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Ultraviolet (UV) A radiation (315–400 nm) is the predominant component of solar UV radiation that reaches the Earth’s surface. However, the underlying mechanisms of the positive effects of UV-A on photosynthetic organisms have not yet been elucidated. In this study, we investigated the effects of UV-A radiation on the growth, photosynthetic ability, and metabolome of the edible cyanobacterium Nostoc sphaeroides. Exposures to 5–15 W m−2 (15–46 µmol photons m−2 s−1) UV-A and 4.35 W m−2 (20 μmol photons m−2 s−1) visible light for 16 days significantly increased the growth rate and biomass production of N. sphaeroides cells by 18%–30% and 15%–56%, respectively, compared to the non-UV-A-acclimated cells. Additionally, the UV-A-acclimated cells exhibited a 1.8-fold increase in the cellular nicotinamide adenine dinucleotide phosphate (NADP) pool with an increase in photosynthetic capacity (58%), photosynthetic efficiency (24%), QA re-oxidation, photosystem I abundance, and cyclic electron flow (87%), which further led to an increase in light-induced NADPH generation (31%) and ATP content (83%). Moreover, the UV-A-acclimated cells showed a 2.3-fold increase in ribulose-1,5-bisphosphate carboxylase/oxygenase activity, indicating an increase in their carbon-fixing capacity. Gas chromatography–mass spectrometry-based metabolomics further revealed that UV-A radiation upregulated the energy-storing carbon metabolism, as evidenced by the enhanced accumulation of sugars, fatty acids, and citrate in the UV-A-acclimated cells. Therefore, our results demonstrate that UV-A radiation enhances energy flow and carbon assimilation in the cyanobacterium N. sphaeroides. IMPORTANCE Ultraviolet (UV) radiation exerts harmful effects on photo-autotrophs; however, several studies demonstrated the positive effects of UV radiation, especially UV-A radiation (315–400 nm), on primary productivity. Therefore, understanding the underlying mechanisms associated with the promotive effects of UV-A radiation on primary productivity can facilitate the application of UV-A for CO2 sequestration and lead to the advancement of photobiological sciences. In this study, we used the cyanobacterium Nostoc sphaeroides, which has an over 1,700-year history of human use as food and medicine, to explore its photosynthetic acclimation response to UV-A radiation. As per our knowledge, this is the first study to demonstrate that UV-A radiation increases the biomass yield of N. sphaeroides by enhancing energy flow and carbon assimilation. Our findings provide novel insights into UV-A-mediated photosynthetic acclimation and provide a scientific basis for the application of UV-A radiation for optimizing light absorption capacity and enhancing CO2 sequestration in the frame of a future CO2 neutral, circular, and sustainable bioeconomy. [ABSTRACT FROM AUTHOR]

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Oxidative stress is a harmful effect induced on the skin by polycyclic aromatic hydrocarbons (PAH), including benzo[a]pyrene (BaP) air pollutants. This effect is amplified by the additive damaging effect of the sun, especially through the UVA light component. Besides being one of the main compounds that make up air pollution, BaP can also be found in tar, tobacco smoke, and various foods. In addition to its direct carcinogenic potential, BaP can act as a photosensitizer absorbing sunlight in the UVA range and thus generating ROS and 8-hydroxy-2′-deoxyguanosine (8-OHdG). Fernblock® (FB) is an aqueous extract from the leaves of Polypodium leucotomos that has been proven to exert photoprotective and antioxidant effects on skin cells. In this study, we evaluate the potential of FB to prevent the damage induced by a combination of BaP and UVA light on human keratinocyte and mouse melanocyte cell lines (HaCaT and B16-F10, respectively). In particular, we have analyzed the capacity of FB to counteract the alterations caused on cellular morphology, viability, oxidative stress and melanogenic signaling pathway activation. Our data indicate that FB prevented cell damage and reduced oxidative stress and melanogenic signaling pathway activation caused by a combination of BaP and UVA light irradiation. Altogether, our findings support the fact that FB is able to prevent skin damage caused by the exposure to a combination of UVA and the air pollutant BaP. [ABSTRACT FROM AUTHOR]

