20) following UVB treatment, P<0.01. However, no significant change in antimycobacterial immunity occurred following UVB exposure. This pilot study in Asian subjects with good baseline tuberculo-immunity has not supported a role for UVB-induced 25-OH D in the immune response to Mycobacterium tuberculosis. [source]

Thalidomide inhibits UVB-induced mouse keratinocyte apoptosis by both TNF-,-dependent and TNF-,-independent pathways

Kurt Q. Lu
Background: Thalidomide is an anti-inflammatory pharmacologic agent that has been utilized as a therapy for a number of dermatologic diseases. Its anti-inflammatory properties have been attributed to its ability to antagonize tumor necrosis factor-alfa (TNF-,) production by monocytes. However, its mechanism of action in the skin is not known. Purpose: To test our hypothesis that thalidomide may antagonize TNF-, production in the skin, we used a mouse model for acute ultraviolet-B (UVB) exposure, a known stimulus for inducing this cytokine. Results: A single bolus dose of thalidomide (either 100 or 400 mg/kg) given immediately before UVB exposure (40,120 mJ/cm2) inhibited, in a dose-dependent manner, sunburn cell formation (i.e. keratinocyte (KC) apoptosis as defined by histologic appearance and confirmed by terminal transferase mediated biotinylated dUTP nick end labelling staining) in mouse skin biopsy specimens. However, this agent did not affect the formation of cyclobutane pyrimidine dimers, a measure of UVB-induced DNA damage, which is an early event associated with apoptosis. RNase protection assays confirmed that high (400 mg/kg), but not low (100 mg/kg), doses of thalidomide inhibited the UVB-induced increase in steady-state TNF-, mRNA. Additionally, our in vitro data using neonatal mouse KCs showed that thalidomide prevented UVB-induced cell death (JAM assay). The antiapoptotic effects of thalidomide can be reversed by the addition of exogenous recombinant mouse TNF-, and hence reconstituting UVB-induced programmed cell death. The inhibition of sunburn cell formation by low-dose thalidomide in the absence of TNF-, inhibition suggests that other, unidentified mechanisms of apoptosis inhibition are active. Conclusions: These data suggest that the anti-inflammatory effects of thalidomide can affect UVB injury, and may, in part, explain its action in photosensitivity diseases such as cutaneous lupus erythematosus. [source]

Genomic scale analysis of the human keratinocyte response to broad-band ultraviolet-B irradiation

Joe Takao
Ultraviolet B (UVB) radiation is an important inducer of many biologic changes in skin, of which keratinocytes are a key target. To gain better insight into changes in gene expression generated in the early phase after UVB exposure, we used complementary RNA (cRNA) microarray hybridization to compare differences in mRNA expression of UVB-irradiated (single dose of 100 J/m2 broad-band UVB) and sham-irradiated primary cultured human keratinocytes. Six hours after irradiation, total RNA was isolated from keratinocytes, and cRNA was synthesized and hybridized to a GeneChip expression array (Affymetrix) consisting of 6800 genes. Based on a threshold of >,twofold change, 187 genes (2.8%) were designated to be the most UVB-responsive. Surprisingly, none of these genes had been shown previously to be modulated by UVB. Conversely, several genes in the microarray that had been reported previously to be UVB- responsive by other methods showed less (< twofold) or no change. Northern blotting of seven differentially modulated genes produced results similar to those derived from microarray technology, thereby validating the accuracy of screening. Clustering based on known or likely functions indicated that among 88 upregulated genes, nine encode for cytochrome c subunits, six for ribosomal proteins, and two for regulators of apoptosis. By contrast, many of the 99 downregulated genes are involved in transcription, differentiation and transport. These findings indicate that keratinocytes respond to a single low dose of broad-band UVB irradiation by enhancing processes involved in energy production and translation, while suppressing those related to transcription, differentiation and transport. [source]

