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Oxidative stress induced by medium-wavelength ultraviolet radiation (UVB) is one of the most dangerous environmental stressors for the skin. Therefore, various medicinal remedies aim to prevent the harmful effects of UVB or support the recovery of the damaged cells. This study aimed to evaluate the impact of bioactive phytocannabinoid cannabigerol (CBG) together with 3-O-ethyl ascorbic acid (EAA), a stable, lipophilic derivative of the antioxidant vitamin C, on UVB-induced changes of proteome in cultured human keratinocytes 24 h after treatment. Surprisingly, proteomic analysis revealed very prominent CBG and EAA effects on kinases. These changes mainly influenced ERK1/2, IKK, MAP3K7, MAPK14, RIPK2, and NLK. Their expression was decreased by CBG and EAA, especially if used together after UVB-irradiation, so the effects of UVB were abolished restoring the profile of kinases to non-irradiated control. Moreover, CBG and EAA also reduced the UVB-induced modifications of proteins by the lipid peroxidation product 4-hydroxynonenal, especially in the case of AKT, Camkk1, cJun, ERK1, IKKα, MAPK11 and PERK. We conclude that, by maintaining proteome stability and kinase-dependent signalling, both CBG and EAA may support the recovery of human keratinocytes exposed to UVB radiation, especially if applied together, while the time-dependence of these effects should be further studied., Competing Interests: Competing interests The authors declare no competing interests., (© 2024. The Author(s).)

In today's evolving global environment, reproductive dysfunctions brought on by various environmental toxins are of greatest concern. Radiation is a constant threat to living things, causing both genetic and cellular changes that result in mutations and cell death. It is thought that ultraviolet B (UVB) radiation we are exposed to daily has biological effects on rats and humans that are both short and long term. Due to the damaging effects of UVB radiation on the living system, this study explores the automatic mechanism by which a certain level of radiation induces oxidative stress, which is further controlled by the antioxidant activity of naringin (NG). In our study, male Swiss albino mice were exposed to UVB irradiation, which altered mice's body and testes weight, hormonal imbalance, biochemical parameters, and histo-morphometric parameter. In addition, we chose naringin's UVB irradiation deterrent effect. Twenty-four healthy adult male Swiss albino mice weighing 25-35 g were chosen at random. For 15 days of exposure, they were divided into four groups at random: group I-control, group II-UVB exposure (2 h per day), group III-UVB exposure with naringin (NG) (80 mg/kg, bw), and group IV-naringin (NG) (80 mg/kg, bw). Compared to the control group, UVB irradiation causes alterations in the animal body weight, testes weight, hormones, enzymatic and non-enzymatic assays, and histological parameters. It was seen that NG retrieved the alterations in parameters caused by UVB irradiation. The UVB radiation exposure on mice caused the testicular dysfunction drastically, while the naringin recapitulates testis functioning., (© 2023. The Author(s), under exclusive licence to Society for Reproductive Investigation.)

Background: Ultraviolet (UV) radiation-induced oxidative stress is the main cause of photodamage to the skin. Glutathione (GSH) serves important physiological functions, including scavenging oxygen-free radicals and maintaining intracellular redox balance. γ-glutamylcysteine (γ-GC), as an immediate precursor of GSH and harboring antioxidant and anti-inflammatory properties, represents an unexplored option for skin photodamage treatment., Purpose: The purpose of this study was to investigate whether γ-GC can reduce UVB-induced NIH-3T3 cell damage., Methods: The experimental groups were as follows: control, UVB radiation, UVB radiation after pretreatment with γ-GC. Cell counting kit-8 (CCK-8) assays were used to measure cell proliferation, flow cytometry, and immunoblotting to detect the apoptosis rate and apoptosis-associated proteins. The levels of Reactive Oxygen Species (ROS), Superoxide Dismutase (SOD), and GSH/GSSG (oxidized GSH) were measured to assess oxidative stress. Immunoblotting and immunofluorescence were used to detect DNA damage. The members of the MAPK signaling pathways were detected by immunoblotting., Results: UVB irradiation significantly reduced cell viability and destroyed the oxidative defense system. Pretreatment with γ-GC reduced UVB-induced cytotoxicity, restored the oxidation defense system, and inhibited activation of the MAPK pathway. It also reduced the apoptosis rate, downregulated the levels of cleaved caspase 3 and cleaved PARP. Furthermore, pretreatment with γ-GC reduced the accumulation of γH2AX after UVB radiation exposure, indicating that γ-GC could protect cells from DNA damage., Conclusion: γ-GC protected NIH-3T3 from damage caused by UVB irradiation. The photoprotective effect of γ-GC is mediated via strengthening the endogenous antioxidant defense system, which prevents DNA damage and inhibits the activation of the MAPK pathway., (© 2022 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

The growing incidence of skin cancer (SC) has prompted the search for additional preventive strategies to counteract this global health concern. Mutant p53 (mutp53), particularly with ultraviolet radiation (UVR) signature, has emerged as a promising target for SC prevention based on its key role in skin carcinogenesis. Herein, the preventive activity of our previously disclosed mutp53 reactivator SLMP53-2 against UVR-induced SC was investigated. The pre-treatment of keratinocyte HaCaT cells with SLMP53-2, before UVB exposure, depleted mutp53 protein levels with restoration of wild-type-like p53 DNA-binding ability and subsequent transcriptional activity. SLMP53-2 increased cell survival by promoting G1-phase cell cycle arrest, while reducing UVB-induced apoptosis through inhibition of c-Jun N-terminal kinase (JNK) activity. SLMP53-2 also protected cells from reactive oxygen species and oxidative damage induced by UVB. Moreover, it enhanced DNA repair through upregulation of nucleotide excision repair pathway and depletion of UVB-induced DNA damage, as evidenced by a reduction of DNA in comet tails, γH2AX staining and cyclobutane pyrimidine dimers (CPD) levels. SLMP53-2 further suppressed UVB-induced inflammation by inhibiting the nuclear translocation and DNA-binding ability of NF-κB, and promoted the expression of key players involved in keratinocytes differentiation. Consistently, the topical application of SLMP53-2 in mice skin, prior to UVB irradiation, reduced cell death and DNA damage. It also decreased the expression of inflammatory-related proteins and promoted cell differentiation, in UVB-exposed mice skin. Notably, SLMP53-2 did not show signs of skin toxicity for cumulative topical use. Overall, these results support a promising protective activity of SLMP53-2 against UVB-induced SC., (Copyright © 2021 Elsevier Ltd. All rights reserved.)

