UVB Damage (uvb + damage)

Distribution by Scientific Domains


Selected Abstracts


Selective down-regulation of the ,6-integrin subunit in melanocytes by UVB light

EXPERIMENTAL DERMATOLOGY, Issue 6 2005
Sven Krengel
Abstract:,In vivo, melanocytes bind to laminin (LM) molecules of the basement membrane (BM) via the integrins ,3,1 and ,6,1, and they adhere to neighbouring keratinocytes via E-cadherin. Only few studies have addressed the impact of ultraviolet (UV) light on the interaction of melanocytes with their microenvironment. In this report, we examined the influence of UVB irradiation on the expression of the most important melanocyte-adhesion molecules (E-, N-cadherin, ,2-, ,3-, ,5-, ,6-, ,V-, ,1-, ,3-integrins and ICAM-1) in vitro by flow cytometry. We were able to demonstrate that the ,6-integrin subunit is selectively and reversibly down-regulated by UVB in a dwzm 150ose-dependent manner. In comparison, keratinocytes lacked UVB-inducible alterations in the expression of ,6-integrin. In the presence of LM-1, the UVB-induced down-regulation of ,6-integrin in melanocytes was significantly reduced. Moreover, LM-1 increased the resistance of melanocytes to UVB-induced cell death, as measured by annexinV-binding analysis. This effect was reversed by preincubation with an ,6-integrin-blocking antibody. By immunofluorescence, we could demonstrate that UVB leads to a dose-dependent internalization of ,6-integrin, providing an obvious explanation for the down-regulation on the outer cell surface observed by flow cytometry. We suggest that adhesion to LM-1 through ,6-integrin represents a protective mechanism for melanocytes to withstand UVB damage. Through ,6-integrin internalization, sunburns might alter the interaction between melanocytes and the BM, resulting in apoptosis induced by loss of anchorage (anoikis). Repeated sunburns may then lead to the selection of a population of melanocytes which are capable of anchorage-independent survival, culminating in solar nevogenesis and melanoma development. [source]


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

GLOBAL CHANGE BIOLOGY, Issue 6 2007
VINCENT O. Van UITREGT
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]


Adaptive response of the skin to UVB damage: role of the p53 protein

INTERNATIONAL JOURNAL OF COSMETIC SCIENCE, Issue 1 2006
L. Verschooten
Synopsis Different adaptation mechanisms like heat shock response, cell cycle arrest and DNA repair, melanin pigmentation and thickening of the epidermis are present in the human skin to protect against the adverse effects of solar UV irradiation. When DNA damage is beyond repair, cells undergo apoptosis to prevent their replication. We discuss the current knowledge on these different adaptation mechanisms to UVB damage, the most energetic fraction of solar UV that reaches the skin. As p53 protein, the guardian of the genome, plays a key role in protective response to genotoxic damage, its role in this adaptive response of the skin to UV will be further discussed. Résumé Pour se protéger contre les effets néfastes de l'irradiation UV de la lumière solaire, la peau humaine dispose de différents mécanismes de protection adaptatifs: résistance au choc thermique, arrêt du cycle cellulaire et réparation de l'ADN, pigmentation mélanique et épaississement de l'épiderme. Quand les altèrations dépassent les capacités de réparation, les cellules entrent en apoptose pour empêcher la réplication d'une cellule avec de l'ADN endommagé. Dans cet article, on passe en revue les connaissances actuelles sur les différents mécanismes d'adaptation de la peau aux altérations provoquées par les UVB, la fraction la plus énergétique des UV solaires qui atteint la peau. Puisque la protéine P53, gardienne du génome, joue un rôle clé dans la réponse de protection aux altérations génotoxiques, son rôle dans la réponse d'adaptation de la peau aux UV sera discuté en détail. [source]


The effects of EGb 761 on lipid peroxide levels and superoxide dismutase activity in sunburn

PHOTODERMATOLOGY, PHOTOIMMUNOLOGY & PHOTOMEDICINE, Issue 3 2002
Mehtap Kilinc Ozkur
Background/Purpose: Free oxygen radicals are involved in inflammatory skin reactions induced by ultraviolet B (UVB). In this study, the effect of a herbal antioxidant Ginkgo biloba extract (EGb 761) was investigated in UVB irradiated mice skin. Methods: The study was carried out on four groups of mice (n = 6 in each group). The first group was a control group (G1). The second group (G2) was only exposed to acute UVB irradiation. The third group (G3) received 100 mg/kg/day of EGb 761 orally for 5 days before UVB irradiation and the fourth group (G4) was given only a single dose of EGb 761 immediately after UVB irradiation. Eighteen hours after exposing to UVB, lipid peroxide levels, and superoxide dismutase (SOD) activities were studied and UVB damage was evaluated histopathologically according to ,sun-burn cell count'. Results: The SOD activities and Malondialdehyde (MDA) levels in G2, G3 and G4 were found to be decreased significantly when compared with G1 (P < 0.05). The SOD activities of G3 and G4 were higher when compared with G2 (P < 0.05). The number of sunburn cells (SBCs) was the highest in G2. Conclusions: Our results suggest that EGb 761 may have an important effect, both as a protective and therapeutic agent, in sunburn after UVB irradiation. [source]