A clinical trial and molecular study of photoadaptation in vitiligo

C.L. Hexsel
Summary Background, Photoadaptation to ultraviolet (UV) B phototherapy is due to both pigmentary and nonpigmentary influences. Objectives, To measure photoadaptation in vitiliginous skin and to compare it with normal pigmented skin. Methods, Seventeen patients with Fitzpatrick skin phototypes III,VI with vitiligo received six to nine UVB treatments, two to three times weekly. Minimal erythema dose (MED) testing was done at baseline and after all treatments; the percentage change in MED was analysed as a measure of photoadaptation. The percentage decrease in cyclobutane pyrimidine dimers (CPDs) over 24 h after a single exposure of 1 MED was analysed on vitiliginous and normal skin. Results, The mean SD percentage change in MED from before to after treatments was: treated vitiliginous skin 285 399% (P = 0015), treated normal skin 359 499% (P = 0015), untreated vitiliginous skin 119 226% (P =0070), untreated normal skin 251 413% (P = 0041). Of these patients, two-thirds had a positive percentage change in MED (photoadaptation). The mean amount of CPDs induced per megabase of DNA immediately after exposure was significantly higher in vitiliginous skin. The mean SD percentage decrease in CPDs (rate of repair) in 24 h was 357 268% in vitiliginous skin (P = 0027) and 462 195% in normally pigmented skin (P = 0001); no difference was noted in the repair in vitiliginous skin compared with normal skin (P = 04). Conclusions, Photoadaptation in vitiliginous and normal skin was observed in two-thirds of patients. Vitiliginous skin had significantly more CPDs following UVB exposure; the rate of repair of UVB-induced DNA damage was equivalent to that in normal skin. [source]

Effect of ultraviolet (UV) A, UVB or ionizing radiation on the cell cycle of human melanoma cells

M. Placzek
Summary Background, One important component of the cellular response to irradiation is the activation of cell cycle checkpoints. It is known that both ultraviolet (UV) radiation and ionizing radiation (IR) can activate checkpoints at transitions from G1 to S phase, from G2 phase to mitosis and during DNA replication. Objectives, To evaluate the effects of irradiation with different wavelengths on cell cycle alterations. Methods, p53-deficient IPC-298 melanoma cells were irradiated with 10 J cm,2 UVA, 40 mJ cm,2 UVB, or with 75 Gy IR. Cell cycle effects were then determined by DNA/5-bromodeoxyuridine dual-parameter flow cytometry. Results, IPC-298 cells irradiated in G1 with UVA were not arrested at the G1/S transition, but at the G2/M transition. Despite p53 deficiency, the cells showed a G1 arrest after UVB exposure. Furthermore, IR did not affect G1 or S phase, but induced G2 phase arrest. Hence, the effects of UVA, but not of UVB, on the cell cycle in p53-deficient melanoma cells are comparable with those of IR. Conclusions, UVA and IR induce radical-mediated strand breaks and DNA lesions, and UVB essentially induces thymine dimers that lead to excision repair-related strand breaks. Different cell cycle effects may be a consequence of different types of DNA damage. The results showed that UVB-irradiated p53-deficient cells are arrested in G1. Irradiation with the solar radiation component UVB can therefore result in a beneficial retardation of tumour promotion in human skin carrying p53-mutated cell clones. [source]

Ultraviolet B induces hyperproliferation and modification of epidermal differentiation in normal human skin grafted on to nude mice

S. Del Bino
Summary Background For ethical and technical reasons, the in vivo biological effects of ultraviolet (UV) radiation on skin are difficult to study in human volunteers. The use of human skin grafted on to nude mice may circumvent this difficulty. Objectives To investigate the effects of a single moderate UVB exposure on human skin grafted on to nude mice. Methods Modifications of epidermal differentiation markers and patterns of keratin expression were assessed from 24 h to 14 days after a physiological UVB irradiation characterized by the induction of sunburn cells. Results During the first 48 h postexposure, involucrin, loricrin, transglutaminase type I, filaggrin and keratin K2e expression were altered together with the formation of abnormal horny layers. Constitutive keratin K14 was increased while keratin K10 expression was delayed. Newly synthesized keratins K6, K16, K17 and K19 were induced in parallel with an increase in the epidermal proliferation rate. A progressive normalization of both keratinocyte proliferation and differentiation took place during the following days, reaching completion within 2 weeks. Conclusions Exposure of human skin to a UVB dose corresponding to a mild sunburn reaction induces epidermal hyperproliferation and alterations of several constitutive differentiation markers, as well as a drastic modification in the pattern of epidermal keratins. Although these modifications were shown to be progressively reversed in a single exposure model, the data also suggest that subsequent UV exposures occurring during the recovery period may lead to potentially deleterious long-term consequences, such as photoageing and photocarcinogenesis. Grafted human skin appeared to be an attractive and promising model for investigating the biological consequences of UVB radiation in vivo. [source]