Cutaneous leishmaniasis is the most common form of leishmaniasis in humans. The disease is caused by several species, such as Leishmania mexicana, a protozoa parasite. Several major risk factors are associated with this disease, including poverty, poor housing, inadequate domestic hygiene, malnutrition, mobility, and occupational exposure. Solar radiation (UVB) has not been considered a risk factor because there is no scientific evidence demonstrating a correlation with increased susceptibility to cutaneous leishmaniasis. In this study, the shaved skin of the back of C57BL/6 mice was irradiated with 24.2 mJ/cm 2 of UVB. A delayed-type hypersensitivity (DTH) reaction was used to assess UV-induced immune suppression. Skin lesions were quantitated, and parasite burden and the presence of anti-Leishmania mexicana antibodies in serum and germinal centers in draining lymph nodes were determined. We found an increased in the lesion size and parasitic load in UVB-irradiated mice compared to the WT mice and B lymphocyte activation in draining lymph nodes and increased IgG1 production. Our results show an important role of UVB-induced suppression in cutaneous leishmaniasis through local production of IL-10 and systemic IgG1antibodies. This is the first study that demonstrates the effects of UVB radiation on cutaneous leishmaniasis by Leishmania mexicana., (Copyright © 2021. Published by Elsevier B.V.)

iTRAQ proteomic profiling was conducted to examine the proteomic responses of the Antarctic copepod Tigriopus kingsejongensis under ultraviolet B (UVB) exposure. Of the 5507 proteins identified, 3479 proteins were annotated and classified into 25 groups using clusters of orthologous genes analysis. After exposing the T. kingsejongensis to 12 kJ/m 2 UVB radiation, 77 biological processes were modulated over different time periods (0, 6, 12, 24, and 48 h) compared with the control. A Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis showed that UVB exposure in T. kingsejongensis downregulated ribosome and glyoxylate and dicarboxylate metabolism at all time points. Furthermore, antioxidant and chaperone proteins were highly downregulated in response to UVB exposure, causing protein damage and activating apoptotic processes in the 48 h UVB exposure group. These proteomic changes show the mechanisms that underlie the detrimental effects of UVB on the cellular defense systems of the Antarctic copepod T. kingsejongensis., (Copyright © 2021 Elsevier Inc. All rights reserved.)

Overexposure to ultraviolet B (UVB) rays can cause damage to the skin. Liquiritin has a variety of pharmacological effects, such as anti-inflammatory and antioxidant. In the present study, the effect of liquiritin on UVB irradiated rat skin was investigated. Results showed that UVB irradiation caused erythema and wrinkles on the skin surface, as well as thickening and loss of elasticity of the epidermis and a significant increase in the level of ROS in the skin tissue. At the same time, western blot detected an increase in nuclear factor kappa-B (NF-κB) and matrix metalloproteinases (MMPs) and Elisa also detected an increase in pro-inflammatory factors. Therefore, we hypothesized that UVB irradiation-induced damage is associated with inflammation. Interestingly, application of liquiritin to exposed skin of rats reduced the increase in ROS, pro-inflammatory factors, and MMPs caused by UVB irradiation and increased the levels of Sirtuin3 (SIRT3) and Collagen α1. In addition, after intraperitoneal injection of the SIRT3 inhibitor 3-TYP in rats, the protective effect of liquiritin against UVB damage was found to be diminished. These results suggested that promotion of SIRT3 with liquiritin inhibits UVB-induced production of pro-inflammatory mediators, possibly acting through the SIRT3/ROS/NF-κB pathway. In conclusion, this study suggests that liquiritin is an effective drug candidate for the prevention of UVB damage., (Copyright © 2021 Elsevier B.V. All rights reserved.)

Broccoli microgreens have shown potential health benefits due to their high glucosinolate (GL) levels. Previously, we observed that postharvest UVB treatment did not have much effect on increasing GLs in broccoli microgreens. In this study, we investigated the influence of preharvest UVB irradiation on GL levels in broccoli microgreens. UHPLC-ESI/ITMS analysis showed that preharvest UVB treatments with UVB 0.09 and 0.27 Wh/m 2 significantly increased the glucoraphanin (GLR), glucoerucin (GLE), and total aliphatic GL levels by 13.7 and 16.9%, respectively, in broccoli microgreens when measured on harvest day. The nutritional qualities of UVB-treated microgreens were stable during 21-day storage, with only small changes in their GL levels. Broccoli microgreens treated before harvest with UVB 0.27 Wh/m 2 and 10 mM CaCl 2 spray maintained their overall quality, and had the lowest tissue electrolyte leakage and off-odor values during the storage. Furthermore, preharvest UVB 0.27 Wh/m 2 treatment significantly increased GL biosynthesis genes when evaluated before harvest, and reduced the expression level of myrosinase, a gene responsible for GL breakdown during postharvest storage. Overall, preharvest UVB treatment, together with calcium chloride spray, can increase and maintain health-beneficial compound levels such as GLs and prolong the postharvest quality of broccoli microgreens.

The high incidence of skin cancers in the Caucasian population is primarily due to the accumulation of DNA damage in epidermal cells induced by chronic ultraviolet B (UVB) exposure. UVB-induced DNA photolesions, including cyclobutane-pyrimidine dimers (CPDs), promote mutations in skin cancer driver genes. In humans, CPDs are repaired by nucleotide excision repair (NER). Several commonly used and investigational medications negatively influence NER in experimental systems. Despite these molecules' ability to decrease NER activity in vitro, the role of these drugs in enhancing skin cancer risk is unclear. In this study, we investigated four molecules (veliparib, resveratrol, spironolactone, and arsenic trioxide) with well-known NER-inhibitory potential in vitro, using UVB-irradiated CHO epithelial and HaCaT immortalized keratinocyte cell lines. Relative CPD levels, hypoxanthine phosphoribosyltransferase gene mutation frequency, cell viability, cell cycle progression, and protein expression were assessed. All four molecules significantly elevated CPD levels in the genome 24 h after UVB irradiation. However, veliparib, spironolactone, and arsenic trioxide reduced the mutagenic potential of UVB, while resveratrol did not alter UVB-induced mutation formation. UVB-induced apoptosis was enhanced by spironolactone and arsenic-trioxide treatment, while veliparib caused significantly prolonged cell cycle arrest and increased autophagy. Spironolactone also enhanced the phosphorylation level of mammalian target of rapamycin (mTOR), while arsenic trioxide modified UVB-driven mitochondrial fission. Resveratrol induced only mild changes in the cellular UVB response. Our results show that chemically inhibited NER does not result in increased mutagenic effects. Furthermore, the UVB-induced mutagenic potential can be paradoxically mitigated by NER-inhibitor molecules. We identified molecular changes in the cellular UVB response after NER-inhibitor treatment, which may compensate for the mitigated DNA repair. Our findings show that metabolic cellular response pathways are essential to consider in evaluating the skin cancer risk-modifying effects of pharmacological compounds.

