Low Doses Of UVB Research Articles

Effects of repeated low‐dose UVB irradiation on the hyphal growth of Candida albicans

Ultraviolet B light (UVB) can have negative phototropic effects on fungi. Candida albicans is often found on human skin exposed to UVB. Therefore, it is of medical interest to know whether a negative phototropic response to UVB irradiation can support an invasive growth of this potentially dangerous agent. In our study we investigated how repeated irradiation with low doses of UVB can influence the hyphal growth of C. albicans. Six randomly chosen strains of C. albicans were tested. Formation of hyphae was induced and maintained within transparent agar plates. The fungi were exposed to UVB three times daily for 7 days from either the observe or the reverse side during incubation. The wavelength spectrum was in the range of 310-315 nm, single doses were between 0.0018 and 0.432 J cm(-2). After 7 days the morphology and growth direction of C. albicans cells were determined microscopically. All six strains showed a common and dose-dependent response to UVB irradiation: the progression of hyphal growth was inhibited, no phototropic effects were seen and as a new finding an increased formation of blastospores was observed. We conclude that an irradiation of human skin colonized by C. albicans with doses of UVB that can occur under natural or artificial conditions is unlikely to trigger skin invasion by C. albicans.

Resistance of Human Melanoma Cells Against the Death Ligand TRAIL Is Reversed by Ultraviolet-B Radiation via Downregulation of FLIP

Tumor necrosis factor related apoptosis-inducing ligand (TRAIL) is a potential anticancer drug since it induces apoptosis preferentially in malignant but not in normal cells. Not all cancer cells, however, are TRAIL susceptible. Chemotherapeutic drugs and ionizing radiation have been found to be able to sensitize resistant tumor cells for TRAIL-induced apoptosis. Since ultraviolet B radiation (UVB) is a potent inducer of apoptosis but exhibits much less adverse effects, we studied whether UVB sensitizes TRAIL-resistant melanoma cells. Therefore, we analyzed the TRAIL-sensitive human cell line A-375 in comparison to the resistant cell line IGR-37. Both cell lines showed expression of the long form of the antiapoptotic FLICE inhibitory protein FLIP(L) which, however, was partially cleaved into the 43 kDa form in A-375 cells. In addition, only IGR-37 cells expressed the short splicing variant FLIP(S), which exerts high antiapoptotic activity. Accordingly, transient overexpression of FLIP(S) rendered A-375 cells resistant to TRAIL. Upon exposure to low UVB doses, TRAIL-treated IGR-37 cells underwent pronounced apoptosis and TRAIL sensitivity of A-375 cells was dramatically increased. In both cases, UVB caused an inhibition of flip expression. This study indicates that (i) the expression level and the processing status of FLIP may play a crucial role in determining the sensitivity of melanoma cells towards TRAIL and (ii) expression of FLIP is regulated by UVB.

Effects of enhanced UV-B radiation on the hormonal content of vegetative and reproductive tissues of two tomato cultivars and their relationships with reproductive characteristics

The effects of enhanced UV-B radiation on hormone changes in vegetative and reproductive tissues of tomato (Lycopersicon esculentum Mill.) and their relationships with reproductive characteristics were studied. Two cultivars, TongHui (TH) and XiaGuang (XG), were grown in the field for one growing season under ambient (Control), ambient plus 2.54 kJ m−2 d−1 (T1) or ambient plus 4.25 kJ m−2 d−1 (T2) of supplemental ultraviolet-B (280–320 nm). The number of open flowers increased significantly in the TH cultivar under T2 while it declined in the XG cultivar under T1. Although pollen germination from both cultivars was inhibited by UV-B treatment, fruit number was enhanced in the TH cultivar at both UV-B doses and in the XG cultivar at the low dose. On the other hand, seed size (dry weight) was reduced in the XG cultivar by both UV-B doses and in the TH cultivar at the low UV-B dose. The final germination rates of seeds from control and UV-B treated plants of both cultivars showed no significant differences (p > 0.05), while germination was delayed in the TH cultivar at both doses of UV-B and in the XG cultivar only for T2. To determine the mechanism of UV-B's effects on developmental processes, hormone concentrations in leaves, pistils and seeds were analyzed using ELISA on partially purified extracts. The results suggested that enhanced UV-B radiation induced hormone changes in both vegetative and reproductive tissues. The alteration of flower number may be associated with the changes of ZR in leaves under enhanced UV-B radiation and the delayed germination may due to the changes in seed ABA and GAs.