Intertidal macroalgae have developed adaptation and acclimation strategies protecting against stressful environments. The red algae, Porphyra sensu lato are well known for their use as human food, but they also present potential applications in cosmeceutics. In order to enhance the content of interested bioactive compounds, this study evaluated the effects of three different stress factors, through two bi-factorial experiments, the combination of PAR and PAR supplemented by UV-A, Violet and Blue radiation (PAR UVAViBl+) with three nutrient concentrations or emersion/immersion conditions. Interactive effects of PAR UVAViBl+ and nutrient concentrations on the daily integrated electron transport rate (ETR int) was observed. This suggests a photoprotective effect of nitrate against the possible damage by UV-A radiation. The emersion produced a decreased in the in situ ETR, followed by a recovery during re-hydration. The energy dissipation rate (EDR), firstly described in this work, increased under nutrient limitation and under PAR UVAViBl+ radiation, as a photoprotection mechanism. At morphological level, the surface/volume (S/V) ratio of the cells increased under nutrient limitation favoring the nitrogen assimilation, although it could be a risk of photodamage under UV-A radiation. Biliproteins and mycosporine-like amino acids (MAAs) increased under high nutrient availability as it was expected due to both are N-compounds. Polyphenols were higher under PAR UVAViBl+ at day 2, indicating a photoprotective mechanism whereas this effect disappeared at day 7 of culture. Emersion seems to induce MAAs accumulation under PAR UVAViBl+ radiation. Antioxidant capacity determined by ABTS assay was positively correlated to antioxidant substances as biliproteins, polyphenols and MAAs. The application of short-term stress conditions (2–7 days) during culture, can be a strategy to increase the content of interesting compounds due to both UV screen properties and antioxidant capacity. • High nitrogen showed a photoprotective response through the accumulation of N-compounds. • The supplementation of Violet-Blue light can reduce or delay the negative effects cause by UV-A radiation on photosynthesis. • The ratio ETR/EDR is a good indicator of the physiological state of algae, since it increased under favorable conditions. • The stressed conditions investigated in the laboratory could be scaled up in land-based aquaculture. [ABSTRACT FROM AUTHOR]

Oxidative stress is a harmful effect induced on the skin by polycyclic aromatic hydrocarbons (PAH), including benzo[a]pyrene (BaP) air pollutants. This effect is amplified by the additive damaging effect of the sun, especially through the UVA light component. Besides being one of the main compounds that make up air pollution, BaP can also be found in tar, tobacco smoke, and various foods. In addition to its direct carcinogenic potential, BaP can act as a photosensitizer absorbing sunlight in the UVA range and thus generating ROS and 8-hydroxy-2′-deoxyguanosine (8-OHdG). Fernblock® (FB) is an aqueous extract from the leaves of Polypodium leucotomos that has been proven to exert photoprotective and antioxidant effects on skin cells. In this study, we evaluate the potential of FB to prevent the damage induced by a combination of BaP and UVA light on human keratinocyte and mouse melanocyte cell lines (HaCaT and B16-F10, respectively). In particular, we have analyzed the capacity of FB to counteract the alterations caused on cellular morphology, viability, oxidative stress and melanogenic signaling pathway activation. Our data indicate that FB prevented cell damage and reduced oxidative stress and melanogenic signaling pathway activation caused by a combination of BaP and UVA light irradiation. Altogether, our findings support the fact that FB is able to prevent skin damage caused by the exposure to a combination of UVA and the air pollutant BaP.

The incidence of melanoma is one of the fastest growing of all tumor types in the United States and the number of cases worldwide has doubled in the past 30 years. Melanoma, which arises from melanocytes, is an extremely aggressive tumor that invades the vascular and lymphatic systems to establish tumors elsewhere in the body. Melanoma is a particularly resilient cancer and systemic therapy approaches have achieved minimal success against metastatic melanoma resulting in only a few FDA-approved treatments with limited benefit. Leading treatments offer minimal efficacy with response rates generally under 15% in the long term with no clear effect on melanoma-related mortality. Even the recent success of the specific BRAF mutant inhibitor vemurafenib has been tempered somewhat since acquired resistance is rapidly observed. Thus, understanding the mechanism(s) of melanoma carcinogenesis is paramount to combating this deadly disease. Not only for the treatment of melanoma but, ultimately, for prevention. In this report, we will summarize our work to date regarding the characterization of ultraviolet radiation (UVR)-mediated melanomagenesis and highlight several promising avenues of ongoing research. © 2014 Elsevier B.V. All rights reserved.