Continuous exposure to ultraviolet B (UVB) can cause photodamage of the skin. This photodamage can be inhibited by the overexpression of the non-coding RNA, nc886, via the protein kinase RNA-activated (PKR) pathway. The study aims to identify how UVB inhibits nc886 expression, and it also seeks to determine whether substances that can control nc886 expression can influence UV-induced inflammation, and the mechanisms involved. The results suggest that UVB irradiation accelerates the methylation of the nc886 gene, therefore, reducing its expression. This induces the activation of the PKR, which accelerates the expression of metalloproteinase-9 (MMP-9) and cyclooxygenase (COX-2), and the production of MMP-9, prostaglandin-endoperoxide synthase (PGE 2 ), and certain pro-inflammatory cytokines, specifically interleukin-8 (IL-8), and tumor necrosis factor- (TNF-). Conversely, in a model of nc886 overexpression, the expression and production of those inflammatory factors are inhibited. In addition, Laminaria japonica extract (LJE) protect the levels of nc886 against UVB irradiation then subsequently inhibit the production of UV-induced inflammatory factors through the PKR pathway., Competing Interests: The authors declare no conflicts of interests.

Background: ultraviolet radiation types A and B (UV) (400-315nm and 315-280nm respectively) are the main components present in sunlight known to cause skin injuries. Arnica montana is a plant that has been widely studied for containing anti-inflammatory, healing and analgesic properties capable of preventing or ameliorating lesions. Here, we investigated the therapeutic effect of topical application of Arnica montana after UVB-induced cutaneous injuries in mice. Methods: mice were exposed to UVB radiation (Philips TL40W/12 RS lamp) in a period of 3 hours. After one hour of radiation exposure, the animals were treated with topical application of Arnica montana ointment (250 mg/g) in the ear. At the time of 16 hours after treatment, the parameters of edema, oxidative stress and inflammatory reaction were measured in the ear of mice. Results: our results demonstrated that topical treatment with Arnica montana reduced the UVB-induced inflammatory response as demonstrated by the reduction of ear edema, inhibition of myeloperoxidase activation, decrease of nuclear factor kappa B levels and reduction of proinflammatory cytokines levels, such as interleukin-1beta, interleukin-6, tumour necrosis factor-alpha and interferon-gamma. In addition, Arnica montana ameliorated oxidative damage mediated by UVB radiation, as demonstrated by the reduction of lipid peroxidation, protein oxidation and increase of tissue antioxidant capacity and glutathione levels in the ear. Conclusion: we concluded that Arnica montana ointment is effective in alleviating the auricular inflammatory process and oxidative damage induced by acute UVB radiation, sustaining the traditional use of Arnica montana for the treatment of skin disorders.

Background and Aims: UVB radiation can rapidly induce gene regulation leading to cumulative changes for plant physiology and morphology. We hypothesized that a transgenerational effect of chronic exposure to solar short UV modulates the offspring's responses to UVB and blue light, and that the transgenerational effect is genotype dependent., Methods: We established a factorial experiment combining two Vicia faba L. accessions, two parental UV treatments (full sunlight and exclusion of short UV, 290-350 nm), and four offspring light treatments from the factorial combination of UVB and blue light. The accessions were Aurora from southern Sweden, and ILB938 from Andean region of Colombia and Ecuador., Key Results: The transgenerational effect influenced morphological responses to blue light differently in the two accessions. In Aurora, when UVB was absent, blue light increased shoot dry mass only in plants whose parents were protected from short UV. In ILB938, blue light increased leaf area and shoot dry mass more in plants whose parents were exposed to short UV than those that were not. Moreover, when the offspring was exposed to UVB, the transgenerational effect decreased in ILB938 and disappeared in Aurora. For flavonoids, the transgenerational effect was detected only in Aurora: parental exposure to short UV was associated with a greater induction of total quercetin in response to UVB. Transcript abundance was higher in Aurora than in ILB938 for both CHALCONE SYNTHASE (99-fold) and DON-GLUCOSYLTRANSFERASE 1 (19-fold)., Conclusions: The results supported both hypotheses. Solar short UV had transgenerational effects on progeny responses to blue and UVB radiation, and they differed between the accessions. These transgenerational effects could be adaptive by acclimation of slow and cumulative morphological change, and by early build-up of UV protection through flavonoid accumulation on UVB exposure. The differences between the two accessions aligned with their adaptation to contrasting UV environments., Competing Interests: Declaration of Competing Interest The authors declare that there are no conflicts of interest., (Copyright © 2020. Published by Elsevier GmbH.)

The extracellular matrix (ECM) is a non-cellular and three-dimensional structure, constituted by a macromolecular dynamic network that involves the cells in all animal tissues, including embryonic ones. Several studies with vertebrates and cell cultures have reported deleterious effects of ultraviolet-B (UVB) radiation on the components associated with the ECM. However, studies focusing on the UVB radiation effects on ECM components of crustaceans during embryonic development are very scarce. Thus, the aim of this study was to identify the coding sequences of components associated with the ECM and to evaluate the effect of UVB radiation on embryos of the ecologically-important decapod Macrobrachium olfersii. To evaluate the modulation of these ECM components during embryonic development, the transcript levels of Col4α1, Itgβ, Lamα, Mmp1 and Timp in M. olfersii embryos were analyzed at early developmental stages (E1, E3 and E4), intermediate developmental stage (E7) and late developmental stages (E10 and E14). In addition, embryos at E7, which correspond to a landmark of crustacean development, were analyzed after 12 h of UVB exposure to verify UVB effects on the ECM components. The ECM component sequences were similar to other decapods, suggesting conservation of these genes among crustaceans. The results showed modulations of the ECM components of M. olfersii embryos that reflect the need for each component in the cellular mechanisms, necessary for normal embryonic development. After UVB exposure, embryos showed opacity of embryonic tissues and it was found the overexpression of Col4α1, Itgβ, Mmp1 and Timp transcript levels (1.82-, 1.52-, 2.34- and 6.27-fold, respectively). These impairments can compromise important events for normal embryonic development, such as growth of optic lobes, caudal papilla, ramification of appendages and differentiation of organic systems. The results presented here, together with the effects on morphology, cell proliferation, differentiation, and apoptosis demonstrated previously, strengthen the knowledge of the complex impacts of UVB radiation on freshwater embryos. Nevertheless, our results encourage further investigations focusing on the assessment of UVB effects on different organisms in order to better understand the myriad of UVB effects on ECM components., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2020 Elsevier B.V. All rights reserved.)

