Comparison of UVA vs UVB Photoaging Rat Models in Short-term Exposure.

Background: Prolonged exposure to sunlight is known to induce photoaging of the skin, leading to various skin changes and disorders, such as dryness, wrinkles, irregular pigmentation, and even cancer. Ultraviolet A (UVA) and ultraviolet B (UVB) radiation are particularly responsible for causing photoaging. Objective: This study aims to identify and compare photoaging rat models exposed to UVA and UVB. Methods: This research method compared macroscopic (scoring degree of wrinkling) and microscopic (histology) signs and symptoms on skin samples of rat exposed to UVA and UVB for 4 weeks at a radiation dose of 840mJ/cm2. Results: The results of this study indicated that the degree of wrinkling was highest in rat skin exposed to UVB rays by 51% (p<0.05). UVB histological results showed that the epidermis layer (40 µm, p<0.05) was thickened and the dermis layer (283 µm, p<0.05) was thinned in the skin of mice exposed to UVB light. The UVB group, showed the density of collagen in the dermis with a mean value of 55% (p<0.05). Conclusion: Our results suggest that short-term exposure to UVB radiation (in the acute, subacute or subchronic phase) induces more rapid and pronounced damage to rat skin when compared to UVA radiation exposure.

Environmental plastics in the context of UV radiation, climate change, and the Montreal Protocol.

There are close links between solar UV radiation, climate change, and plastic pollution. UV-driven weathering is a key process leading to the degradation of plastics in the environment but also the formation of potentially harmful plastic fragments such as micro- and nanoplastic particles. Estimates of the environmental persistence of plastic pollution, and the formation of fragments, will need to take in account plastic dispersal around the globe, as well as projected UV radiation levels and climate change factors.

A systematic review of the risk of cutaneous malignancy associated with ultraviolet nail lamps: what is the price of beauty?

Gel manicures have become part of a popular personal care service in the last two decades due to increased longevity of the polish and the added strength to the nail plate. Prolonged exposure to nail ultraviolet (UV) lamps is required to cure the gel polish. Despite the increased use of UV nail lamps, there is limited consensus in the literature on the risk of skin malignancy associated with UV nail lamps. The objective of this article was to provide a systematic review of the risk of skin malignancy associated with the use of UV nail lamps and to synthesize evidence-based recommendations on their safe usage. A systematic review of the literature was conducted on the databases, Medline and Embase, in accordance with PRISMA guidelines. The search yielded 2,331 non-duplicate articles. Nine were ultimately included, of which three were case reports, one was a cross-sectional study, and five were experimental studies. The risk of bias per the Joanna Briggs Institute guidelines was high or unclear, likely due to the number of case reports included. Prolonged and repeated exposure to UV nail lamps may pose a low risk of skin cancer. It is important to note that the available evidence is weak, and patients should be informed about the limited data to make their own decisions. Dermatologists and other healthcare providers should be updated with the latest evidence to address patients' concerns about gel manicures and suggest practices which can effectively reduce the risk of cutaneous malignancy associated with gel manicures, such as the use of UV-blocking gloves or properly applied sunscreens.

Interferon alpha promotes caspase-8 dependent ultraviolet light-mediated keratinocyte apoptosis via interferon regulatory factor 1.

Introduction: Ultraviolet (UV) light is a known trigger of both cutaneous and systemic disease manifestations in lupus patients. Lupus skin has elevated expression of type I interferons (IFNs) that promote increased keratinocyte (KC) death after UV exposure. The mechanisms by which KC cell death is increased by type I IFNs are unknown. Methods: Here, we examine the specific cell death pathways that are activated in KCs by type I IFN priming and UVB exposure using a variety of pharmacological and genetic approaches. Mice that overexpress Ifnk in the epidermis were exposed to UVB light and cell death was measured. RNA-sequencing from IFN-treated KCs was analyzed to identify candidate genes for further analysis that could drive enhanced cell death responses after UVB exposure. Results: We identify enhanced activation of caspase-8 dependent apoptosis, but not other cell death pathways, in type I IFN and UVB-exposed KCs. In vivo, overexpression of epidermal Ifnk resulted in increased apoptosis in murine skin after UVB treatment. This increase in KC apoptosis was not dependent on known death ligands but rather dependent on type I IFN-upregulation of interferon regulatory factor 1 (IRF1). Discussion: These data suggest that enhanced sensitivity to UV light exhibited by lupus patients results from type I IFN priming of KCs that drives IRF1 expression resulting in caspase-8 activation and increased apoptosis after minimal exposures to UVB.