Effect of low doses of UV-A and UV-B radiation on photosynthetic activities inPhaseolus mungo L.

The effect of low doses of UV-A (320–400 nm) and UV-B (280–320 nm) radiation on photosynthetic activities inPhaseolus mungo L. was investigated under field condition. Supplementation of UV-A enhanced the synthesis of chlorophyll and carotenoids than the UV-B supplemented plants. Significant increase was seen in the concentration of UV-B absorbing compounds of UV-B treated plants. Increase of PS 2 activity in UV-A treated plants was seen. Changes in photosynthetic activity were measured in terms of PS 2 mediated O2 evolution and Chl a fluorescence.

Vertical migration as a response to UVR stress in Calanus finmarchicus females and nauplii

We conducted laboratory experiments to study the behavioural responses of Calanus finmarchicus females and nauplii exposed to artificial ultraviolet radiation (UVR) and photosynthetically active radiation (PAR). Both nauplii and females migrated downwards when exposed to UVR. Nauplii reacted mainly to UV-B radiation, while females responded also to UV-A. Nauplii were also collected in the field to check if vertical distributions supported the experimental findings. Light measurements in Vestfjorden showed that plankton were exposed to quite low doses of UVR most of the time. However, on days with a thin ozone layer, clear sky and low turbidity UV-B doses in the surface waters might be harmful. Strong turbulence in the surface layer prevents nauplii from adjusting their position, exposing them to fluctuating levels of UVR due to vertical mixing. Under calm conditions, however, copepods could migrate sufficiently to avoid harmful UVR doses.

UV dose-dependent caspase activation in a corneal epithelial cell line

Purpose. To characterize the UVB radiation-dependent patterns of caspase activation and cell death in SV 40 immortalized corneal epithelial cells. Methods. Cell death in immortalized human corneal epithelial cells (T-HCEC) was induced by exposure to low (50mJ/cm 2) and high (450mJ/cm 2) doses of UVB. Cell death morphology was examined by fluorescence microscopy using the cell death marker propidium iodide (PI). Apoptosis of T-HCEC was analyzed by DNA fragmentation assays, and enzyme activity was measured for caspase 3 and 9 by fluorophotometry. Changes in mitochondrial inner membrane potential were measured by flow cytometry using the fluorescent marker, rhodamine 123. Redistribution of cytochrome c, the upstream trigger of caspase 9, was measured in the cytosol fraction of T-HCEC following irradiation. Results. PI staining revealed a fragmented staining pattern of the nucleus consistent with apoptosis in detached cells irradiated with low-dose UVB, while cells receiving high dose UVB demonstrated round, well bordered staining of the nucleus. Flow cytometry revealed irreversible mitochondrial damage in the high dose group shown by decreased levels of rhodamine 123 fluorescence. Cells in the low-dose group had intact mitochondrial inner membrane potential, increased cytosolic cytochrome c, and showed a significantly higher rate of DNA fragmentation and caspase activation than the high dose group. Conclusion. Low dose UVB caused cytochrome c redistribution, caspase activation and apoptosis of corneal epithelial cells, which was not observed at high irradiation levels of UVB.

Effects of UVB preconditioning on heat tolerance of cucumber ( Cucumis sativus L.)