Chronic exposure of human skin to solar ultraviolet radiation (UVR) induces a range of biological reactions which may directly or indirectly lead to the development of skin cancer. In order to overcome these damaging effects of UVR and to reduce photodamage, the skin's endogenous defence system functions in concert with the various exogenous photoprotectors. Growth factors, particularly insulin-like growth factor-I (IGF-I), produced within the body as a result of cellular interaction in response to UVR demonstrates photoprotective properties in human skin. This review summarises the impact of UVR-induced photolesions on human skin, discusses various endogenous as well as exogenous approaches of photoprotection described to date and explains how IGF-I mediates UVR photoprotective responses at the cellular and mitochondrial level. Further, we describe the current interventions using growth factors and propose how the knowledge of the IGF-I photoprotection signalling cascades may direct the development of improved UVR protection and remedial strategies., Competing Interests: Declaration of Competing Interest None., (Copyright © 2019 Elsevier Ltd. All rights reserved.)

Daphniopsis tibetana Sars lives in elevation, usually with strong solar UV radiation. We speculate that UV may have an effect on the ecology and evolutionary biology of this species. However, the regulatory effect and mechanism of UV on D. tibetana have not been studied previously. Here, our results showed that UVB could act as a positive factor in the relative body lengths, reproductive parameters, and population growth parameters of D. tibetana when UVB radiation is 20-170 mJ cm -2 , compared with the control group. Strikingly, these parameters were highest at 120 mJ cm -2 . To explore the mechanism underlying the UVB irradiation effects, we conducted a transcriptome analysis using the Trinity platform. The results indicated that differentially regulated genes were mostly enriched in lipid transport and lipid localization by Gene Ontology (GO) enrichment analysis of 146 differentially expressed genes (83 upregulated and 63 downregulated). This is the first study of UVB radiation of D. tibetana to reveal genes that may have crucial roles in survival, growth, and reproduction and could be candidates for future functional studies. Additionally, the study could supply a substantial resource for investigating and elucidating lipids that could play important roles in a physiological context.

The present study, we investigate the preventive role of naringin, a dietary flavonoid, against ultraviolet-B (UVB) radiation (280-320 nm) induced oxidative damage and inflammatory responses in mouse embryonic fibroblast cell lines (NIH-3T3). In this study, 20 mJ/cm 2 of UVB radiation induces cell cytotoxicity, reactive oxygen species (ROS) generation, DNA damage, and antioxidants depletion in NIH-3T3 cells. Treatment with naringin (60 µM) prior UVB exposure prevented the cell cytotoxicity, ROS generation, DNA damage, and antioxidants depletion in NIH-3T3 cells. Furthermore, naringin prevents UVB-induced mitogen-activated protein kinase families and nuclear factor-κB (NF-κB)-mediated activation of inflammatory factors, that is TNF-α, IL-6, IL-10, and COX-2 in NIH-3T3 cells. Peroxisome proliferator-activated receptor γ (PPARγ) is an anti-inflammatory agent and it suppressed the UVB-mediated oxidative and inflammatory responses. In this study, naringin activates PPARγ and prevents inflammatory biomarkers in NIH-3T3 cells. Thus, naringin prevents UVB-mediated inflammation and oxidative damage in NIH-3T3 cells probably over controlling NF-κB expression and activation of PPARγ., (© 2018 Wiley Periodicals, Inc.)

Natured botanical extract has attracted considerable attention recently in the field of skin anti-ultraviolet (UV) radiation. As a medicinal herb, Sophora japonica flower buds contained several components such as flavonoids, isoflavonoids, triterpenes, alkaloids and polysaccharides, which have multiple pharmacological properties except hemostatic agents which have been used in China and Korea for centuries. The purpose of our study was to investigate whether polysaccharide extracted from Sophora japonica L. flower buds (PS) was able to attenuate UVB-induced damage using a human keratinocyte cell line (HaCaT cells). HaCaT cells were pretreated with PS in a serum-free medium for 2 h and then irradiated with different doses of UVB rays. The results showed that the PS attenuated UVB-induced cytotoxicity which was verified by MTT method and morphology feature assay. UVB exposure (30-120 mJ/cm 2 ) reduced HaCaT cells viability significantly following with the increased irradiation dose 24 h later, while pretreatment with PS (0.25-2.0 mg/mL) attenuated UVB-induced cytotoxicity significantly and increased cell viability in a dose-dependent manner except 30 mJ/cm 2 group. The PS reduced the ROS generation, down-regulated the expression of phosphor-JNK and phosphor-p38 MAPK proteins significantly through MAPK pathway in UVB-irradiated HaCaT cells. It also decreased the apoptosis rate at low dose of UVB ray and protected the cells from apoptosis which had been identified by the down-regulated level of active-caspase3 in UVB-irradiated HaCaT cells. In conclusion, PS pretreatment protected HaCaT keratinocytes from UVB irradiation-induced skin injuries effectively, and the underlying mechanism may involve MAPK signaling pathway which contribute to apoptotic cell death. However, further studies especially whose using human systems are needed to determine efficacy of PS in vivo., (Copyright © 2018. Published by Elsevier B.V.)