Keratocyte repopulation in UVB-exposed thioltransferase knockout mice

Purpose: Thioltransferase is involved in cell protein homeostasis and DNA synthesis. It inhibits apoptosis and stimulates cell proliferation. Keratocyte repopulation after ultraviolet B (UVB) damage was studied in corneas of thioltransferase (-/-) mice. Methods: Six wild type mice and six thioltransferase (-/-) mice corneas were exposed at 300 nm UV-radiation at a dose producing damage in the corneal stroma (8 kJ/m2). Animals were killed 3 and 7 days after exposure. Corneas were processed for light microscopy. Results: All corneas of wild type mice and thioltransferase (-/-) mice showed extensive damage 3 days after UVB exposure. Keratocytes disappeared throughout the entire thickness of the UVB-damaged central stroma. Corneal thickness was nearly doubled compared with non-treated control corneas. However, 7 days after UVB exposure corneas of wild type mice were almost completely repopulated by keratocytes, only superficial of the stroma was still free of keratocytes. Corneal thickness was almost normal. Corneal stroma in the thioltransferase (-/-) mice 7 days after UV exposure was still not repopulated by keratocytes and the corneas were still very thick. Conclusions: The keratocyte repopulation in thioltransferase (-/-) mice is delayed. Thioltransferase seems to play an important role in the corneal wound healing and keratocyte repopulation after UVB induced damage. [source]

Cooler temperatures increase sensitivity to ultraviolet B radiation in embryos and larvae of the frog Limnodynastes peronii

Abstract Recent studies suggest that complex interacting processes are driving global amphibian declines. Increased ultraviolet B (UVB) radiation in the solar spectrum associated with ozone depletion has been implicated in declines, and evidence suggests that the effects of UVB radiation on amphibians may be greater at cooler temperatures. We tested the thermal sensitivity of UVB effects on amphibians in a controlled factorial experiment using the striped marsh frog, Limnodynastes peronii as a model species. We compared survival, growth and locomotor performance of embryonic and larval L. peronii reared under low and high UVB exposures at both 20 and 30 C. Embryonic and larval L. peronii proved extremely sensitive to UVB damage and exhibited greater sensitivity at 20 C compared with 30 C. Embryonic survival to Gosner stage 25 was unaffected by UVB exposure at 30 C, but at 20 C survival was reduced to 52% under high UVB. Larval survival exhibited a similar trend. At 20 C, all tadpoles survived under low UVB, whereas under high UVB there was 100% mortality after 15 days of exposure. At 30 C, 86% survived under low UVB, but only 46% survived under high UVB. Sublethal effects such as, embryonic malformation, retarded larval growth and reduced larval swimming performance were also greater at 20 C compared with 30 C. Our results strongly indicate that UVB damage in amphibians is markedly increased at cooler temperatures. Thus, populations of UVB sensitive species occurring at cold climates may be at greater risk of declines due to increased solar UVB radiation. [source]

Combination of narrow band UVB and topical calcipotriol for the treatment of vitiligo

EO Goktas
Abstract Background, Narrow band ultraviolet B (NB-UVB) phototherapy has been used successfully for the treatment of vitiligo. Recently, topical calcipotriol has also been claimed to be effective, either as monotherapy or as a part of combination therapies. Objective, The aim of the present study was to compare the clinical efficacy of NB-UVB and NB-UVB plus topical calcipotriol in the treatment of vitiligo. Methods, NB-UVB treatment was given to 24 patients with generalized vitiligo three times weekly. Topical calcipotriol cream was only applied to the lesions located on the right side of the body. Treatment was continued for 6 months. Treatment efficacy was evaluated by determining the average response rates of the lesions at 3-month intervals. Results, The average response rates of patients receiving combination of NB-UVB plus calcipotriol and NB-UVB alone were 51 19.6% and 39 18.9%, respectively. The median cumulative UVB dose and number of UVB exposures for initial repigmentation were 6345 mj/cm2 (range; 2930,30980) and 18 (range; 12,67) for the combination therapy, and 8867.5 mj/cm2 (range; 2500,30980) and 24 (range; 15,67) for the narrow band UVB therapy, respectively. Conclusions, These findings indicate that concurrent topical calcipotriol potentates the efficacy of NB-UVB in the treatment of vitiligo. This combination not only provides earlier pigmentation with lower total UVB dosage and less adverse UVB effects, but also reduces the duration and cost of treatment as well. [source]