Comprehensive Analysis of Exosomal MicroRNAs Derived from UVB-Irradiated Keratinocytes as Potential Melanogenesis Regulators.

The exosomes derived from keratinocytes can have a substantial impact on melanogenesis by influencing melanocytes. MicroRNAs (miRNAs) encapsulated within exosomes are implicated in the control of melanogenesis, particularly when under the influence of UVB irradiation. This investigation explores UVB-induced exosomal miRNAs from keratinocytes as potential regulators of melanogenesis. UVB-irradiated, keratinocyte-derived exosomes were observed to augment melanogenesis in melanocytes, resulting in an upregulation of MITF, TRP1, TRP2, and TYR expression compared to non-UVB-irradiated exosomes. Additionally, a subset of exosomal miRNAs was differentially selected and confirmed to exert both enhancing and inhibitory effects on melanogenesis through functional assays. Notably, hsa-miR-644a, hsa-miR-365b-5p, and hsa-miR-29c-3p were found to upregulate melanogenesis, while hsa-miR-18a-5p, hsa-miR-197-5p, and hsa-miR-4281 downregulated melanogenesis. These findings suggest the involvement of keratinocyte-derived exosomal miRNAs in melanogenesis regulation within melanocytes. The expression levels of exosomal miRNAs from keratinocytes exhibited a UVB-dependent increase, indicating a potential role for these miRNAs as regulators of melanogenesis in response to UVB irradiation. Furthermore, melanogenesis was found to be dependent on exosomes derived from keratinocytes. This underscores the potential of UVB-induced exosomal miRNAs derived from keratinocytes as regulators of melanogenesis. Moreover, this study unveils a significant role for exosomes in melanocyte pigmentation, presenting a novel pathway in the intricate process of melanogenesis.

Betanin Attenuates Epigenetic Mechanisms and UV-Induced DNA Fragmentation in HaCaT Cells: Implications for Skin Cancer Chemoprevention.

Dermal photoaging refers to the skin's response to prolonged and excessive ultraviolet (UV) exposure, resulting in inflammation, changes to the tissue, redness, swelling, and discomfort. Betanin is the primary betacyanin in red beetroot (Beta vulgaris) and has excellent antioxidant properties. Yet, the specific molecular mechanisms of betanin in HaCaT cells have not been fully clarified. The objective of this study was to investigate the activity of betanin and the underlying mechanisms in HaCaT cells; furthermore, in this study, we explored the protective effect of various concentrations of betanin against UVB irradiation on HaCaT cells. Additionally, we assessed its influence on the transcription of various epigenetic effectors, including members of the DNA methyltransferase (DNMT) and histone deacetylase (HDAC) families. Our findings demonstrate a notable downregulation of genes in HaCaT cells, exhibiting diverse patterns upon betanin intake. We considered the involvement of DNMT and HDAC genes in distinct stages of carcinogenesis and the limited exploration of the effects of daily exposure dosages. Our results indicate that betanin may protect the skin from damage caused by UV exposure. Further investigation is essential to explore these potential associations.

Limited contribution of photoenzymatic DNA repair in mitigating carry-over effects from larval UVB exposure: Implications for frog recruitment.

