Doses Of ultraviolet-B Radiation Research Articles

Exposure to ultraviolet-B radiation increases the susceptibility of mosquitoes to infection with dengue virus.

By 2100, greenhouse gases are predicted to reduce ozone and cloud cover over the tropics causing increased exposure of organisms to harmful ultraviolet-B radiation (UVBR). UVBR damages DNA and is an important modulator of immune function and disease susceptibility in humans and other vertebrates. The effect of UVBR on invertebrate immune function is largely unknown, but UVBR together with ultraviolet-A radiation impairs an insect immune response that utilizes melanin, a pigment that also protects against UVBR-induced DNA damage. If UVBR weakens insect immunity, then it may make insect disease vectors more susceptible to infection with pathogens of socioeconomic and public health importance. In the tropics, where UVBR is predicted to increase, the mosquito-borne dengue virus (DENV), is prevalent and a growing threat to humans. We therefore examined the effect of UVBR on the mosquito Aedes aegypti, the primary vector for DENV, to better understand the potential implications of increased tropical UVBR for mosquito-borne disease risk. We found that exposure to a UVBR dose that caused significant larval mortality approximately doubled the probability that surviving females would become infected with DENV, despite this UVBR dose having no effect on the expression of an effector gene involved in antiviral immunity. We also found that females exposed to a lower UVBR dose were more likely to have low fecundity even though this UVBR dose had no effect on larval size or activity, pupal cuticular melanin content, or adult mass, metabolic rate, or flight capacity. We conclude that future increases in tropical UVBR associated with anthropogenic global change may have the benefit of reducing mosquito-borne disease risk for humans by reducing mosquito fitness, but this benefit may be eroded if it also makes mosquitoes more likely to be infected with deadly pathogens.

Maslinic acid attenuates UVB-induced oxidative damage in HFF-1 cells.

Oxidative damage is one of the major mechanisms of ultraviolet B (UVB)-induced damage to the skin. Maslinic acid (MA) is a natural compound of pentacyclic triterpene acids. It has been proved to have anti-inflammatory and antioxidant properties. This study aimed to explore the effects of MA on oxidative damage in human foreskin fibroblast cells (HFF-1) and the potential molecular mechanisms. A specific dose of UVB radiation was used to induce oxidative damage in HFF-1. Based on this, we performed measurements of cell proliferation, reactive oxygen species (ROS) levels, antioxidant enzyme activity, inflammation-related mediators, and NF-κB nuclear localization with or without the addition of MA. MA significantly promoted cell proliferation viability at 10 and 20 μM. The addition of MA 24 h before UVB irradiation was more effective at enhancing cell proliferation and also produced lower ROS levels compared to co-cultured fibroblasts and MA for 24 h after irradiation. However, there was no statistically significant difference between groups at concentrations of 10 and 20 μM. The pretreatment group with MA had elevated superoxide dismutase and catalase activities, decreased IL-6 generation, and lowered mRNA levels of IL-6, TNF-α and MMP3 in comparison with the UVB-irradiated group without additional MA. Meanwhile, the nuclear translocation of NF-κB and the degradation of IκB were inhibited by MA pretreatment. Taken together, these findings suggest that MA may alleviate UVB-induced oxidative damage in HFF-1 by inhibiting the nuclear translocation of NF-κB.

Preharvest UV-B Treatment Improves Strawberry Quality and Extends Shelf Life

Postharvest ultraviolet B (UV-B) radiation has been used to control pathogen incidence on fresh produce, but little attention has been paid to preharvest UV-B effect on strawberry fruit quality and storage. In this study, strawberry (Fragaria × ananassa Duch. cv Albion) plants grown in greenhouse were irradiated with UV-B lamps with an intensity of 0.7362 J/s m2 for 1 and 2 h every day from 5–7 pm after flowering. Fruits were harvested at red stage for quality evaluation. The results indicated that the preharvest UV-B-treated fruits had lighter color (increased L*) than the control. Total soluble solids (TSS), total phenolics content (TPS) and total anthocyanin content (TAC) of UV-B-treated fruits were higher than for the control fruits. There were no significant differences in any of the quality traits between UV-B one-hour and two-hour treatments. We further evaluated the fruit quality when stored at 5 °C on day 7 and day 14. Compared to untreated control, UV-B-treated fruits retarded decrease in L*, TSS, TPS, TAC and firmness, and reduced fruit decay. Examination of expression of genes related to UV-B signaling indicated that HY5 was the major component of UV-B signaling during the green and white stages. However, anthocyanin genes were highly responsive to UV-B treatment during the red stage. Our results suggest that utilization of a low dose of UV-B radiation during the growth stage can improve strawberry fruit quality, and extend shelf life. This research facilitates the utilization of preharvest UV-B treatment for improving fruit quality in controlled environment agriculture.