Ultraviolet (UV) B radiation can cause skin aging by increasing matrix metalloproteinase (MMP) production and collagen degradation, leading to the formation of wrinkles. This study investigated whether hawthorn polyphenol extract (HPE) protects against UVB-induced skin photoaging using HaCaT human keratinocytes, normal human dermal fibroblasts (HDFs), and mice. Analysis of the phenol composition of HPE by high-performance liquid chromatography-mass spectrometry showed that chlorogenic acid (13.5%), procyanidin B2 (19.2%), and epicatechin (18.8%) collectively accounted for 51.4% of total phenol content and represent the active ingredients of hawthorn fruit. A cell viability assay revealed that HPE treatment promoted cell proliferation in HaCaT cells and HDFs. On the other hand, MMP-1 and type I procollagen production was decreased and increased, respectively, in UVB-exposed cells treated with HPE as compared with those without treatment, as determined by enzyme-linked immunosorbent assay. Hematoxylin and eosin and Weigert staining of dermal tissue specimens from mice demonstrated that HPE also reversed UVB-induced epidermal thickening and dermal damage. The increase in production of reactive oxygen species and decrease in antioxidant enzyme activity as well as the increase in nuclear factor-κB activation and mitogen-activated protein kinase phosphorylation induced by UVB irradiation were reversed by HPE (100 or 300 mg/kg body weight), which also suppressed MMP expression and stimulated the production of type I procollagen in the dorsal skin of UVB-irradiated mice. These results suggest that HPE is a natural product that can prevent UVB radiation-induced skin photoaging.

Persistent exposure to solar ultraviolet radiation (UVR) causes continuous damages to skin, including progressive impairment of epidermal stem cells (ESCs) capacities. Ghrelin is the only known endogenous orexigenic hormone, which has displayed its various pharmacological functions. In the current study, we found that the specific receptor of ghrelin, growth hormone secretagogue receptor (GHS-R), is expressed in ESCs. Interestingly, GHS-R expression is significantly upregulated in response to ultraviolet B (UVB) radiation. We also found that ghrelin treatment prevented UVB radiation-induced reduction in cell viability and the release of lactate dehydrogenase (LDH). Additionally, ghrelin reduced UVB radiation-induced generation of reactive oxygen species (ROS) and restored the intracellular level of reduced glutathione (GSH). UVB radiation significantly suppressed the expressions of integrin β1 and Krt19, the two major ESC markers, which were restored by ghrelin. Notably, knockdown of GHS-R abolished the effects of ghrelin on the expressions of integrin β1 and Krt19, suggesting the involvement of GHS-R. Also, we found that ghrelin treatment inhibited UVB radiation- induced reduction of Wnt1, Wnt3a, Myc, and cyclin D1 at both the mRNA levels and the protein levels. Taken together, our findings identify a novel function of ghrelin on maintaining the capacities of ESCs against UVB radiation., (Copyright © 2018 Elsevier Masson SAS. All rights reserved.)

The total phenolic content (TP) and antioxidant activity of the ethanolic extract and fractions that were obtained from the leaves of Nectandra hihua were assessed using different methods. The ethanolic extract (EE) and ethyl acetate fraction (EAF) had the best antioxidant capacity, which was comparable to butylated hydroxytoluene and quercetin (ABTS + 2.55 ± 0.06, 3.54 ± 0.03 mmol TE/g; DPPH IC 50 10.27 ± 0.05, 9.88 ± 0.02 μg/mL; FRAP 2.17 ± 0.08, 2.38 ± 0.04 mmol TE/g; ORAC 5.16 ± 0.08, 5.35 ± 0.07 mmol TE/g; TP 568.05 ± 18.15, 397.20 ± 17.88 mg GAE/g, respectively). The cytoprotective effect, reactive oxygen species (ROS) and lipid peroxidation inhibitions on L929 fibroblasts irradiated with UVB (600 mJ/cm 2 ) in pre- and post-treatments with EE and EAF were determined. These plant materials demonstrated high ROS scavenging activity and lipid peroxidation inhibition on L929 fibroblasts in both treatments, especially with pre-treatment (EE 38.47 ± 1.95% and EAF 40.20 ± 4.5% inhibition of ROS production, and EE 39.03 ± 3.33% and EAF 41.67 ± 7.6% of lipid peroxidation inhibition), indicating the best cytoprotection with pre-treatment (13.52 ± 1.66% and 13.34 ± 2.61% increases in cell viability). The antioxidant flavonoids quercitrin, avicularin, juglalin, afzelin and astragalin were isolated from EAF. The results obtained indicate that EE and EAF present photodamage attenuating potential against UVB-induced oxidative stress and can be useful as a starting point for developing dermatological products to prevent oxidative skin damage., (Copyright © 2018 Elsevier B.V. All rights reserved.)

This study analyzed fruit stem extract (MGFE) from Muscat Bailey A grape (Vitis labrusca × Vitis vinifera) for their ameliorative effects on Ultraviolet B (UVB)-induced skin damage in Balb/c mice. Well established in vivo assays were used to determine the biological effects of MGFE upon UVB irradiation of BALB/c mice. The results showed that treatment with MGFE recovered glutathione depletion, prevented lipid peroxidation of tissues and decreased the expression of DNA repair enzyme oxo guanine glycosylase-1. MGFE recovered the skin conditions in UVB-irradiated Balb/c mice. Moreover, MGFE inhibited dermal infiltration of inflammatory cells and reduced serum tumor necrosis factor alpha and interleukin-6 levels. Finally, MGFE treatment inhibited UVB-induced melanin formation and collagen fiber destruction through the inhibition of matrix metalloproteinase-1 expression. Through high-performance liquid chromatography analysis, catechin, epicatechin, and trans-resveratrol were found to be among the main active compounds present in MGFE. Taken together, these results indicated that MGFE has potentials as topical therapeutic materials against skin damage by inhibiting oxidative stress and inflammatory., (Copyright © 2017. Published by Elsevier Masson SAS.)