To study the preconditioning effects of exposure to UVB on heat tolerance (44–48 °C), 10-day-old cucumber ( Cucumis sativus L.) seedlings were irradiated for 6 days with a daily dose of either 3.4, 5.5 or 10.6 kJ m −2 of biologically effective UVB (UVB BE). Cellulose diacetate-filtered UVB lamps were used to supply UVB. These approximated low, ambient (medium) and twice-ambient (high) UVB doses, respectively, at 42°N latitude on a clear day during the summer solstice. A parallel group of control plants, held under polyester (PE)-filtered UVB lamps, received no UVB. UVB treatment increased the level of methanol-extractable UV-absorbing phenols in cotyledons and primary leaves. In a further HPLC analysis of acid-hydrolyzed leaf extract, eight peaks were separated. The two major peaks were co-chromatographed with authentic flavonoids, quercetin and kaempferol. The quercetin-like compound was preferentially enhanced in UVB-exposed plants. When the low and medium UVB-irradiated plants were later heat-stressed (46 °C, 1 h), survival improved by 112 and 82% and height growth increased by 35 and 40%, respectively, compared with controls that received no UVB. In contrast to low and ambient levels of UVB, which reduced membrane leakage, twice-ambient levels increased lipid peroxidation and electrolyte leakage. Although exposure to above-ambient levels of UVB was injurious, low and ambient doses of UVB promoted survival and growth of cucumber seedlings. Such a synergism between UVB and heat tolerance could be used to precondition seedlings grown in UVB-deficient greenhouses and may benefit plants under the predicted global warming scenario.

20 years after--milestones in molecular photobiology.

Ultraviolet radiation represents one of the most relevant environmental factors because of its hazardous health effects, which include induction of skin cancer, premature skin aging, and exacerbation of infectious diseases. The biologic effects exerted by ultraviolet radiation have been well characterized by a variety of in vitro and in vivo studies. The events taking place inside the cell during the ultraviolet response, however, remained unclear for quite a long time. Molecular photobiology has increased our knowledge about ultraviolet-induced signal transduction enormously within the last 10 years. For a long time, nuclear DNA has been regarded as the only chromophore for ultraviolet radiation. Today we know that ultraviolet radiation can affect also other molecular targets located in the cytoplasm and at the cell membrane. These targets include cell surface receptors, kinases, phosphatases, and transcription factors. Detailed knowledge about ultraviolet-induced signal transduction will certainly increase our understanding of how ultraviolet radiation exerts its biologic effects and furthermore will provide us with tools to interfere with these pathways, thereby reducing the adverse effects of ultraviolet radiation.

Effect of ultraviolet B radiation and 100 Hz electromagnetic fields on proliferation and DNA synthesis of Jurkat cells.

The use of ultraviolet B light (UVB) has been proven to be highly effective for treatment of various inflammatory skin diseases, but UVB phototherapy is limited by its carcinogenic side effects. It is necessary to uncover effectors that augment UVB so that similar or improved efficacy can be obtained with lower UVB doses. We found that low frequency, low intensity electromagnetic fields (EMFs) can act as such an effector and synergistically inhibit T lymphocyte proliferation. We first characterized the effects of UVB on Jurkat cells, a model for cutaneous T lymphocytes, and determined UVB's dose dependent inhibition of cell proliferation and induction of apoptosis. Cells exposed to a sublethal UVB dose retained their sensitivity to UVB, but repetitive irradiation seemed to cause accumulation of delayed DNA damage. We then exposed cells to combinations of UVB plus EMFs and found that 100 Hz, 1 mT EMFs decrease DNA synthesis of UVB-activated Jurkat cells by 34 +/- 13% compared to UVB alone. The decrease is, however, most effective when relatively high UVB doses are employed. Since EMFs alone had only a very weak inhibitory effect (10 +/- 2%), the data suggest that EMFs augment the cell killing effects of UVB in a synergistic way. These findings could provide the basis for development of new and improved clinical phototherapy protocols.