Ultraviolet (UV) A radiation (315-400 nm) is the predominant component of solar UV radiation that reaches the Earth's surface. However, the underlying mechanisms of the positive effects of UV-A on photosynthetic organisms have not yet been elucidated. In this study, we investigated the effects of UV-A radiation on the growth, photosynthetic ability, and metabolome of the edible cyanobacterium Nostoc sphaeroides . Exposures to 5-15 W m -2 (15-46 µmol photons m -2 s -1 ) UV-A and 4.35 W m -2 (20 μmol photons m -2 s -1 ) visible light for 16 days significantly increased the growth rate and biomass production of N. sphaeroides cells by 18%-30% and 15%-56%, respectively, compared to the non-UV-A-acclimated cells. Additionally, the UV-A-acclimated cells exhibited a 1.8-fold increase in the cellular nicotinamide adenine dinucleotide phosphate (NADP) pool with an increase in photosynthetic capacity (58%), photosynthetic efficiency (24%), Q A re-oxidation, photosystem I abundance, and cyclic electron flow (87%), which further led to an increase in light-induced NADPH generation (31%) and ATP content (83%). Moreover, the UV-A-acclimated cells showed a 2.3-fold increase in ribulose-1,5-bisphosphate carboxylase/oxygenase activity, indicating an increase in their carbon-fixing capacity. Gas chromatography-mass spectrometry-based metabolomics further revealed that UV-A radiation upregulated the energy-storing carbon metabolism, as evidenced by the enhanced accumulation of sugars, fatty acids, and citrate in the UV-A-acclimated cells. Therefore, our results demonstrate that UV-A radiation enhances energy flow and carbon assimilation in the cyanobacterium N. sphaeroides .IMPORTANCEUltraviolet (UV) radiation exerts harmful effects on photo-autotrophs; however, several studies demonstrated the positive effects of UV radiation, especially UV-A radiation (315-400 nm), on primary productivity. Therefore, understanding the underlying mechanisms associated with the promotive effects of UV-A radiation on primary productivity can facilitate the application of UV-A for CO 2 sequestration and lead to the advancement of photobiological sciences. In this study, we used the cyanobacterium Nostoc sphaeroides , which has an over 1,700-year history of human use as food and medicine, to explore its photosynthetic acclimation response to UV-A radiation. As per our knowledge, this is the first study to demonstrate that UV-A radiation increases the biomass yield of N. sphaeroides by enhancing energy flow and carbon assimilation. Our findings provide novel insights into UV-A-mediated photosynthetic acclimation and provide a scientific basis for the application of UV-A radiation for optimizing light absorption capacity and enhancing CO 2 sequestration in the frame of a future CO 2 neutral, circular, and sustainable bioeconomy., Competing Interests: The authors declare no conflict of interest.

The fluoroquinolones absorb light in the 320 to 330 nm ultraviolet A (UV‐A) wavelength and produce reactive oxygen species (ROS) such as superoxide anion, hydroxyl radical, and hydrogen peroxide; thus, the photodynamic generation of ROS may be the basis of phototoxicity of quinolones in human beings and animals. This study aimed to evaluate the damaging effects of UV‐A radiation at different periods of exposure on rats' brains administered with ciprofloxacin. Ciprofloxacin administration in UV‐A exposed animals exaggerated the brain‐oxidative stress biomarkers and decreased the locomotor activity. Exposure of rats to UV‐A for 60 minutes induced a significant increase of malondialdehyde (MDA), myeloperoxidase (MPO), and a decrease in the values of superoxide dismutase (SOD), glutathione (GSH) compared to a normal one; these changes were UV‐A exposure time–dependent. However, the administration of vitamin C to the UV‐60‐treated group decreased the values of MDA, MPO, and shifted the values of SOD, GSH toward the normal values. Vitamin C, probably due to its strong antioxidant properties, could improve and partially counteract the toxic effect of UV‐A on oxidative stress parameters and prevent the damage in rat's brain tissues. [ABSTRACT FROM AUTHOR]

Paraoxonase-2 (PON2) is an intracellular protein, that exerts a protective role against cell oxidative stress and apoptosis. Genetic and environmental factors (i.e. dietary factors, cigarette smoke, drugs) are able to modulate cellular PON2 levels. The effect of ultraviolet A radiation (UVA), the oxidizing component of sunlight, on PON2 in human dermal fibroblasts (HuDe) has not been previously explored. Excessive UVA radiation is known to cause direct and indirect skin damage by influencing intracellular signalling pathways through oxidative stress mediated by reactive oxygen species (ROS) that modulate the expression of downstream genes involved in different processes, e.g. skin photoaging and cancer. The aim of this study was, therefore, to investigate the modulation of PON2 in terms of protein expression and enzyme activity in HuDe exposed to UVA (270 kJ/m2). Our results show that PON2 is up-regulated immediately after UVA exposure and that its levels and activity decrease in the post-exposure phase, in a time-dependent manner (2–24 h). The trend in PON2 levels mirror the time-course study of UVA-induced ROS. To confirm this, experiments were also performed in the presence of a SPF30 sunscreen used as shielding agent to revert modulation of PON2 at 0 and 2 h post-UVA exposure where other markers of photo-oxidative stress were also examined (NF-KB, γH2AX, advanced glycation end products). Overall, our results show that the upregulation of PON2 might be related to the increase in intracellular ROS and may play an important role in mitigation of UVA-mediated damage and in the prevention of the consequences of UV exposure, thus representing a new marker of early-response to UVA-induced damage in skin fibroblasts. • PON2 is expressed in skin fibroblasts and is upregulated by UVA exposure. • PON2 modulation is reverted when skin cells are shielded by a sunscreen. • PON2 appears to act as a defense in skin cells against UVA-induced oxidative stress. • PON2 could represent a novel marker of early-response to skin UVA-induced damage. • PON2 could be used to determine the efficacy of photoprotective agents. [ABSTRACT FROM AUTHOR]