Annually, more skin cancer cases are diagnosed than the collective incidence of the colon, lung, breast, and prostate cancer. Persistent contact with sunlight is a primary cause for all the skin malignancies. UVB radiation induces reactive oxygen species (ROS) production in the skin which eventually leads to DNA damage and mutation. Various delivery approaches for the skin cancer treatment/prevention have been evolving and are directed toward improvements in terms of delivery modes, therapeutic agents, and site-specificity of therapeutics delivery. The effective chemoprevention activity achieved is based on the efficiency of the delivery system used and the amount of the therapeutic molecule deposited in the skin. In this article, we have discussed different studies performed specifically for the chemoprevention of UVB-induced skin cancer. Ultra-flexible nanocarriers, transethosomes nanocarriers, silica nanoparticles, silver nanoparticles, nanocapsule suspensions, microemulsion, nanoemulsion, and polymeric nanoparticles which have been used so far to deliver the desired drug molecule for preventing the UVB-induced skin cancer., (© 2017 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Skin aging is a complex process that is strongly affected by UV radiation, which stimulates the production of reactive oxygen species (ROS) in the epidermis and dermis and subsequently causes skin damage. Among the major consequences are increased collagen degradation and reduced collagen synthesis. Previous reports have demonstrated the beneficial effects of polyphenols for healthy skin. Passiflora tarminiana Coppens & V.E. Barney, a species of the Passifloraceae family, is widely distributed in South America and is rich in flavonoids. We show that UVB radiation increases metalloproteinase 1 (MMP-1) and reduces procollagen production in human dermal fibroblast (HDF) cells in a dose- and time-dependent manner. We examined the antioxidant and antiaging effects of the extract and fractions of P. tarminiana fruits. The fractions showed high polyphenol content (620mg EAG/g) and antioxidant activity, as measured by ORAC (4097μmol ET/g) and ABTS (2992μmol ET/g) assays. The aqueous fraction drastically inhibited the collagenase enzyme (IC 50 0.43μg/mL). The extract and fractions presented photoprotective effects by reducing UVB-induced MMP-1 production, increasing UVB-inhibited procollagen production, and decreasing ROS production after UVB irradiation in HDF. Finally, the polyphenol contents of the extracts and fractions from P. tarminiana were analyzed by HPLC-DAD-ESI-MS n , and procyanidins and glycosylated flavonoids were identified., (Copyright © 2017 Elsevier B.V. All rights reserved.)

Lippia graveolens HBK (Mexican oregano) is a species that is regularly used as a condiment in Mexican cuisine. In traditional medicine, it is used for the treatment of respiratory and digestive illnesses, headaches, rheumatism and inflammation-related disorders. The main chemical components reported in this species include the following: terpenoids, iridoids and flavonoids. The aim of this study was to determine the potential photochemopreventive effect of the methanolic extract of Lippia graveolens (MELG) against ultraviolet B (UVB)-induced skin cancer in SKH-1 mice. The phenolic content, radical scavenger activity, penetration and genotoxicity of the MELG were also evaluated. The MELG exhibited scavenging activity against 1,1-diphenyl-2-picrylhydrazyl, superoxide and hydroxyl radicals, and it did not exhibit genotoxic activity in the micronucleus test. In addition, the MELG absorbed UVB (280nm) electromagnetic radiation. The main components detected in the plant extract were naringenin and galangin, and pinocembrin was also isolated and identified through spectroscopic analysis. The MELG demonstrated a photoprotective effect against UVB-induced cell death in Escherichia coli. In chronic challenge experiments, the MELG protected against UVB-induced skin cancer in SKH-1 mice. The MELG penetrated the skin of mice. Topical administration of the MELG protected against chronic UVB-induced damage in mouse SKH-1 skin. Our results suggest that the MELG has photochemopreventive activity and may potentially prevent photo-tumorigenesis., (Copyright © 2016 Elsevier B.V. All rights reserved.)

The leaves of Petasites japonicus are used for their anti-allergic properties in traditional Korean, Japanese, and Chinese medicine. This study aimed to identify bioactive compounds isolated from P. japonicus leaves. All compounds were assessed for their ability of transcriptional activation, induction of phase 2 enzymes and heat shock proteins (HSPs), as well as protection against the UVB-induced apoptotic cell death. Bioactive compounds were isolated from P. japonicus leaves. All compounds were evaluated for their protective effect using human dermal fibroblasts (HDF) and human epidermal keratinocyte cells (HEKC) treated with UVB radiation. Four flavonoids were isolated from the leaves of P. japonicus and identified as kaempferol-3-O-(6″-acetyl)-β-D-glucoside (1), quercetin-3-O-(6″-acetyl)-β-D-glucoside (2), kaempferol-3-O-β-D-glucoside (3), and quercetin-3-O-β-D-glucoside (4). These compounds activated nuclear factor (erythroid-derived 2)-like 2 (Nrf2) and heat-shock response transcription elements (HSE) that resulted in the induction of heme oxygenase-1 (HO-1) and HSP70, respectively. Activation of these pathways provided protection to the skin cells against UVB radiation. The isolated compounds activated the Nrf2 and HSE pathways and could protect against UVB-induced apoptosis.

Vitamin D is known as the sunshine vitamin. During exposure to sunlight the skin transforms 7-dehydrocholesterol into vitamin D 3 . Throughout evolution vitamin D 3 has played a pivotal role in the evolution of vertebrates. Vitamin D is not only critically important for bone health but has a multitude of other biologic functions to help reduce chronic illnesses. This Chapter reviews how vitamin D is produced in the skin, factors that affect its production and a prospective on how to obtain vitamin D from sensible sun exposure.

The usage of active compounds of dietary phytochemicals in prevention of UV-induced skin diseases is increasingly gaining attention in the development of skin care products. The purpose of this study was to measure the influence of delphinidin (as a botanical agent) on the cell mechanical properties evaluated by the atomic force microscopy (AFM) technique in the immortalized human keratinocyte cell line (HaCaT) exposed to UVB radiation. The cells were treated with various doses of UVB radiation with and without pre and post-treatment with selected concentrations of delphinidin. The measurements of the elastic properties revealed that the exposure of HaCaT cells to high dose of the UVB radiation (100mJ/cm 2 ) caused a decrease in the cell elastic modulus. It was accompanied by the decrease of metabolic activity, rearrangement of actin cytoskeleton and disappearance of the cell repair marker 53BP1. Both pre-treatment and post-treatment with delphinidin at non-cytotoxic concentrations (5 or 10μM), restored the elastic modulus of irradiated keratinocytes. A direct AFM analysis showed that the UVB-mediated decrease of the cell stiffness was restored more effectively when cells were treated with delphinidin after the UVB irradiation. The results demonstrate the regenerative effect of delphinidin on the mechanical properties of cells exposed to UVB radiation (100mJ/cm 2 ), which may be due to antioxidant and inhibitory effect on matrix metalloproteinases activation., (Copyright © 2016 Elsevier B.V. All rights reserved.)