HPV-16 E6/7 Immortalization Sensitizes Human Keratinocytes to Ultraviolet B by Altering the Pathway from Caspase-8 to Caspase-9-dependent Apoptosis

UVB from solar radiation is both an initiating and promoting agent for skin cancer. We have found that primary human keratinocytes undergo an apoptotic response to UVB. To determine whether these responses are altered during the course of immortalization, we examined markers of apoptosis in primary human foreskin keratinocytes (HFK) transduced with either a retroviral vector expressing the E6 and E7 genes of HPV-16 or with empty vector alone (LXSN-HFK). Whereas LXSN-HFK as well as early passage keratinocytes expressing HPV-16 E6 and E7 (p7 E6/7-HFK) were both moderately responsive to UVB irradiation, late passage-immortalized keratinocytes (p27 E6/7-HFK) were exquisitely sensitive to UVB-induced apoptosis. After exposure to UVB, enhanced annexin V-positivity and internucleosomal DNA fragmentation were observed in p27 E6/7-HFK compared with either LXSN- or p7 E6/7-HFK. Caspase-3 fluorometric activity assays as well as immunoblot analysis with antibodies to caspase-3 and poly(ADP-ribose) polymerase revealed elevated caspase-3 activity and processing at lower UVB doses in p27 E6/7-HFK compared with LXSN- or p7 E6/7-HFK. In addition, the caspase inhibitor DEVD-CHO reduced the apoptotic response and increased survival of all three HFK types. Immunoblot analysis revealed that caspase-8 was activated in all three cell types, but caspase-9 was only activated in p27 E6/7-HFK. Cell cycle analysis further showed that only p27 E6/7-HFK exhibit G(2)/M accumulation that is enhanced by UVB treatment. This accumulation was associated with a rapid down-regulation of Bcl-2 in these cells. The immortalization process subsequent to the expression of HPV E6 and E7 may therefore determine UVB sensitivity by switching the mode of apoptosis from a caspase-8 to a Bcl-2-caspase-9-mediated pathway of apoptosis.

Detection of poly(ADP-ribose) by immunocytochemistry: a sensitive new method for the early identification of UVB- and H2O2-induced apoptosis in keratinocytes.

Apoptosis is an active form of cell death that is initiated by a variety of stimuli, including reactive oxygen species (ROS) and ultraviolet (UV) radiation. Poly (ADP-ribose) (PAR) is formed upon activation of the DNA repair enzyme poly(ADP-ribose) polymerase (PARP), and therefore was suggested as a new marker of apoptosis. Since DNA of epidermal cells represents a well-known chromophore for UVB irradiation, and UVB is known to generate H2O2 in keratinocytes, we hypothesized that PAR is a very sensitive marker of UVB- and H2O2-induced apoptosis in keratinocytes. In order to test this hypothesis, human immortalized keratinocytes (HaCaT) were UVB-irradiated or treated with H2O2, and subsequently apoptosis was identified by comparing conventional parameters such as morphological analysis, DNA laddering, and TUNEL assay, with PAR formation. Both, UVB and H2O2 treatment induced PAR formation in HaCaT cells in a dose-dependent manner, and its formation was detected as early as 4 h after irradiation, and at lower UVB doses (10 mJ/cm2) than observed by DNA laddering and the TUNEL assay. In conclusion, the detection of PAR formation is a very sensitive and early method for the identification of apoptotic cells in UVB-induced apoptosis of human keratinocytes.

Ultraviolet B radiation enhances a phytochrome-B-mediated photomorphogenic response in Arabidopsis.

Ultraviolet B radiation (UV-B, 290-315 nm) can cause damage and induce photomorphogenic responses in plants. The mechanisms that mediate the photomorphogenic effects of UV-B are unclear. In etiolated Arabidopsis seedlings, a daily exposure to 2.5 h of UV-B enhanced the cotyledon opening response induced by a subsequent red light (R) pulse. An R pulse alone, 2.5 h of UV-B terminated with a far-red pulse, or 2.5 h of continuous R caused very little cotyledon opening. The enhancing effect of UV-B increased with fluence rate up to approximately 7.58 micromol m(-2) s(-1); at higher fluence rates the response to UV-B was greatly reduced. The phyA, phyA cry1, and cry1 cry2 mutants behaved like the wild type when exposed to UV-B followed by an R pulse. In contrast, phyB, phyB cry1, and phyB phyA mutants failed to open the cotyledons. Thus, phytochrome B was required for the cotyledon opening response to UV-B --> R treatments, whereas phytochrome A and cryptochromes 1 and 2 were not necessary under the conditions of our experiments. The enhancing effect of low doses of UV-B on cotyledon opening in uvr1 uvr2 and uvr1 uvr3 mutants, deficient in DNA repair, was similar to that found in the wild type, suggesting that this effect of UV-B was not elicited by signals derived from UV-B-induced DNA lesions (cyclobutane pyrimidine dimers and 6-4 photoproducts). We conclude that low doses of UV-B, perceived by a receptor system different from phytochromes, cryptochromes, or DNA, enhance a de-etiolation response that is induced by active phytochrome B.