Solar ultraviolet-B (UVB) radiation has increased due to stratospheric ozone depletion, climate and ecosystem changes and is a driver of amphibian population declines. Photoenzymatic repair (PER) is a critical mechanism for limiting UVB lethality in amphibian larvae. However, the link between PER and the UVB-induced effects remains understudied through long-term investigations in vivo. Here, we assessed how larval PER determines the lethal and sublethal effects induced by environmentally relevant acute UVB exposure until the juvenile phase in the Neotropical frog Odontophrynus americanus. We conducted laboratory-based controlled experiments in which tadpoles were or were not exposed to UVB and subsequently were exposed to light (for PER activation) or dark treatments. Results showed that the rates of mortality and apoptosis observed in post-UVB dark treatment are effectively limited in post-UVB light treatment, indicating PER (and not dark repair, i.e. nucleotide excision repair) is critical to limit the immediate genotoxic impact of UVB-induced pyrimidine dimers. Nonetheless, even tadpoles that survived UVB exposure using PER showed sublethal complications that extended to the juvenile phase. Tadpole responses included alterations in morphology, chromosomal instability, increased skin susceptibility to fungal proliferation, as well as increased generation of reactive oxygen species. The short-term effects were carried over to later stages of life because metamorphosis time increased and juveniles were smaller. No body abnormalities were visualized in tadpoles, metamorphs, and juveniles, suggesting that O. americanus is UVB-resistant concerning these responses. This study reveals that even frog species equipped with an effective PER are not immune to carry-over effects from early UVB exposure, which are of great ecological relevance as late metamorphosis and smaller juveniles may impact individual performance and adult recruitment to breeding. Future ecological risk assessments and conservation and management efforts for amphibian species should exercise caution when linking PER effectiveness to UVB resistance.

Current insights and future perspectives of ultraviolet radiation (UV) exposure: Friends and foes to the skin and beyond the skin.

Ultraviolet (UV) radiation is ubiquitous in the environment, which has been classified as an established human carcinogen. As the largest and outermost organ of the body, direct exposure of skin to sunlight or UV radiation can result in sunburn, inflammation, photo-immunosuppression, photoaging and even skin cancers. To date, there are tactics to protect the skin by preventing UV radiation and reducing the amount of UV radiation to the skin. Nevertheless, deciphering the essential regulatory mechanisms may pave the way for therapeutic interventions against UV-induced skin disorders. Additionally, UV light is considered beneficial for specific skin-related conditions in medical UV therapy. Recent evidence indicates that the biological effects of UV exposure extend beyond the skin and include the treatment of inflammatory diseases, solid tumors and certain abnormal behaviors. This review mainly focuses on the effects of UV on the skin. Moreover, novel findings of the biological effects of UV in other organs and systems are also summarized. Nevertheless, the mechanisms through which UV affects the human organism remain to be fully elucidated to achieve a more comprehensive understanding of its biological effects.

Efficacy of a facial-aging web app on sun protection behaviors among primary school students in Iran: a randomized controlled trial.

BACKGROUND: Skin cancers resulting from excessive exposure to solar ultraviolet (UV) radiation are on the rise. This study aims to investigate the impact of facial-aging app intervention on promoting safe and healthy behaviors and its influence on reducing students' UV exposure. METHOD: Utilizing a Pretest-Posttest repeated-measures design, we developed a theory-guided web app on the WhatsApp platform, named the Sunshine and Skin Health app. This app allows users to visualize their altered faces in three stages of adolescence, middle age, and old age based on sun protection behavior. The intervention continued within WhatsApp, incorporating 27 health messages grounded in the PMT theory, eight educational files, and a skin cancer video clip. The primary outcome is the change in sun protection behavior between the two groups (intervention and control) immediately after the intervention (T2) and the secondary outcome is the change in sun protection behavior between the two groups at 3 months follow-up (T3). The data are analyzed in SPSS 22 and a significance level of 0.05 is considered. RESULTS: The results revealed no significant difference between the two groups before the intervention. However, in the intervention group, there were significant differences in the utilization of sunglasses, hats, and sunscreen in the last month, as well as sunscreen reapplication after washing their hands and face, both immediately after the intervention and at the 3-month follow-up, compared to the control group (P = 0.001). Furthermore, a significant intervention effect, time effect, and interaction effect between group and time were observed in behaviors related to using sunscreen in the last month and sunscreen reapplication after washing hands and face (P = 0.001). Specifically, the intervention group exhibited a significant difference from Time 1 to 2 and from Time 1 to 3 (p = 0.001), but no significant difference from Time 2 to 3. In contrast, the control group did not show any significant differences over time. CONCLUSIONS: This study indicated that the Facial-Aging web app can effectively encourage safe behaviors in sunlight. To ensure the maintenance and sustainability of these behaviors over the long term, it is crucial to consider implementing booster sessions. TRIAL REGISTRATION: Iranian Registry of Clinical Trials IRCT20200924048825N1. Registered prospectively on 8 February 2021.