Purpose: The purpose was to compare transepithelial versus epithelium off technique of corneal collagen crosslinking (CXL) in patients of keratoconus. Materials and Method: Totally, 40 eyes (40 patients) with progressive keratoconus were subjected to transepithelial CXL (20 eyes; Group I), and conventional CXL (20 eyes; Group II). Patients were evaluated for uncorrected distance visual acuity, best corrected visual acuity (BCVA), slit lamp-biomicroscopy, keratometry, 9-point pachymentry, orbscan II, and endothelial cell count at baseline and post CXL at 1, 3, and 6 months. Results: The two groups were similar with respect to the evaluated parameters both at baseline and at the end of 6 months. There was an improvement in mean BCVA from Log Mar 0.327 ± 0.1 (Group 1), 0.36 ± 0.08 (Group 2) to 0.23 ± 0.08 (Group 1; P < 0.001), 0.22 ± 0.06 (Group 2; P < 0.001), respectively, at 6 months. Mean Sim K astigmatism decreased from 6.6 ± 1.93 D (Group 1), 6.64 ± 1.93 D (Group 2) to 5.14 ± 1.86 D (Group 1; P = 0.001), and 4.77 ± 0.06 (Group 2; P = 0.001), respectively, at 6 months. The mean pachymetry increased from 432.05 ± 19.36 μm (Group 1), 429.91 ± 16.66 μm (Group 2) to 447.8 ± 16.09 μm (Group 1; P < 0.001), 440.25 ± 11.18 um (Group 2; P = 0.002), respectively, at 6 months. All cases showed stabilization of keratoconus two eyes in epithelium off group developed persistent stromal haze. Most of the patients in Group II experienced pain and photophobia during first 2 days, but not of Group I. Conclusion: Trans-epithelial technique offers visual and topographic outcomes similar to the conventional method with superior patient comfort postintervention.

Abstract Aims This study aims to evaluate the protective effect of alpha pinene (AP), an essential oil monoterpene, against ultraviolet-A (UVA; 320–400 nm) induced cellular damages in human skin epidermal keratinocytes (HaCaT cells). Materials and methods In this study, HaCaT cells were subjected to single UVA-irradiation (10 J/cm2) in the presence and absence of AP (30 μM) then different cellular end points were analyzed. The protective effect of AP against UVA-induced cytotoxicity was evaluated by MTT-based metabolic assay. Generation of reactive oxygen species (ROS), alteration of mitochondrial membrane potential (MMP), DNA single- and double strand breaks (SSBs and DSBs) and apoptotic morphological changes during different treatment conditions were measured by fluorescence microscopy and spectrofluorometry. Modulatory role of AP against UVA-mediated inflammatory markers expression, nucleotide excision repair (NER) proteins and apoptotic markers expression during AP and/or UVA treatment were studied by western blot. Key findings Pretreatment with AP prevented UVA-induced cytotoxicity, generation of ROS, lipid peroxidation and DNA stand breaks probably through its antioxidant property. AP also inhibited UVA-induced inflammatory mediators such as NF-κB, TNF-α and IL-6 expression in HaCaT cells. Further, AP modulates NER proteins via activation of p53 and p21 thereby subsequently prevent the formation of UVA-induced cyclobutane pyrimidine dimers (CPDs). We also noticed that AP inhibits apoptotic cell death by preventing UVA-induced loss of mitochondrial membrane potential through modulating Bax/Bcl-2 expression in HaCaT cells. Significance The present findings suggest that AP prevent UVA-induced oxidative stress, inflammation, DNA damages and apoptosis in human skin cells. [ABSTRACT FROM AUTHOR]