Temperature causes species-specific responses to UV-induced DNA damage in amphibian larvae.

Anthropogenic ozone depletion has led to a 2–5% increase in ultraviolet B radiation (UVBR) levels reaching the earth's surface. Exposure to UVBR causes harmful DNA damage in amphibians, but this is minimized by DNA repair enzymes such as thermally sensitive cyclobutane pyrimidine dimer (CPD)-photolyase, with cool temperatures slowing repair rates. It is unknown whether amphibian species differ in the repair response to a given dose of UVBR across temperatures. We reared larvae of three species (Limnodynastes peronii, Limnodynastes tasmaniensis and Platyplectrum ornatum) at 25°C and acutely exposed them to 80 µW cm−2 UVBR for 2 h at either 20°C or 30°C. UVBR-mediated DNA damage was measured as larvae repaired damage in photoreactive light at their exposure temperatures. Cool temperatures increased DNA damage in two species and slowed DNA repair rate in P. ornatum. The magnitude of DNA damage incurred from UVBR was species-specific. Platyplectrum ornatum had the lowest CPDs and DNA repair rates, and the depressive effects of low temperature on photorepair were greater in L. tasmaniensis. Considering the susceptibility of most aquatic organisms to UVBR, this research highlighted a need to consider the complexity of species-specific physiology when forecasting the influence of changing UVBR and temperature in aquatic ecosystems.

Moderate Low UVB Irradiation Modulates Tumor-associated Macrophages and Dendritic Cells and Promotes Antitumor Immunity in Tumor-bearing Mice.

Excessive, high doses of ultraviolet B (UVB) UVB irradiation are known to cause skin cancer, aging and immunosuppression. On the contrary, moderate low doses of UVB irradiation are shown to be essential and beneficial to human health, including a tumor-suppressive effect. However, the mechanism by which low levels of UVB suppress tumorigenesis remains unclear. Here, using tumor-bearing mouse models, we show that moderate low repetitive UVB irradiation increases the percentage of activated CD4+ and CD8+ T cells, and CD103+ conventional type 1 dendritic cells (cDC1s), while it decreases the number of immunosuppressive, M2-like macrophages in the tumors. Finally, in mice, deletion of Batf3, a transcription factor critical for the development of conventional dendritic cells, including the CD103+ cDC1s, showed increased tumor growth in both sham- and UVB-irradiated mice. Our findings demonstrate that moderate low UVB irradiation inhibits M2-like tumor-associated macrophages, increases CD103+ cDC1s and promotes antitumor immunity in mice with an established tumor.

Dietary Restriction Attenuates Inflammation and Protects Mouse Skin from High-Dose Ultraviolet B Irradiation.

Ultraviolet B (UVB) radiation may influence the occurrence or even worsen cutaneous disorders from inflammatory to neoplastic disorders. Dietary restriction (DR) is a well-known regimen that can retard aging-associated pathologies, and is shown by us and others that it can significantly inhibit inflammation under various conditions, including in both undisturbed and stressed settings. It is unknown whether DR could act as a nonpharmacological factor to protect skin against UVB-induced damage. In this study, we performed 30% DR to mice 1 week before UVB irradiation (798.6 mJ/cm2). Remarkably, continuous DR significantly ameliorated UVB-induced skin damage and histological changes, associated with a great reduction in the inflammatory responses in the skin. Intriguingly, refed DR mice with ad libitum diet even 24 hours postirradiation reinflamed the inflammatory responses and induced significantly strong damage to the skin. Together, this study provides the first experimental evidence that DR greatly protects mouse skin from high dose of UVB irradiation, which if translatable could have great implications in human beings.