Low Doses of UVB or UVA Induce Chromosomal Aberrations in Cultured Human Skin Cells

Chromosomal defects are frequently present in malignant and premalignant skin disorders; however, it is not known whether ultraviolet radiation from sunlight plays a role in their induction. To obtain information on the ability of ultraviolet A and ultraviolet B to induce chromosomal aberrations, cultured melanocytes and fibroblasts were exposed to physiologic doses of ultraviolet A or ultraviolet B and, for comparison, to gamma rays. As a measure of chromosomal aberrations, the formation of micronuclei was determined. To obtain sufficient statistical data on induced micronuclei and cell kinetics, a flow cytometry method has been modified and applied. The flow cytometry method analysis is based on staining the DNA with ethidium bromide and the cell membranes with 1,6-diphenyl-1,3,5,-hexatriene. We observed dose-dependent micronuclei formation after gamma or ultraviolet B irradiation in both cell types and also for ultraviolet A in fibroblasts. The yield of micronuclei induced in fibroblasts by ultraviolet A was only a factor 15 smaller than that induced by ultraviolet B (313 nm). The results indicate that 10 kJ per m2 (equivalent to 1 minimal erythema dose) of ultraviolet B and 150 kJ per m2 of ultraviolet A (0.2 minimal erythema dose) can induce 1% of micronuclei in fibroblasts, equivalent to the induction due to 0.6 Gy of gamma radiation. In conclusion, physiologic doses of sunlight can induce chromosomal aberrations at a level comparable with that observed after exposure to approximately 1 Gy of ionizing radiation. Therefore, sunlight can be considered a potential inducer of chromosomal aberrations in skin cells, which may contribute to skin carcinogenesis.

Effects of UVB radiation on cytokine generation, cell adhesion molecules, and cell activation markers in T-lymphocytes and peripheral blood HPCs.

Immunomodulatory effects of UV light have increasingly become a focus in transfusion medicine, BMT and transplantation immunology. In the transplant setting, the use of UVB radiation may reduce or abolish T-cell activation without compromising either bone marrow (BM) engraftment or graft-versus-leukemia effect. In this study, BM and apheresis-derived peripheral blood HPCs were used to investigate the effects of UVB on colony-forming ability, CD34+ cell viability, and growth potential, as well as on the secretion of MNC cytokines and the expression of cell surface markers and adhesion molecules. After UVB radiation, enriched populations of T cells and antigen-presenting cells (APCs) were treated with PHA, and the MNC response was measured, as was colony-forming ability. CD34+ cells were quantified and their growth potential was determined in culture. Next, T-cell activation status, cell adhesion molecule and cell surface activation marker expression, and cytokine profiles were evaluated, and cytokine mRNA was quantitated. Parallel studies were done in unirradiated control cell populations. Low-dose (10 mJ/cm(2)) UVB mitigates MNC proliferative responses by 94 percent while maintaining 60 and 80 percent of colony-forming ability in peripheral blood HPC and BM preparations, respectively, and >50 percent of colony-forming ability in CD34+ cell-enriched samples. Low-dose UVB radiation also significantly reduces T-cell production of TNFalpha, TNFalpha mRNA, TNFbeta, IL-2, and IL-6 and downregulates T-cell expression of CD28, CD25, CD69, and intercellular adhesion molecule 1. These findings have shown that a "window" of low-dose UVB radiation (10 mJ/cm(2)) exists, at which BM- and peripheral blood-derived MNC proliferation is inactivated, while the HPCs are relatively spared. UVB light selectively affects T cells, while APCs are resistant to low doses of UVB. UVB radiation also alters the expression of some cell surface markers and cytokines that are important in T-cell activation pathways. Reduction of T-cell activation without cytocidal effect may allow UVB radiation to become an immunomodulating agent in BM or HPC transplantation.