The growing incidence of melanoma is a serious public health issue that merits a thorough understanding of potential causative risk factors, which includes exposure to ultraviolet radiation (UVR). Though UVR has been classified as a complete carcinogen and has long been recognized for its ability to damage genomic DNA through both direct and indirect means, the precise mechanisms by which the UVA and UVB components of UVR contribute to the pathogenesis of melanoma have not been clearly defined. In this review, we therefore highlight recent studies that have addressed roles for UVA radiation in the generation of DNA damage and in modulating the subsequent cellular responses to DNA damage in melanocytes, which are the cell type that gives rise to melanoma. Recent research suggests that UVA not only contributes to the direct formation of DNA lesions but also impairs the removal of UV photoproducts from genomic DNA through oxidation and damage to DNA repair proteins. Moreover, the melanocyte microenvironment within the epidermis of the skin is also expected to impact melanomagenesis, and we therefore discuss several paracrine signaling pathways that have been shown to impact the DNA damage response in UV‐irradiated melanocytes. Lastly, we examine how alterations to the immune microenvironment by UVA‐associated DNA damage responses may contribute to melanoma development. Thus, there appear to be multiple avenues by which UVA may elevate the risk of melanoma. Protective strategies against excess exposure to UVA wavelengths of light therefore have the potential to decrease the incidence of melanoma. Environ. Mol. Mutagen. 59:438–460, 2018. © 2018 Wiley Periodicals, Inc. [ABSTRACT FROM AUTHOR]

Purpose: The purpose was to compare transepithelial versus epithelium off technique of corneal collagen crosslinking (CXL) in patients of keratoconus. Materials and Method: Totally, 40 eyes (40 patients) with progressive keratoconus were subjected to transepithelial CXL (20 eyes; Group I), and conventional CXL (20 eyes; Group II). Patients were evaluated for uncorrected distance visual acuity, best corrected visual acuity (BCVA), slit lamp-biomicroscopy, keratometry, 9-point pachymentry, orbscan II, and endothelial cell count at baseline and post CXL at 1, 3, and 6 months. Results: The two groups were similar with respect to the evaluated parameters both at baseline and at the end of 6 months. There was an improvement in mean BCVA from Log Mar 0.327 ± 0.1 (Group 1), 0.36 ± 0.08 (Group 2) to 0.23 ± 0.08 (Group 1; P < 0.001), 0.22 ± 0.06 (Group 2; P < 0.001), respectively, at 6 months. Mean Sim K astigmatism decreased from 6.6 ± 1.93 D (Group 1), 6.64 ± 1.93 D (Group 2) to 5.14 ± 1.86 D (Group 1; P = 0.001), and 4.77 ± 0.06 (Group 2; P = 0.001), respectively, at 6 months. The mean pachymetry increased from 432.05 ± 19.36 μm (Group 1), 429.91 ± 16.66 μm (Group 2) to 447.8 ± 16.09 μm (Group 1; P < 0.001), 440.25 ± 11.18 um (Group 2; P = 0.002), respectively, at 6 months. All cases showed stabilization of keratoconus two eyes in epithelium off group developed persistent stromal haze. Most of the patients in Group II experienced pain and photophobia during first 2 days, but not of Group I. Conclusion: Trans-epithelial technique offers visual and topographic outcomes similar to the conventional method with superior patient comfort postintervention. [ABSTRACT FROM AUTHOR]

This study aimed to investigate whether α-tocopherol is able to protect keratinocytes against ultraviolet A (UVA) radiation by increasing glutathione (γ-glutamylcysteinylglycine; GSH) levels or decreasing lipid peroxidation and reactive oxygen species (ROS) generation. The cell survival fraction was 43.6% when keratinocytes were irradiated with UVA at a dose of 8 J/cm². α-Tocopherol was added prior to UVA irradiation and the cell viability was assayed. The cell survival fractions were 60.2, 77.1, 89.0, 92.9 and 96.2% when α-tocopherol was added at concentrations of 2.9, 5.9, 8.8, 11.8 and 14.7 IU/ml, respectively. These results suggested that α-tocopherol is capable of protecting keratinocytes against UVA irradiation. Furthermore, the levels of GSH, lipid peroxidation and ROS were measured. The levels of GSH were 0.354 and 0.600 mmol/g protein in keratinocytes irradiated with UVA (8 J/cm²) and in non-irradiated cells, respectively, whereas they were 0.364, 0.420, 0.525, 0.540 and 0.545 mmol/g protein when α-tocopherol was added at concentrations of 2.9,5.9,8.8,11.8 and 14.7 IU/ml, respectively. The levels of lipid peroxidation were 20.401 or 5.328 µmollg [malondialdehyde (MDA)/protein] in keratinocytes irradiated with UVA (8 J/cm²) and in non-irradiated cells, respectively, whereas they were 11.685,6.544,5.847,4.390 and 2.164 µmol/g (MDA/protein) when α-tocopherol was added at concentrations of 2.9, 5.9, 8.8, 11.8 and 14.7 IU/ml, respectively. The levels of ROS were 3,952.17 or 111.87 1/mg protein in keratinocytes irradiated with UVA (8 J/cm²) and in non-irradiated cells, respectively, whereas they were 742.48, 579.36, 358.16, 285.63 and 199.82 1/mg protein when α-tocopherol was added at concentrations of 2.9, 5.9, 8.8, 11.8 and 14.7 IU/ml, respectively. These findings suggested that α-tocopherol protects keratinocytes against UVA irradiation, possibly through increasing the levels of GSH or decreasing the levels of lipid peroxidation and ROS generation. [ABSTRACT FROM AUTHOR]