Calculation of solar ultraviolet influx in the eye considering the field of view and pupillary dilation due to sunglasses.

The media and even the specialized literature report that the ultraviolet (UV) protection for sunglasses is critical, on the grounds that sunglasses can have a counter effect if the lenses do not provide adequate UV protection. They reason that the primary and natural mechanism is that the pupil of the eye contracts to attenuate radiation and protect the inner eye under sun exposure. Therefore, if dark lenses do not provide appropriate UV protection, there is an increased UV incidence in the inner eye due to pupil dilation, which enhances the adverse effects and impacts the ocular tissues more severely than in situations without UV protection. However, no existing literature properly quantified or supported this argument. In this work, the influx of solar UV throughout the pupil of the eye was calculated in two situations: when a person wear sunglasses and when he/she does not. In both situations, the pupil dilation and the field of view (squint) were considered with their dependence on the brightness of the ambient, calculated by modeling the solar irradiation. Finally, it was assessed whether sunglasses with poor UV protection actually increase the UV influx throughout the dilated pupil compared to the non-dilated pupil. A set of 214 sunglasses lenses were tested and the results show that pupil dilation does not play an important role in the UV influx throughout the pupil. It was observed that the FOV is the main player, surpassing the pupil size contribution by up to 314.3%, disproving the common explanation. Because of the major role of the FOV, our results show that sunglasses with UV-A protection below 86% may have a slight potential to increase hazards to the eye compared to not wearing sunglasses at all. These results can have direct impact on sunglasses standards regarding the UV protection linked to the category of the lenses.

Effects of ambient UVB light on Pacific oyster Crassostrea gigas mantle tissue based on multivariate data.

Ambient ultraviolet radiation (UVB) from solar and artificial light presents serious environmental risks to aquatic ecosystems. The Pacific oyster, Crassostrea gigas, perceives changes in the external environment primarily through its mantle tissue, which contains many nerve fibers and tentacles. Changes within the mantles can typically illustrate the injury of ambient UVB. In this study, a comprehensive analysis of phenotypic, behavioral, and physiological changes demonstrated that extreme UVB radiation (10 W/m²) directly suppressed the behavioral activities of C. gigas. Conversely, under ambient UVB radiation (5 W/m²), various physiological processes exhibited significant alterations in C. gigas, despite the behavior remaining relatively unaffected. Using mathematical model analysis, the integrated analysis of the full-length transcriptome, proteome, and metabolome showed that ambient UVB significantly affected the metabolic processes (saccharide, lipid, and protein metabolism) and cellular biology processes (autophagy, apoptosis, oxidative stress) of the C. gigas mantle. Subsequently, using Procrustes analysis and Pearson correlation analysis, the association between multi-omics data and physiological changes, as well as their biomarkers, revealed the effect of UVB on three crucial biological processes: activation of autophagy signaling (key factors: Ca2+, LC3B, BECN1, caspase-7), response to oxidative stress (reactive oxygen species, heat shock 70, cytochrome c oxidase), and recalibration of energy metabolism (saccharide, succinic acid, translation initiation factor IF-2). These findings offer a fresh perspective on the integration of multi-data from non-model animals in ambient UVB risk assessment.

Genotoxicity of ultraviolet light and sunlight in the bacterium Caulobacter crescentus: Wavelength-dependence.

The ultraviolet (UV) component of sunlight can damage DNA. Although most solar UV is absorbed by the ozone layer, wavelengths > 300 nm (UVA and UVB bands) can reach the Earth's surface. It is essential to understand the genotoxic effects of UV light, particularly in natural environments. Caulobacter crescentus, a bacterium widely employed as a model for cell cycle studies, was selected for this study. Strains proficient and deficient in DNA repair (uvrA-) were used to concurrently investigate three genotoxic endpoints: cytotoxicity, SOS induction, and gene mutation, using colony-formation, the SOS chromotest, and RifR mutagenesis, respectively. Our findings underscore the distinct impacts of individual UV bands and the full spectrum of sunlight itself in C. crescentus. UVC light was highly genotoxic, especially for the repair-deficient strain. A UVB dose equivalent to 20 min sunlight exposure also affected the cells. UVA exposure caused a significant response only at high doses, likely due to activation of photorepair. Exposure to solar irradiation resulted in reduced levels of SOS induction, possibly due to decreased cell survival. However, mutagenicity is increased, particularly in uvrA- deficient cells.