Effect of Ultraviolet B Irradiation on Melanin Content Accompanied by the Activation of p62/GATA4-Mediated Premature Senescence in HaCaT Cells.

ObjectiveTo explore the effect and mechanism of ultraviolet B (UVB) on melanin synthesis and premature senescence in human immortalized keratinocytes (HaCaT) cells.MethodsHaCaT cells were irradiated with 0, 20, 50, 80, 100, 150, and 200 mJ/cm2 of UVB. NaOH method was used for melanin content assay, cellular tyrosinase (TYR) activity was determined by 3,4-Dihydroxy-L-phenylalanine (L-DOPA) oxidation to dopachrome, premature senescence was analyzed by senescence-associated beta-galactosidase (SA-β-gal) staining kit, and the levels of p21, p16, p62, and GATA4 proteins were detected by Western blotting. Premature senescence was inhibited by the inhibitors of ataxia telangiectasia mutated (ATM) or ataxia telangiectasia and Rad3–related (ATR), and the p53 signaling pathway was activated by Nutlin-3. The mRNA levels of senescence-associated secretory phenotype (SASP) factors including tumor necrosis factor alpha (TNF-α), vascular endothelial growth factor A (VEGF-A), and interleukin-8 (IL-8) were measured by real-time quantitative polymerase chain reaction in HaCaT cells after 80 mJ/cm2 of UVB irradiation.ResultsThe melanin level increased significantly with the elevation of irradiation dose (F = 28.19, 43.82, 143.60, P < .05), reaching the peak at the dose of 80 mJ/cm2. The tyrosinase activity increased significantly (F = 84.50, P < .05), the percentage of premature senescence increased (F = 16.31, P < .05), the levels of p62 decreased, and the level of GATA4 increased obviously with the increase of UVB dose after irradiation. The UVB-induced promotion of GATA4 level was significantly inhibited by being treated with ATM or ATR inhibitor. However, this did not occur in the Nutlin-3-treated group. The mRNA and protein expression of TNF-α increased significantly at 72 h at 80 mJ/cm2 of UVB irradiation.ConclusionsMelanin contents increased first and decreased afterward with the increasing of UVB irradiation. The decrease of p62-mediated selective autophagy was accompanied by the accumulation of GATA4 after different doses of UVB irradiation. Activation of this p62/GATA4 pathway depends on the ATM and ATR but is independent of p53, and the SASP factor was activated in HaCaT cells at 80 mJ/cm2 of UVB irradiation.

Engineered nanoceria modulate neutrophil oxidative response to low doses of UV-B radiation through the inhibition of reactive oxygen species production.

To avoid aging and ultraviolet mediated skin disease the cell repair machinery must work properly. Neutrophils, also known as polymorphonuclear leukocytes, are the first and most abundant cell types which infiltrate sites of irradiation and play an important role in restoring the microenvironment homeostasis. However, the infiltration of neutrophils in ultraviolet-B (UV-B) irradiated skin might also contribute to the pathophysiology of skin disease. The polymorphonuclear leukocytes activation induced by UV-B exposure may lead to prolonged, sustained NADPH oxidase activation followed by an increase in reactive oxygen species (ROS) production. Our previous work showed that cerium oxide nanoparticles can protect L929 fibroblasts from ultraviolet-B induced damage. Herein, we further our investigation of engineered cerium oxide nanoparticles (CNP) in conferring radiation protection specifically in modulation of neutrophils' oxidative response under low dose of UV-B radiation. Our data showed that even low doses of UV-B radiation activate neutrophils' oxidative response and that the antioxidant, ROS-sensitive redox activities of engineered CNPs are able to inhibit the effects of NADPH oxidase activation while conferring catalase and superoxide dismutase mimetic activity. Further, our investigations revealed similar levels of total ROS scavenging for both CNP formulations, despite substantial differences in cerium redox states and specific enzyme-mimetic reaction activity. We therefore determine that CNP activity in mitigating the effects of neutrophils' oxidative response, through the decrease of ROS and of cell damage such as chromatin condensation, suggests potential utility as a radio-protectant/therapeutic against UV-B damage.