Ultraviolet A (UVA) radiation, the major component of solar ultraviolet (UV) radiation reaching the earth's surface, leads to negative effects in insects, such as oxidative stress, photoreceptor damage, and cell death. To better understand the molecular mechanisms of insect response to UVA radiation, suppression subtractive hybridization (SSH) and real-time quantitative polymerase chain reaction approaches were combined to reveal differential transcript expression in Drosophila melanogaster Meigen, 1830 (Diptera: Drosophilidae). In this study, two subtractive cDNA libraries were constructed and sequenced, obtaining 131 high-quality unique expressed sequence tags (ESTs) that were up- or downregulated in D. melanogaster exposed to UVA radiation for 0.5 h. Of the 131 ESTs, 102 unique ESTs were differentially expressed and classified into 10 functional categories. The results showed that UVA radiation induces expression of genes related to stress and defense response and metabolism. Potential transcription factor binding motifs upstream of these genes are associated with multiple signaling pathways that may help the insect cope with the stress of UVA radiation. To our knowledge, this is the first analysis of insect response to UVA radiation at the transcriptional level. Our results reveal that UVA radiation influences the expression profiles of stress-responsive genes and provide further insights into the mechanisms of adaptive response to UVA radiation stress. [ABSTRACT FROM AUTHOR]

Abstract: 7,8-dihydro-8-oxo-guanine (8-oxoG) is a mutagenic DNA lesion that is induced by ultraviolet A (UVA) radiation. 8-oxoG results in increased frequency of GC→TA transversion mutations. UVA-induced mutant frequency was measured in the guanine phosphoribosyl transferase (gpt) gene of Chinese hamster ovary cells (AS52) that were stably transfected to overexpress the hOGG1 protein, the human DNA repair glycosylase for 8-oxoG. This mutant frequency was compared with ultraviolet A-induced mutant frequency in AS52 cells stably transfected with the same vector without the hOGG1 gene. The mutant frequency was significantly decreased in the hOGG1 overexpressing cells irradiated with 300 and 400kJ/m2 ultraviolet A radiation, corresponding to 25% and 10% cell survival, respectively. The hOGG1 overexpressing cells repaired oxidative DNA lesions three times faster than the vector only cells as measured by a semi-automated alkaline elution assay using FPG enzyme, the bacterial OGG1 analogue, to cut DNA at oxidative base modifications. Thus, the lower mutation frequency in UVA-induced mutations of the hOGG1 overexpressing cells may be related to the increased repair of 8-oxoG. No GC→TA mutations were detected in the UVA-irradiated hOGG1 overexpressing cells. The results suggest a link between the 8-oxoG lesion and UVA-induced mutagenesis. We propose that hOGG1 has a role in maintaining genomic stability in mammalian cells after oxidative stress. [Copyright &y& Elsevier]

An increasingly popular theory ascribes UVA (>320–400 nm) carcinogenicity to the ability of this wavelength to trigger intracellular photosensitization reactions, thereby giving rise to promutagenic oxidative DNA damage. We have tested this theory both at the genomic and nucleotide resolution level in mouse embryonic fibroblasts carrying the lambda phage cll transgene. We have also tested the hypothesis that inclusion of a cellular photosensitizer (riboflavin) can intensify UVA-induced DNA damage and mutagenesis, whereas addition of an antioxidant (vitamin C) can counteract the induced effects. Cleavage assays with formamidopyrimidine DNA glycosylase (Fpg) coupled to alkaline gel electrophoresis and ligation-mediated PCR (LM-PCR) showed that riboflavin treatment (1 μM) combined with UVA1 (340–400 nm) irradiation (7.68 J/cm²) or higher dose UVA1 irradiation alone induced Fpg-sensitive sites (indicative of oxidized and/or ring-opened purines) in the overall genome and in the cll transgene, respectively. Also, the combined treatment with riboflavin and UVA1 irradiation gave rise to single-strand DNA breaks in the genome and in the cll transgene determined by terminal transferase-dependent PCR (TD-PCR). A cotreatment with vitamin C (1 mM) efficiently inhibited the formation of the induced lesions. Mutagenicity analysis showed that riboflavin treatment combined with UVA1 irradiation or high-dose UVA1 irradiation alone significantly increased the relative frequency of cll mutants, both mutation spectra exhibiting significant increases in the relative frequency of G:C → T:A transversions, the signature mutations of oxidative DNA damage. The induction of cll mutant frequency was effectively reduced consequent to a cotreatment with vitamin C. Our findings support the notion that UVA-induced photosensitization reactions are responsible for oxidative DNA damage leading to mutagenesis. [ABSTRACT FROM AUTHOR]