Successful separation of apoptosis and necrosis pathways in HaCaT keratinocyte cells induced by UVB irradiation.

UVB irradiation can induce apoptotic, necrotic, and differentiation pathways in normal human keratinocytes. The present study was undertaken to determine at what dose of UVB each of these pathways is induced and whether these pathways are distinct or overlapping. We have observed that UVB induces fragmentation of DNA in human HaCaT keratinocytes, in a bimodal manner. Low doses of UVB, 5-20 mJ/cm2, increase the levels of apoptosis as shown by increased levels of fragmented DNA, Fas, PARP, and FasL protein, and the number of apoptotic cells as assessed by FACS analysis. At higher doses of UVB (20 and 30 mJ/cm2) the number of apoptotic cells becomes reduced, as does the amount of Fas, PARP, and FasL protein. At these higher doses, cell viability is decreased as measured by DNA synthesis (BrdU labeling) neutral red uptake, which represents an increasing necrotic phenotype. Expression of markers of keratinocyte differentiation, involucrin, keratin K1, and keratin K10, are also observed to decrease with increasing UVB dose. These changes are accompanied by a further increase in DNA fragmentation. We conclude that low doses of UVB (5-20 mJ/cm2) induced an apoptotic pathway, whereas increasing doses (greater than 20 mJ/cm2) of UVB produce a direct necrotic effect and inhibit terminal differentiation.

DNA damage formation, DNA repair, and survival after exposure of DNA repair-proficient and nucleotide excision repair-deficient human lymphoblasts to UVA1 and UVB

Purpose : The comet assay has been used to visualize DNA damage in single cells after exposure to UV light. These comets are commonly thought to reflect transient, repair-induced DNA breaks. The goal of the work presented here was to further characterize the nature of UV-induced comets and to further elucidate DNA damage formation by different wavelengths of ultraviolet light. Materials and methods : Detailed dose–response and time-course experiments with comet formation were carried out with normal and nucleotide excision repair (NER)-deficient xeroderma pigmentosum (XP) lymphoblasts. Irradiation was carried out with low, intermediate, or high doses of UVA1 or UVB, comet formation was observed, cell survival and viability were determined, and UV-induced apoptosis was measured. Results : All responses were dose-dependent. With the intermediate dose of UVA1, a pronounced comet formation was observed without subsequent growth inhibition. Raising levels of porphyrins, which act as photosensitizers, by preincubation with 5-amino-levulinic acid increased comet formation with UVA1, but not with UVB. UVA1-sensitivity and comet formation in XP cells was not significantly different from the normal cells. With UVB no comet formation was seen without subsequent apoptotic cell death. XP cells exhibited the known UVB-hypersensitivity, but their comet formation was not significantly different from that of normal cells. Conclusions : The findings are compatible with the hypothesis that UV-induced comets represent transient repair-induced DNA breaks. Both, the NER of dimers and the base excision repair of oxidative DNA modifications are thought to contribute to comet formation.

Ultraviolet radiation-induced tolerance.

Ultraviolet (UV) radiation is one of the most important environmental factors. Besides its well-known advantages and its indispensable effects on human life, UV light, particularly the middle wavelength range (290-320 nm [UVB]), can harm human health by inducing skin cancer, premature skin aging, inflammation, and cell death (1-4). Over the last 25 years, it has become apparent that exposure to UVB radiation may also suppress immune reactions. Review of the numerous studies on the immunosuppressive properties of UV radiation led to two quite surprising observations: 1) that UV exposure can have systemic immunologic consequences 2) that UV radiation can induce antigen-specific tolerance. This paper briefly reviews the phenomenon of UV-induced tolerance.