Identification of UV-B radiation responsive microRNAs and their target genes in chrysanthemum (Chrysanthemum morifolium Ramat) using high-throughput sequencing

MicroRNAs (miRNA) play a key roles in ultraviolet-B (UV-B) induced accumulation of bioactive ingredients in plants. Chrysanthemum (Chrysanthemum morifolium Ramat) is a popular ornamental herb with numerous biological activities, but its miRNAs and their roles in UV-B-induced active ingredient accumulation remain unexplored. High-throughput miRNA sequencing technology was used to identify miRNAs responsive to UV-B radiation. Four libraries were constructed from Chrysanthemum ‘Xiaoyangju’ leaves harvested at different time points under UV-B radiation. In total, 245 miRNAs belonging to 42 classical families were identified. Under UV-B treatment, 137 miRNAs showed differential expression, including 71 known and 67 novel miRNAs,. In addition, 1,779 unique target genes involving diverse biological processes were predicted for 80 known and 85 novel miRNAs. Three key glycolysis genes, Glyceraldehyde-3-Phosphate Dehydrogenase, Pyruvate Kinase and Glucan Endo-1,3-beta-D-Glucosidase, were predicated as potential target genes of miR396f-5p, PC-5p-294053_21 and miR397a, respectively. Among identified target genes, five key genes involved in the biosynthesis of chlorogenic acids and flavonoids were predicated as potential targets genes of MIR4367-p5, PC-3p-40855_284, MIR393b-p5, and PC-3p-114893_93. The expression of identified miRNAs relating to bioactive ingredient biosynthesis was significantly affected by UV-B radiation, suggesting a strong effect of UV-B radiation on bioactive ingredient accumulation in Chrysanthemum. Interestingly, several miRNAs related to flavonoids biosynthesis such as PC-3p-114893_93 and MIR4367-p5, were inhibited by short-term UV-B radiation, suggesting that the contribution of UV-B to flavonoids accumulation depends on a low dose of UV-B radiation.

Comparative proteomic analysis of Nostoc flagelliforme reveals the difference in adaptive mechanism in response to different ultraviolet-B radiation treatments.

Nostoc flagelliforme is a pioneer organism in the desert and highly resistant to ultraviolet B (UV-B) radiation, while the involved adaptive mechanism has not been fully explored yet. To elucidate the responsive mechanism, two doses of UV-B radiation (low: 1W/m2 and high: 5W/m2) were irradiated for 6h and 48h, respectively, and their effects on global metabolism in N. flagelliforme were comprehensively investigated. In this study, we used iTRAQ-based proteomic approach to explore the proteomes of N. flagelliforme, and 151, 172, 124 and 148 differentially expressed proteins were identified under low and high UV-B doses for 6h and 48h, respectively. Functional classification analysis showed these proteins were mainly involved in photosynthesis, amino acid metabolism, antioxidant activity and carbohydrate metabolism. Further analysis revealed that UV-B imposed restrictions on primary metabolism including photosynthesis, Calvin cycle, and amino acid metabolism, and cells started defense mechanism through repair of DNA and protein damage, increasing antioxidant activity, and accumulating extracellular polysaccharides to minimize the damage. Moreover, high UV-B dose imposed more severe restrictions and activated stronger defense mechanism compared with low dose. The results would improve the understanding of molecular mechanisms of UV-B-stress adaption in N. flagelliforme.

Effect of Lycium barbarum polysaccharide on expression of vascular endothelial growth factor and hypoxia inducible factor-1α in ultraviolet B-radiated HaCaT cells