Acute as well as chronic sun exposure induces biologically damaging effects in skin including photoageing and cancer. Ultraviolet (UV)A radiation is involved in this process; it is therefore important that sunscreen products provide efficient and stable protection in this range of wavelengths.This study based onin vitroapproaches was performed to demonstrate that photostability is an essential requirement to protect against UVA-induced genetic and dermal alterations.The protection afforded by two sunscreen products, differing with regard to their photostability, was studied using biological markers related to the genotoxic or photoageing impact of UVA or simulated solar UV radiation (UV-SSR). Comet assay was used to assess direct DNA breakage, photo-oxidized purines and lomefloxacin-induced DNA breaks in nuclei of normal human keratinocytes in culture. In similar conditions, detection of p53 accumulation was performed. The use of reconstructed skinin vitroallowed us to use a three-dimensional model to analyse the dermal and epidermal damage induced by UVA or UV-SSR exposure. Abnormal morphological features of the tissue as well as fibroblast alterations and matrix metalloproteinase-1 release induced by UV exposure have been studied after topical application of products on the skin surface.The results showed that the photostable product afforded better protection with regard to all the criteria studied, compared with the photounstable product.These data demonstrate that the loss of absorbing efficiency within the UVA wavelength domain due to photoinstability may have detrimental consequences on cell function and lead to impairments that have been implicated in genotoxic events as well as in the photoageing process. [ABSTRACT FROM AUTHOR]

The dominant skin pigment melanin is believed to protect human skin against several harmful effects of ultraviolet radiation. It is not clear, however, how melanin located inside melanin-producing melanocytes modulates the effect of ultraviolet radiation on melanocytes themselves. We have determined membrane damage in pigmented and unpigmented albino mouse melanocytes after ultraviolet A radiation, which is suspected to induce melanoma. Unpigmented cells were much more susceptible to ultraviolet-A-induced membrane permeability than pigmented cells. Unpigmented cells were also more susceptible to ultraviolet-A-induced lipid peroxidation than strongly pigmented cells. Furthermore, unpigmented cells were much more susceptible to ultraviolet-A-induced depletion of glutathione than pigmented cells. Reduced glutathione is known to be a major antioxidant of unpigmented skin cells such as fibroblasts and keratinocytes. To examine whether or not glutathione is also a major antioxidant in melanocytes, melanocytes were depleted of glutathione by means of buthionine sulfoximine. We found that depletion of glutathione in pigmented melanocytes did not change lipid damage induced by ultraviolet A radiation. In unpigmented melanocytes, however, depletion of glutathione significantly increased lipid damage induced by ultraviolet A radiation. Thus, pigmented melanocytes apparently contain antioxidants more potent than glutathione, protecting them from ultraviolet-A-induced membrane damage. [ABSTRACT FROM AUTHOR]

Ultraviolet Al (UVA1) radiation generates reactive oxygen species and the oxidative stress is known as a mediator of DNA damage and of apoptosis. We exposed cultured human cutaneous fibroblasts to UVA1 radiation (wavelengths in the 340–450-nm range with emission peak at 365 nm) and, using the alkaline unwinding method, we showed an immediate significant increase of DNA strand breaks in exposed cells. Apoptosis was determined by detecting cytoplasmic nucleosomes (enzyme-linked immunosorbent assay method) at different time points in fibroblasts exposed to different irradiation doses. In our conditions, UVA1 radiation induced an early (8 h) and a delayed (18 h) apoptosis. Delayed apoptosis increased in a UVA dosedependent manner. Zinc is an important metal for DNA protection and has been shown to have inhibitory effects on apoptosis. The addition of zinc (6.5 mg/L) as zinc chloride to the culture medium significantly decreased immediate DNA strand breaks in human skin fibroblasts. Moreover, zinc chloride significantly decreased UVA1-induced early and delayed apoptosis. Thus, these data show for the first time in normal cutaneous cultured cells that UVA1 radiation induces apoptosis. This apoptosis is biphasic and appears higher 18 h after the stress. Zinc supplementation can prevent both immediate DNA strand breakage and early and delayed apoptosis, suggesting that this metal could be of interest for skin cell protection against UVA1 irradiation. [ABSTRACT FROM AUTHOR]