This study was conducted to explore the role of UVB on benzanthrone (BA)-induced skin inflammation and its mechanism/s. SKH-1 hairless mice were topically exposed with BA (25 and 50 mg/kg b.wt) either alone or along with UVB (50 mJ/cm(2)) for 24 h and estimation of ROS, histopathological analysis, myeloperoxidase (MPO) activity, mast cell staining, immunohistochemistry for COX-2 and iNOS as well as western blotting for MAPKs, p-NF-κB, c-jun, c-fos COX-2 and iNOS were carried out. Enhanced ROS generation, increased epidermal thickness, mast cell number, MPO activity, enhanced expression of COX-2 and iNOS, MAPKs, c-jun, c-fos, NF-κB were found in BA either alone or when followed by UVB treatment, compared to the control groups. Expression of COX-2, iNOS and phosphorylation of ERK1/2 were found to be more enhanced in BA and UVB- exposed group compared to BA and UVB only group, while phosphorylation of JNK1/2, p38, NF-κB and expression of c-jun and c-fos were comparable with BA and UVB only groups. In summary, we suggest that UVB exposure enhanced BA-induced SKH-1 skin inflammation possibly via oxidative stress-mediated activation of MAPKs-NF-κB/AP-1 signalling, which subsequently increased the expression of COX-2 and iNOS and led to inflammation in SKH-1 mouse skin., (Copyright © 2016 Elsevier Ltd. All rights reserved.)

UV-induced reactive oxygen species (ROS) have been implicated in photocarcinogenesis and skin aging. This is because UV-induced ROS can induce DNA damage that, if unrepaired, can lead to carcinogenesis. Sunscreens contain UV attenuators, such as organic chemical and/or physical UV filters, which can prevent all forms of damage from UV irradiation. In recent years, the effective broad-spectrum UV attenuation properties of ZnO-nanoparticles (ZnO-NPs) have made them attractive as active components in sunscreens and other personal care products. As the use of ZnO-NPs in sunscreens is on the rise, so is public concern about their safety, particularly with exposure to sunlight. Therefore, in the present study, using various experimental approaches, we investigated the possible toxic effects resulting from exposure to UVB and ZnO-NPs in primary mouse keratinocytes (PMKs) as well as in the skin of SKH-1 hairless mice. The findings of the present study demonstrated that co-exposure to UVB and ZnO-NPs: (1) translocated the ZnO-NPs into the nucleus of PMKs; (2) caused enhanced generation of ROS; (3) induced more severe DNA damage as evident by alkaline comet assay and immunocytochemistry for γ-H2AX and 8-hydroxy-2'-deoxyguanosine (8-OHdG); and (4) subsequently caused much more pronounced cell death in PMKs. Further, to elucidate the physiological relevance of these in vitro findings, SKH-1 hairless mice were topically treated with ZnO-NPs and after 30min irradiated with UVB (50mJ/cm(2)). Interestingly, we found that co-exposure of ZnO-NPs and UVB caused increased oxidative DNA damage and cell death, indicated by immunostaining for 8-OHdG and TUNEL assay in sections of exposed mouse skin. Thus, collectively, our findings suggest that UVB exposure increases ZnO-NPs-mediated oxidative stress and oxidative damage, thereby enhancing ZnO-NPs-induced cell death., (Copyright © 2016 Elsevier B.V. All rights reserved.)

Ultraviolet B (UVB) irradiation alters multiple molecular pathways in the skin, thereby inducing skin damage. Human dermal fibroblasts (HDFa) were subjected to single UVB-irradiation (18mJ/cm(2)) resulting in reactive oxygen species (ROS) generation, oxidative DNA damage and upregulation of nuclear factor kappa B (NF-κB) expression. Further, it has been observed that there was a significant cytokine production (TNF-α and IL-6) in UVB irradiated HDFa cells. Our results show that 7-hydroxycoumarin (7-OHC) prevents UVB-induced activation of NF-κB thereby subsequently preventing the overexpression of TNF-α and IL-6 in HDFa cells. Further, 7-OHC prevents UVB-induced activation of cyclooxygenase-2 (COX-2) expression, an inflammatory mediator in skin cells. Moreover, 7-OHC inhibited mRNA expression pattern of matrix metalloproteinases (MMP-1 and MMP-9) in UVB irradiated skin cells. Furthermore, 7-OHC restored antioxidant status, thereby scavenging the excessively generated ROS; consequently preventing the oxidative DNA damage. It has also been noticed that 7-OHC prevents UVB mediated DNA damage through activation of DNA repair enzymes such as XRCC1 and HOGG1. In this study, we treated HDFa cells with 7-OHC before and after UVB irradiation and we found that pretreatment showed better results when compared to posttreatment. Further, 7-OHC showed 9.8416 sun protection factor (SPF) value and it absorbs photons in the UVB wavelength rage. Thus, it has been concluded that sunscreen property, free radical scavenging potential and prevention of NF-κB activation play a role for photoprotective property of 7-OHC., (Copyright © 2016 Elsevier B.V. All rights reserved.)

Purpose In this paper, the contribution of different genes involved in DNA repair for both survival and SOS induction in Escherichia coli mutants exposed to ultraviolet B radiation (UVB, [wavelength range 280-315 nm]) was evaluated. Materials and methods E. coli strains defective in uvrA, oxyR, recO, recN, recJ, exoX, recB, recD or xonA genes were used to determine cell survival. All strains also had the genetic sulA::lacZ fusion, which allowed for the quantification of SOS induction through the SOS Chromotest. Results Five gene products were particularly important for survival, as follows: UvrA > RecB > RecO > RecJ > XonA. Strains defective in uvrA and recJ genes showed elevated SOS induction compared with the wild type, which remained stable for up to 240 min after UVB-irradiation. In addition, E. coli strains carrying the recO or recN mutation showed no SOS induction. Conclusions The nucleotide excision and DNA recombination pathways were equally used to repair UVB-induced DNA damage in E. coli cells. The sulA gene was not turned off in strains defective in UvrA and RecJ. RecO protein was essential for processing DNA damage prior to SOS induction. In this study, the roles of DNA repair proteins and their contributions to the mechanisms that induce SOS genes in E. coli are proposed.