Objective To evaluate effects of Lycium barbarum polysaccharide (LBP) on expression of vascular endothelial growth factor (VEGF) and hypoxia inducible factor-1α (HIF-1α) in ultraviolet B (UVB) -radiated HaCaT cells. Methods Conventionally cultured HaCaT cells were divided into control group and LBP groups, which were firstly treated with DMEM, 12.5, 25.0, 50.0 and 100 μg/ml LBP solution respectively for 4 hours, and then were irradiated by UVB at different intensity of 0, 20, 40, 60 mJ/cm2 separately. After 24-hour continuing culture, CCK-8 assay was performed to determine the cell survival rate, and an enzymatic-biochemical method to estimate the activity of superoxide dismutase (SOD) . RT-PCR and Western blot analysis were conducted to measure the mRNA and protein expression of HIF-1α and VEGF respectively. Results Compared with the control group at the same UVB radiation dose, the 12.5-, 25.0-and 100.0-μg/ml LBP groups showed different extents of increase in survival rates of UVB-radiated cells (P < 0.05) , and the 50.0-μg/ml LBP group showed the highest cell survival rate (P < 0.01) . Among all the LBP groups, SOD activity was highest in the 50.0-μg/ml LBP group (P < 0.01) . Along with the increase of UVB radiation dose, the mRNA and protein expression of HIF-1α and VEGF all gradually increased. Compared with the control group, the 50.0-μg/ml LBP group could effectively reduce the mRNA and protein expression of HIF-1α and VEGF in HaCaT cells (all P < 0.05) . Conclusion LBP may play a role in protecting cells from UVB radiation-mediated damage, likely by influencing the mRNA and protein expression of HIF-1α and VEGF in HaCaT cells. Key words: Ultraviolet rays; Lycium barbarum; Polysaccharides; Endothelial growth factors; Hypoxia inducible factor 1α; HaCaT cells

Mirabilis Jalapa L. Protein as Inductor of Apoptosis on UVB-induced Skin Damage in Mice

Background: Mirabilis jalapa L. protein (MJ-Protein) has been shown to have antioxidant and anti-inflammatory effects in vitro. Thus, it has a potential protective effect against ultraviolet B (UVB)-induced skin damage.Objective: To determine the protective effect and mechanism of MJ protein in UVB-radiation exposed mouse skin.Methods: In this experimentalstudy, 30 female BALB/c mice aged 6 weeks were exposed to a single dose of UVB irradiation with 3 minimal erythema doses (MEDs) and continued with the treatment of 0.6 mg MJ-Protein topically. The number of apoptotic body (sunburn cells) formed in epidermal layers of mouse dorsal skin was assessed at 1, 24, 48, 72, 96 and 120h after UVB irradiation was compared to that of the control group. The difference in the sunburn cells number between two groups were analyzed using independent T-test with the level of significance of 0.05. The apoptosis mechanism was confirmed qualitatively by caspase-3 and DNA fragmentation analysis in vitro.Results:At 24 h after the UVB exposure (peak time for sunburn cells formation), there was a significant increase in the sunburn cells number in the group treated with topical application of MJ-Protein. There was increased caspase-3 expression and DNA fragmentation in HeLa cells treated with MJ-Protein.Conclusions: MJ-Protein protects againts UVB-induced skin damage in mice trough apoptosis induction.Bangladesh Journal of Medical Science Vol.16(3) 2017 p.423-427

Distinct physiological and metabolic reprogramming by highbush blueberry (Vaccinium corymbosum) cultivars revealed during long-term UV-B radiation.

Despite the Montreal protocol and the eventual recovery of the ozone layer over Antarctica, there are still concerns about increased levels of ultraviolet-B (UV-B) radiation in the Southern Hemisphere. UV-B induces physiological, biochemical and morphological stress responses in plants, which are species-specific and different even for closely related cultivars. In woody plant species, understanding of long-term mechanisms to cope with UV-B-induced stress is limited. Therefore, a greenhouse UV-B daily course simulation was performed for 21 days with two blueberry cultivars (Legacy and Bluegold) under UV-BBE irradiance doses of 0, 0.07 and 0.19 W m-2 . Morphological changes, photosynthetic performance, antioxidants, lipid peroxidation and metabolic features were evaluated. We found that both cultivars behaved differently under UV-B exposure, with Legacy being a UV-B-resistant cultivar. Interestingly, Legacy used a combined strategy: initially, in the first week of exposure its photoprotective compounds increased, coping with the intake of UV-B radiation (avoidance strategy), and then, increasing its antioxidant capacity. These strategies proved to be UV-B radiation dose dependent. The avoidance strategy is triggered early under high UV-B radiation in Legacy. Moreover, the rapid metabolic reprogramming capacity of this cultivar, in contrast to Bluegold, seems to be the most relevant contribution to its UV-B stress-coping strategy.

Hsa-miR-520d-5p promotes survival in human dermal fibroblasts exposed to a lethal dose of UV irradiation.