UV light-mediated corneal crosslinking as (lymph)angioregressive pretreatment to promote graft survival after subsequent high-risk corneal transplantation (CrossCornealVision): protocol for a multicenter, randomized controlled trial.

BACKGROUND: Good vision highly depends on the transparency of the cornea, which is the "windscreen" of the eye. In fact, corneal blindness due to transparency loss is the second most common cause of blindness worldwide, and corneal transplantation is the main cure. Importantly, the cornea is normally avascular but can secondarily be invaded by pathological (blood and lymphatic) vessels due to severe inflammation, and the survival prognosis of a corneal graft mainly depends on the preoperative vascular condition of the recipient's cornea. Whereas transplants placed into avascular recipient beds enjoy long-term survival rates of > 90%, survival rates significantly decrease in pathologically pre-vascularized, so-called high-risk recipients, which account for around 10% of all performed transplants in Germany and > 75% in lower and middle-income countries worldwide. METHODS: This parallel-grouped, open-randomized, multicenter, prospective controlled exploratory investigator-initiated trial (IIT) intends to improve graft survival by preconditioning pathologically vascularized recipient corneas by (lymph)angioregressive treatment before high-risk corneal transplantation. For this purpose, corneal crosslinking (CXL) will be used, which has been shown to potently regress corneal blood and lymphatic vessels. Prior to transplantation, patients will be randomized into 2 groups: (1) CXL (intervention) or (2) no pretreatment (control). CXL will be repeated once if insufficient reduction of corneal neovascularization should be observed. All patients (both groups) will then undergo corneal transplantation. In the intervention group, remaining blood vessels will be additionally regressed using fine needle diathermy (on the day of transplantation). Afterwards, the incidence of graft rejection episodes will be evaluated for 24 months (primary endpoint). Overall graft survival, as well as regression of corneal vessels and/or recurrence, among other factors, will be analyzed (secondary endpoints). DISCUSSION: Based on preclinical and early pilot clinical evidence, we want to test the novel concept of temporary (lymph)angioregressive pretreatment of high-risk eyes by CXL to promote subsequent corneal graft survival. So far, there is no evidence-based approach to reliably improve graft survival in the high-risk corneal transplantation setting available in clinical routine. If successful, this approach will be the first to promote graft survival in high-risk transplants. It will significantly improve vision and quality of life in patients suffering from corneal blindness. TRIAL REGISTRATION: ClinicalTrials.gov NCT05870566. Registered on 22 May 2023.

Antioxidants in Photoaging: From Molecular Insights to Clinical Applications.

Photoaging (PA) is considered a silent disease affecting millions of people globally and is defined as skin damage due to prolonged exposure to ultraviolet radiation (UVR) from the sun. Physiologically, the skin is in a state of renewal and synthesis of components of the extracellular matrix (ECM). However, exposure to UVR affects the production of the ECM, and the functioning and response of skin cells to UVR begins to change, thus expressing clinical and phenotypic characteristics of PA. The primary mechanisms involved in PA are direct damage to the DNA of skin cells, increases in oxidative stress, the activation of cell signaling pathways responsible for the loss of skin integrity, and cytotoxicity. The medical and scientific community has been researching new therapeutic tools that counteract PA, considering that the damage caused by UVR exceeds the antioxidant defense mechanisms of the skin. Thus, in recent years, certain nutraceuticals and phytochemicals have been found to exhibit potential antioxidant and photoprotective effects. Therefore, the main objective of this review is to elucidate the molecular bases of PA and the latest pharmaceutical industry findings on antioxidant treatment against the progression of PA.

Dietary Isoeugenol Supplementation Attenuates Chronic UVB-Induced Skin Photoaging and Modulates Gut Microbiota in Mice.