Toxic effects of petroleum to marine zooplankton have been generally investigated using dissolved petroleum hydrocarbons and in the absence of sunlight. In this study, we determined the influence of natural ultraviolet B (UVB) radiation on the lethal and sublethal toxicity of dispersed crude oil to naupliar stages of the planktonic copepods Acartia tonsa, Temora turbinata and Pseudodiaptomus pelagicus. Low concentrations of dispersed crude oil (1 μL L(-1)) caused a significant reduction in survival, growth and swimming activity of copepod nauplii after 48 h of exposure. UVB radiation increased toxicity of dispersed crude oil by 1.3-3.8 times, depending on the experiment and measured variables. Ingestion of crude oil droplets may increase photoenhanced toxicity of crude oil to copepod nauplii by enhancing photosensitization. Photoenhanced sublethal toxicity was significantly higher when T. turbinata nauplii were exposed to dispersant-treated oil than crude oil alone, suggesting that chemical dispersion of crude oil may promote photoenhanced toxicity to marine zooplankton. Our results demonstrate that acute exposure to concentrations of dispersed crude oil and dispersant (Corexit 9500) commonly found in the sea after oil spills are highly toxic to copepod nauplii and that natural levels of UVB radiation substantially increase the toxicity of crude oil to these planktonic organisms. Overall, this study emphasizes the importance of considering sunlight in petroleum toxicological studies and models to better estimate the impact of crude oil spills on marine zooplankton., (Copyright © 2016 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Exposure to ultraviolet B (UVB; 280-320 nm) radiation induces the formation of reactive oxygen species (ROS) in the biological system. In this study, we examined the protective effect of carvacrol on UVB-induced lipid peroxidation and oxidative DNA damage with reference to alterations in cellular an-tioxidant status in human lymphocytes. A series of in vitro assays (hydroxyl radical, superoxide, nitric oxide, DPPH (2,2-Diphenyl-1-picryl hydrazyl), and ABTS (2,2-azino-bis-3-ethylbenzothiazoline-6-sulfonic acid) radical scavenging assays) demonstrate antioxidant property of carvacrol in our study. UVB exposure significantly increased thiobarbituric acid reactive substances (TBARS), lipid hydroperoxides (LHPs), % tail DNA and tail moment; decreased % cell viability and antioxidant status in UVB-irradiated lymphocytes. Treatment with carvacrol 30 min prior to UVB-exposure resulted in a significant decline of TBARS, LHP, % tail DNA, and tail moment and increased % cell viability as carvacrol concentration increased. UVB irradiated lymphocytes with carvacrol alone (at 10 μg/mL) gave no significant change in cell viability, TBARS, LHP, % tail DNA, and tail moment when compared with normal lymphocytes. On the basis of our results, we conclude that carvacrol, a dietary antioxidant, mediates its protective effect through modulation of UVB-induced ROS., (© 2010 Wiley Periodicals, Inc.)

Many amphibian species are dependent on ex situ conservation interventions for their long-term persistence. However, projects have been jeopardised by husbandry issues involving poor calcium metabolism and nutritional metabolic bone disease (NMBD). Healthy calcium metabolism requires appropriate dietary calcium content and access to vitamin D3 . In many animals, vitamin D3 can be photobiosynthesised in skin exposed to UVB radiation, as well as extracted from the diet, but the extent of vitamin D3 photobiosynthesis in amphibians is poorly known. Additionally, prey insects for captive amphibians are deficient in calcium and calcium content must be artificially increased, but the effects of different levels of augmentation and their interaction with UVB exposure are also little understood. We fed captive fire-bellied toads (Bombina orientalis) with crickets augmented to contain 5% and 10% calcium and housed them with and without UVB exposure. Despite additional dietary vitamin D3 supplementation, we found that toads exposed to UVB radiation exhibited significantly higher serum vitamin D3 levels, indicating that this species may partly rely on photobiosynthesis sources of vitamin D3 . These data are the first to show a direct link between UVB exposure and serum vitamin D3 in an amphibian. We found significant positive effects of UVB exposure and 10% dietary calcium content on skeletal structure, as well as complex interactions between treatments. We also found UVB radiation exposure resulted in more rapid natural coloration acquisition. Together, this indicates that standard calcium plus vitamin D3 supplementation methods may not fully substitute for UVB exposure and for increased feeder insect calcium content. This may have implications for the success of ex situ amphibian conservation, as well as for the welfare of captive amphibians in general. Our data lend support for the provision of UVB radiation for captive, basking amphibians., (Journal of Animal Physiology and Animal Nutrition © 2014 Blackwell Verlag GmbH.)

Tropical animals are regularly exposed to solar UV radiation. The generation and accumulation of free radicals as a result of UVB incidence causes tissue damage. In the present study we report that the irradiation of Funambulus pennanti by 1.5 J/cm(2) of UVB caused significant oxidative damage to the spleen. The systemic immunity suffered collateral damage as depicted by results of total leukocyte count (TLC) while an increase in the thiobarbituric acid reactive substances (TBARS) and decline in the activities of enzymes superoxide dismutase (SOD), Glutathione peroxidase (GSH-Px) and Catalase (CAT) denoted oxidative tissue damage. Melatonin the indole-amine with known antioxidative properties when administered subcutaneously (s.c 100 μg/100 gm body weight), before the UVB irradiation recovered the damages caused by UVB radiation in the spleen. The action of melatonin was direct and might have involved its membrane receptor (MT1) as well as nuclear receptor (RORα) indicating the fact that the mode of action of melatonin in ameliorating UVB radiation induced free radical load may be receptor mediated. Our study hence reports for the first time that UVB radiation incurred oxidative damage to the spleen and suppressed the normal tissue functions. This UVB mitigated oxidative stress was recovered by the free radical scavenging and anti-apoptotic functions of melatonin when administered prior to UVB irradiation., (Copyright © 2014 Elsevier B.V. All rights reserved.)

The vulnerability and acclimation to increased UVB radiation in three macroalgae of different morpho-functional groups collected in the Mediterranean coastal waters were evaluated. The algae were submitted for 7 days to increased (PAB+) and decreased (PAB-) UVB radiation. The thickness and morphology influenced the response to increased UVB radiation, being Cystoseira tamariscifolia the less vulnerable algae followed by Ellisolandia elongata. The highest resistance to increased UVB radiation in C. tamariscifolia was related to the accumulation of polyphenols and high antioxidant activity, whereas E. elongata was due to its high reflectance. Finally, Ulva rigida suffered the highest photoinhibition under PAB+ culture. The latest species presented 10 times lower polyphenol content and antioxidant activity than C. tamariscifolia. The three species showed different acclimation patterns to the changes of UVB radiation related to the morphology, photosynthetic activity, accumulation of photoprotectors and antioxidant activities. The ecological implications of the UVB variations on macroalgae are discussed., (Copyright © 2014 Elsevier Ltd. All rights reserved.)