We previously reported that hsa-miR-520d-5p is functionally involved in the induction of the epithelial–mesenchymal transition and stemness-mediated processes in normal cells and cancer cells, respectively. On the basis of the synergistic effect of p53 upregulation and demethylation induced by 520d-5p, the current study investigated the effect of this miRNA on apoptotic induction by ultraviolet B (UVB) light in normal human dermal fibroblast (NHDF) cells. 520d-5p was lentivirally transfected into NHDF cells either before or after a lethal dose of UVB irradiation (302 nm) to assess its preventive or therapeutic effects, respectively. The methylation level, gene expression, production of type I collagen and cell cycle distribution were estimated in UV-irradiated cells. NHDF cells transfected with 520d-5p prior to UVB irradiation had apoptotic characteristics, and the transfection exerted no preventive effects. However, transfection with 520d-5p into NHDF cells after UVB exposure resulted in the induction of reprogramming in damaged fibroblasts, the survival of CD105-positive cells, an extended cell lifespan and prevention of cellular damage or malfunction; these outcomes were similar to the effects observed in 520d-5p-transfected NHDF cells (520d/NHDF). The gene expression of c-Abl (Abelson murine leukemia viral oncogene homolog 1), ATR (ataxia telangiectasia and Rad3-related protein), and BRCA1 (breast cancer susceptibility gene I) in transfectants was transcriptionally upregulated in order. These mechanistic findings indicate that ATR-dependent DNA damage repair was activated under this stressor. In conclusion, 520d-5p exerted a therapeutic effect on cells damaged by UVB and restored them to a normal senescent state following functional restoration via survival of CD105-positive cells through c-Abl-ATR-BRCA1 pathway activation, p53 upregulation, and demethylation.

Postharvest UV-B treatments increased fructose content of tomato (Solanum lycopersicon L. cv. Tayfun F1) harvested at different ripening stages

In the postharvest stage, taste and flavor are the key components of the marketability of tomato. Therefore, greater emphasis is now being placed on improving traits such as sugar content. In this study postharvest ultraviolet-B (UV-B) treatments on sugar, total soluble solids, and color of tomatoes harvested at different stages were investigated. Tomatoes harvested at turning, pink, and red stages were treated with two different doses of UV-B irradiation: UVB4 and UVB8. Color L* and hue angle values of tomatoes treated with UV-B were found to be high, which means the red color of tomatoes was improved. UVB4 treatments increased the color a* and saturation index values of tomatoes at pink and red harvest stage, although it did not affect at the turning stage. Additionally, UV-B irradiation treatments had no effect on sucrose content of the tomatoes. Fructose, glucose, and TSS content of tomatoes treated with UVB8 at red harvest stage were found to be high. Hence, the results obtained from this study are of great importance in terms of providing an increase in the amount of sugar without the need for breeding, and also consumer satisfaction.

Molecular and sensory mechanisms to mitigate sunlight-induced DNA damage in treefrog tadpoles

The increased incidence of solar ultraviolet B (UVB) radiation has been proposed as an environmental stressor, which may help to explain the enigmatic decline of amphibian populations worldwide. Despite growing knowledge regarding the UV-induced biological effects in several amphibian models, little is known about the efficacy of DNA repair pathways. In addition, little attention has been given to the interplay between these molecular mechanisms with other physiological strategies that avoid the damage induced by sunlight. Here, DNA lesions induced by environmental doses of solar UVB and UVA radiation were detected in genomic DNA samples of treefrog tadpoles (Hypsiboas pulchellus) and their DNA repair activity was evaluated. These data were complemented by monitoring the induction of apoptosis in blood cells and tadpole survival. Furthermore, the tadpoles' ability to perceive and escape from UV wavelengths was evaluated as an additional strategy of photoprotection. The results show that tadpoles are very sensitive to UVB light, which could be explained by the slow DNA repair rates for both cyclobutane pyrimidine dimers (CPDs) and pyrimidine (6,4) pyrimidone photoproducts (6,4PPs). However, they were resistant to UVA, probably as a result of the activation of photolyases during UVA irradiation. Surprisingly, a sensory mechanism that triggers their escape from UVB and UVA light avoids the generation of DNA damage and helps to maintain the genomic integrity. This work demonstrates the genotoxic impact of both UVB and UVA radiation on tadpoles and emphasizes the importance of the interplay between molecular and sensory mechanisms to minimize the damage caused by sunlight.