Photoaging, the primary cause of skin aging damage, results from chronic ultraviolet (UV) exposure, leading to dryness and wrinkle formation. Nutritional intervention has emerged as a practical approach for preventing and addressing the effect of skin photoaging. The primary aromatic compound isolated from clove oil, isoeugenol (IE), has antibacterial, anti-inflammatory, and antioxidant qualities that work to effectively restrict skin cancer cell proliferation. This investigation delved into the advantages of IE in alleviating skin photoaging using UVB-irradiated skin fibroblasts and female SKH-1 hairless mouse models. IE alleviated UVB-induced photodamage in Hs68 dermal fibroblasts by inhibiting matrix metalloproteinase secretion and promoting extracellular matrix synthesis. In photoaged mice, dietary IE reduced wrinkles, relieved skin dryness, inhibited epidermal thickening, and prevented collagen loss. Additionally, the intestinal dysbiosis caused by prolonged UVB exposure was reduced with an IE intervention. The results of Spearman's analysis showed a strong correlation between skin photoaging and gut microbiota. Given the almost unavoidable UVB exposure in contemporary living, this research demonstrated the efficacy of dietary IE in reversing skin photoaging, presenting a promising approach to tackle concerns related to extrinsic skin aging.

Myconoside and Calceolarioside E Restrain UV-Induced Skin Photoaging by Activating NRF2-Mediated Defense Mechanisms.

Chronic and excessive ultraviolet (UVA/UVB) irradiation exposure is known as a major contributor to premature skin aging, which leads to excessive reactive oxygen species generation, disturbed extracellular matrix homeostasis, DNA damage, and chronic inflammation. Sunscreen products are the major preventive option against UVR-induced photodamage, mostly counteracting the acute skin effects and only mildly counteracting accelerated aging. Therefore, novel anti-photoaging and photopreventive compounds are a subject of increased scientific interest. Our previous investigations revealed that the endemic plant Haberlea rhodopensis Friv. (HRE) activates the antioxidant defense through an NRF2-mediated mechanism in neutrophiles. In the present study, we aimed to investigate the photoprotective potential of HRE and two of its specialized compounds-the phenylethanoid glycosides myconoside (MYC) and calceolarioside E (CAL)-in UVA/UVB-stimulated human keratinocytes in an in vitro model of photoaging. The obtained data demonstrated that the application of HRE, MYC, and CAL significantly reduced intracellular ROS formation in UVR-exposed HaCaT cells. The NRF2/PGC-1α and TGF-1ß/Smad/Wnt signaling pathways were pointed out as having a critical role in the observed CAL- and MYC-induced photoprotective effect. Collectively, CAL is worth further evaluation as a potent natural NRF2 activator and a promising photoprotective agent that leads to the prevention of UVA/UVB-induced premature skin aging.

Ferrostatin 1 ameliorates UVB-induced damage of HaCaT cells by regulating ferroptosis.

Ferroptosis, a type of programmed cell death, occurs when there is oxidative stress and lipid peroxides. This condition is marked by lipid peroxidation that relies on iron and the reduction of cellular defences against oxidation. To investigate the effect of UVB irradiation on ferroptosis of human keratinocytes HaCaT cells, the cells were pretreated with Ferrostatin 1 (Fer-1, 10 µM), an ferroptosis inhibitor and then irradiated with UVB (20 mJ/cm2 ) for 30 min to detect related indexes of ferroptosis through MTT assay, quantitative real-time polymerase chain reaction, flow cytometry, reactive oxygen species (ROS) assay, western blotting. Results showed that UVB significantly reduced cell activity, promoted apoptosis and ROS level, whereas Fer-1 significantly increased cell activity, and reduced apoptosis and ROS level. In addition, UVB significantly reduced levels of ferroptosis-related proteins and skin barrier-related proteins, and increased levels of γ-H2AX and iron, whereas Fer-1 significantly increased their protein levels, and reduced levels of γ-H2AX and iron. Conjoint analysis of transcriptomic and proteomic revealed that UVB significantly reduced the levels of TIMP metallopeptidase inhibitor 3 (TIMP3), and coagulation factor II thrombin receptor (F2R), whereas Fer-1 significantly promoted the levels of TIMP3, and F2R. Therefore, our results indicated that Fer-1 significantly ameliorates UVB-induced damage of HaCaT cells by regulating the levels of TIMP3 and F2R.