Vitality of plaice embryos ( Pleuronectes platessa) at moderate UV-B exposure

The effects of moderate UV-B radiation (280–320 nm) on mortality and on physiologically vital parameters (heart rate, quality of respiratory control) were studied in plaice embryos ( Pleuronectes platessa L.). If UV-B exposure started at the early embryonic stage Ib (with a daily dose similar to present maximum outdoor levels in mid-April: 4.86 kJ m −2), 100% of embryos were dead after 5 days (control: 61% mortality). If light exposure started later (after gastrulation at stage II), however, mortality in test (UV-B irradiated) and control embryos (not UV-B irradiated) was not significantly different. Instantaneous or short-term effects of UV-B exposure on heart rate were absent even at high intensity (0.5 W m −2). With exposure to a daily dose of 4.86 kJ m −2, long-term accumulated effects of UV-B on heart rate were not detectable: heart rate in test and control embryos increased similarly during development from stage IIIγ to hatching. Exposure for a few days at a daily dose of 8.64 kJ m −2 (similar to present maximum outdoor levels in mid-May), however, resulted in significantly lower heart rates in test embryos than in control embryos at stage IVβ. Even 45 days after exposure, sublethal effects of UV-B on dry weight of the larvae, heart rate and quality of respiratory control were detectable in test animals. It is concluded that the vitality of plaice embryos can be impaired, either by relatively low UV-B doses during early development or by higher UV-B doses during late development.

UVB Irradiation Stimulates Deposition of New Elastic Fibers by Modified Epithelial Cells Surrounding the Hair Follicles and Sebaceous Glands in Mice

UVB irradiation stimulates the synthesis of elastin in the skin of humans and experimental animals. In this study we localized the site and the cells that are responsible for the synthesis of murine dermal elastic fibers. SKH-1 hairless mice were irradiated with UVB and the skin removed for light microscopy, electron microscopy, in situ hybridization, immunohistochemistry, and biochemical studies. In response to chronic low doses of UVB there was an initial moderate increase in tropoelastin mRNA in the papillary dermis. By contrast, there was a continuous marked elevation of collagen alpha1(I) message localizing to sites of inflammatory cell influx throughout the upper and lower dermis. After 25 wk of UV irradiation there was a 2-fold increase in skin elastin, yet total collagen remained unchanged. Serial desmosine analysis from en face sections indicated the increase in elastin content was due to dermal elastic fibers, an increase in the size and number of the dermal cysts, and an increase in subpanniculus elastic fibers. Elastin stains of en face sections suggested that the elastic fibers in the upper dermis were exclusively derived from cells lining the epithelial root sheath and sebaceous glands. In response to UV irradiation, the elastic fibers increased in number and size, wrapping around these structures and aligning in both directions as long fibers parallel to the body axis. Electron micrographs indicated that modified epithelial cells in close proximity to the flattened epithelial cells that encircled the root sheath and sebaceous glands were the source of the elastic fibers.

Effects of UV-B radiation on photosynthetic reactions in Rhizophora apiculata

Influences of UV-B radiation on Rhizophora apiculata were studied in terms of chlorophylls, their presence in protein complexes of the chloroplast, PS I and PS II photochemical activities, in vitro absorption spectrum of the chloroplast, in vivo leaf fluorescence and UV absorbing compounds. The seedlings were exposed to the various levels of UV-B radiations, equivalent to 0 (control), 10, 20, 30 and 40% stratospheric ozone depletion of the study area. The low doses of UV-B (10 and 20%) increased the reaction centre chlorophyll (10 and 8%) and activities of PS-I (98 and 39%) and PS-II (77 and 38%) respectively; whereas, 30 and 40% UV-B treatments decreased the reaction centre chlorophylls by 11 and 33% and PS II activity by 0 and 20%; while PS I activity did not show any inhibitory effect. Chloroplasts isolated from control and 10% UV-B treated plants exhibited the same level of absorption at 676 nm. In vivo leaf fluorescence was found to be diminished with UV-B radiation and at the 10% UV-B, variable fluorescence was promoted significantly by 10%. The content of UV-absorbing compounds was progressively enhanced with doses of UV-B radiation along with higher absorption at 276 and 330 nm.