Response of two cultivars of Phaseolus vulgaris L. (French beans) plants exposed to enhanced UV-B radiation under mountain ecosystem.

Enhanced solar ultraviolet-B (UV-B) irradiance resulting from depletion in the ozone layer has the potential to cause detrimental effects on plants. Higher altitudes tend to receive higher doses of ambient UV-B radiation. The present study was carried out to assess the effects of enhanced UV-B (ambient + 10.2 kJ m(-2) day(-1)) radiation on two cultivars of Phaseolus vulgaris L. (cv. Pusa Himlata and Pusa Parvati) at growth, physiological, and biochemical levels grown under mountain ecosystem. The magnitudes of negative effects of enhanced UV-B radiation were found more in Pusa Parvati as compared to Pusa Himlata. Non-enzymatic (total phenolics and flavonoids content) and enzymatic antioxidants (superoxide dismutase, catalase, and peroxidase) were increased in both cultivars at both the ages of growth but increase was found more in Pusa Himlata as compared to Pusa Parvati. The study further showed that the economic yield of Pusa Himlata and Pusa Parvati was decreased by 14 and 44%, respectively, due to enhanced UV-B radiation. The higher decrease in the economic yield of Pusa Parvati depicted that increased amounts of total flavonoids content and stimulation of their antioxidant defense mechanism via increasing the activities of enzymatic antioxidants were not able to completely detoxify the produced reactive oxygen species under enhanced UV-B radiation and made it more sensitive to applied stress. From the present study, it can be concluded that enhanced UV-B radiation in the mountain areas of the Indian Himalayan Regions could be one of the environmental causes for lower yields of agricultural crops. Cultivation of P. vulgaris L. cv. Pusa Himlata should be promoted at higher altitudes of the Indian Himalayan Regions.

Dietary Milk Sphingomyelin Prevents Disruption of Skin Barrier Function in Hairless Mice after UV-B Irradiation.

Exposure to ultraviolet-B (UV-B) irradiation causes skin barrier defects. Based on earlier findings that milk phospholipids containing high amounts of sphingomyelin (SM) improved the water content of the stratum corneum (SC) in normal mice, here we investigated the effects of dietary milk SM on skin barrier defects induced by a single dose of UV-B irradiation in hairless mice. Nine week old hairless mice were orally administrated SM (146 mg/kg BW/day) for a total of ten days. After seven days of SM administration, the dorsal skin was exposed to a single dose of UV-B (20 mJ/cm2). Administration of SM significantly suppressed an increase in transepidermal water loss and a decrease in SC water content induced by UV-B irradiation. SM supplementation significantly maintained covalently-bound ω-hydroxy ceramide levels and down-regulated mRNA levels of acute inflammation-associated genes, including thymic stromal lymphopoietin, interleukin-1 beta, and interleukin-6. Furthermore, significantly higher levels of loricrin and transglutaminase-3 mRNA were observed in the SM group. Our study shows for the first time that dietary SM modulates epidermal structures, and can help prevent disruption of skin barrier function after UV-B irradiation.

Effects of different light conditions on repair of UV-B-induced damage in carpospores of Chondrus ocellatus Holm

We evaluated the effects of ultraviolet-B (UV-B) radiation and different light conditions on the repair of UV-B-induced damage in carpospores of Chondrus ocellatus Holm (Rhodophyta) in laboratory experiments. Carpospores were treated daily with different doses of UV-B radiation for 48 days, when vertical branches had formed in all treatments; after each daily treatment, the carpospores were subjected to photosynthetically active radiation (PAR), darkness, red light, or blue light during a 2-h repair stage. Carpospore diameters were measured every 4 days. We measured the growth and cellular contents of cyclobutane pyrimidine dimers (CPDs), chlorophyll a, phycoerythrin, and UV-B-absorbing mycosporine-like amino acids (MAAs) in carpospores on Day 48. Low doses of UV-B radiation (36 and 72 J/m2) accelerated the growth of C. ocellatus. However, as the amount of UV-B radiation increased, the growth rate decreased and morphological changes occurred. UV-B radiation significant damaged DNA and photosynthetic pigments and induced three kind of MAAs, palythine, asterina-330, and shinorine. PAR conditions were best for repairing UV-B-induced damage. Darkness promoted the activity of the DNA darkrepair mechanism. Red light enhanced phycoerythrin synthesis but inhibited light repair of DNA. Although blue light, increased the activity of DNA photolyase, greatly improving remediation efficiency, the growth and development of C. ocellatus carpospores were slower than in other light treatments.