Painting of 3,3′,4′,5-tetrachlorosalicylanilide (TCSA) plus ultraviolet A (UVA) irradiation to the same site induces contact photosensitivity (CPS), but at the same time results in death of the photohapten-modified cells. Using an in vitro immune lymph node cell (LNC) proliferation system, we investigated the mechanism of induction and elicitation of CPS by TCSA painting plus UVA irradiation. The proliferation of LNC from TCSA-photosensitized mice was not augmented by the addition of TCSA-photocoupled syngeneic spleen cells (SC) or epidermal cells (EC), whereas the picryl chloride immune LNC proliferation was activated by trinitrophenyl-coupled (TNP-coupled) SC or EC. While the viability of SC and EC was unchanged even after TNP haptenization, cells showed very low levels of viability after TCSA photohaptenization. This suggests that the inability of photoTCSA-modified cells to activate LNC proliferation is because of their low viability. Nylon wool column purified lymph node T cells from TCSA-photosensitized mice were activated by photohapten-conjugated SC or photohaptenized EC fragments only in the presence of peritoneal macrophages (M Φ). The function of live M Φ was not replaced by interleukin-1 (IL-1), suggesting that M Φ were required for processing and/or presentation of photohapten rather than simply providing IL-1. Our in vitro study implies that photoTCSA-modified cells generated in vivo require intact antigen-presenting cells to effectively induce and elicit the CPS reaction. [ABSTRACT FROM AUTHOR]

Background While morbidity and mortality related to HIV are decreasing, age-related chronic conditions are becoming more common in people living with HIV (PLWH). We hypothesized that multimorbidity prevalence among PLWH would increase from 2006 to 2016 and that multimorbidity would be associated with demographic and healthcare system-level factors. Methods Cohorts included PLWH aged 45–89 who received care at the University of Virginia (UVA) Ryan White HIV clinic in 2006 (Cohort 1) and 2016 (Cohort 2). Multimorbidity was defined as the co-occurrence of ≥2 age-related chronic diseases. Demographics, HIV-specific clinical characteristics and multimorbidity were compared between the cohorts using a generalized linear model fit using a generalized estimating equation that accounted for repeated measures. Within each cohort, multivariable binary logistic regression was used to assess the association between participants' characteristics and multimorbidity. Results Cohort 1 had 198 participants, and Cohort 2 had 378 participants. Cohort 1 represented 33% of the 2006 clinic population, and Cohort 2 represented 54% of the 2016 clinic population. Less Cohort 2 participants were uninsured (5% vs. 22%, P < 0.001) and more had private insurance (44% vs. 26%, P < 0.001). The prevalence of multimorbidity was higher in Cohort 2 (28% vs 21%, P < 0.001). For Cohort 1, multimorbidity was less likely for those with private insurance (8%, adjusted Odds Ratio [aOR] 0.81, 95% Confidence Interval [CI] 0.69–0.90) compared with those with Medicare (32%). For Cohort 2, multimorbidity was more likely for those with incomes < 100% Federal Poverty Level (FPL; 34%) compared with those with incomes 101–250% FPL (27%, aOR 0.86, 95% CI 0.74–1.00) and 251–500% FPL (21%, aOR 0.78, 95% CI 0.64–0.95). For Cohort 2, multimorbidity was associated with female sex (40%, aOR 1.21, 95% CI 1.01–1.45) compared with male sex (24%). Conclusion Older PLWH represented an increasing proportion of the studied Southeastern clinic population. Multimorbidity prevalence was higher in 2016 compared with 2006. Insurance status was associated with multimorbidity for Cohort 1. For Cohort 2, incomes < 100% FPL and female sex were associated with increased likelihood of multimorbidity. Future research will need to assess the reasons for these disparities. Disclosures All authors: No reported disclosures. [ABSTRACT FROM AUTHOR]

Ultraviolet (UV) radiation is responsible for various damages to the skin, collectively referred to as photoaging. A key UV-induced effect on the skin is excessive degradation of collagen and related structural abnormalities. Camellia japonica is a flowering plant with cosmeceutical properties. In the present study, Camellioside A (CMDA), a triterpene saponin, was investigated for its effects against UVA-induced photoaging in HaCaT keratinocytes. CMDA was analyzed to determine its attenuating effects against UVA-induced overproduction of the collagen degradation enzyme, matrix metalloproteinase-1 (MMP-1), in UVA-irradiated immortalized human HaCaT keratinocytes. UVA irradiation significantly increased MMP-1 release from keratinocytes in addition to suppressing type Iα1 pro-collagen production. Treatment with CMDA reversed the effects of UVA irradiation on the production of MMP-1 and type Iα1 pro-collagen. UVA irradiation also stimulated the activation of p38, ERK and JNK mitogen-activated protein kinases (MAPKs) and their downstream transcription factor activator protein 1 (a heterodimer of c-Fos and c-Jun). MAPK activation and consequent phosphorylation of c-Fos and c-Jun were also inhibited by CMDA treatment. In conclusion, the present study indicated that CMDA may have potential antiphotoaging properties due to suppression of UVA-mediated MMP-1 production., (Copyright © 2020, Spandidos Publications.)