Effects of ultraviolet B on the expressions of nuclear factor-κB p65 and its inhibitory factor IκBα in keratinocytes

Objective To investigate the regulatory effects of different doses of ultraviolet B (UVB) radiation on the expressions of nuclear factor (NF)-κB p65 and its inhibitory factor IκBα in human keratinocytes cultured in vitro.Methods A human keratinocyte cell line CRL-2310 and primary human keratinocytes were used in this study.Both CRL-2310 and primary human keratinocytes were irradiated with 4.5,10 and 50 mJ/cm2 UVB,with unirradiated cells serving as the control.Western blot was performed to determine the expression levels of total IκBα,NF-κB p65 and IKKβ1 proteins in the cells at 4 hours after the irradiation.Some primary human keratinocytes were irradiated with 50 mJ/cm2 UVB,and Western blot was conducted to measure the expression levels of total and phosphorylated IκBα,NF-κB p65 and IKKβ1 proteins in these cells at 2,4,8,and 12 hours after the irradiation respectively.The optical density of protein bands was analyzed by the Quantity One software (version 4.6.8),the product of the optical density and area of each band was calculated for IKKβ,IκBα,NF-κB p65,β-actin as well as phosphorylated IKKβ,IκBα,and NF-κB p65 separately,and the expression levels of target proteins were expressed as the ratio of the product for the target proteins to that for β-actin.All experiments were repeated for three times,and the average expression levels were calculated for these proteins.Results No significant changes were observed in the CRL-2310 keratinocytes or the primary keratinocytes for the protein expression levels of total IKKβ,IκBα and NF-κB p65 at 4 hours after UVB radiation at 4.5 and 10 mJ/cm2,or for those of total IKKβ at 4 hours after UVB radiation at 50 mJ/cm2 compared with the unirradiated controls (all P ＞ 0.05).However,there was a statistical decrease in the expression levels of IκBα and NF-κB p65 in primary keratinocytes (0.173 ± 0.055 vs.0.462 ± 0.142,t =5.64,P ＜ 0.05; 0.076 ± 0.030 vs.0.120 ± 0.034,t =5.40,P ＜ 0.05),as well as a slight reduction in the expression level of IκBα (0.160 ± 0.046 vs.0.398 ± 0.136,t =4.37,P ＜ 0.05) with no statistical changes in the expression level of NF-κB p65 (P ＞ 0.05) in CRL-2310 keratinocytes,at 4 hours after 50 mJ/cm2 UVB radiation when compared with the unirradiated controls.After irradiation with 50 mJ/cm2 UVB,the expression level of IκBα in primary keratinocytes began to decrease at 2 hours compared with the unirradiated keratinocytes (0.140 ± 0.034 vs.0.208 ± 0.031,t =17.55,P ＜ 0.05),and the degree of decrease increased over time; the expression level of NF-κB p65 showed no changes at 2 or 4 hours (both P ＞ 0.05),but a significant decrease at 8 and 12 hours (1.162 ± 0.345 vs.1.235 ± 0.349,t =36.67,P ＜ 0.05; 1.061 ± 0.246 vs.1.390 ± 0.226,t =28.71,P ＜ 0.05),but remained unchanged afterwards.No significant differences were noted in the protein expression levels of IKKβ,phosphorylated IKKα/β (ser176/180),phosphorylated IκBα (ser32) or phosphorylated NF-κB p65 (ser536) between the irradiated and unirradiated primary keratinocytes at the 4 time points (all P ＞ 0.05).Conclusions High dose of UVB radiation (50 mJ/cm2) can significantly suppress the protein expression of IκBα,but slightly decrease the protein expression of NF-κB p65 in human primary keratinocytes,suggesting that UVB radiation induces the activation of NF-κB p65 through another potential pathway. Key words: Ultraviolet rays; Keratinocytes; NF-kappa B