Photochemistry and Photobiology最新文献

Alternative splicing of precursor messenger RNA (pre-mRNA), including linear splicing and back splicing, produces multiple isoforms that lead to diverse cell fates in response to stimuli including ultraviolet radiation (UVR). Although UVR-induced linear gene splicing has been extensively studied in skin cells, the UVR-induced gene back-splicing events that lead to the production of circular RNAs (circRNAs) have not been thoroughly investigated. The present study used circRNA transcriptome sequencing to screen the differentially expressed circRNAs in human keratinocytes (HaCaT) after UVA irradiation. A total of 312 differentially expressed circRNAs were found in HaCaT cells post-UVR. Among the UVA-induced differentially expressed circRNAs, circUBE2I-a novel circRNA formed by exons 2-6 of the UBE2I gene-was the most significantly upregulated circRNA. RT-qPCR assay further confirmed the increase of circUBE2I level in HaCaT cells after UVA irradiation or H₂O₂ treatment. RNase R digestion experiment revealed the stability of circUBE2I. Overexpression of circUBE2I in keratinocytes induced ferroptosis after UVA or H₂O₂, preventable by the ferroptosis inhibitor ferrostatin-1. Our study provides new insights into the role of circular RNAs in UVA-induced skin cell damage and suggests that circUBE2I could be a therapeutic target in UVR-aroused ferroptosis in skin cells.

There has been much recent interest in whole-room far-UVC (wavelength around 222 nm) to markedly and safely reduce overall levels of airborne pathogens in occupied indoor locations. Far-UVC light produces very low levels of ozone-in real-world scenarios induced ozone levels of less than 10 ppb, and much less in moderately or well-ventilated rooms compliant with US far-UVC dose recommendations, and very much less in rooms compliant with international far-UVC dose standards. At these very low ozone levels, there is no epidemiological evidence of increased health risks from any of the very large outdoor ozone studies, whether from ozone alone or from ozone plus associated pollutants. Indoors, at the low ozone concentrations of relevance here, ozone does not react rapidly enough with preexisting airborne volatile organic compounds to compete with even extremely low levels of room ventilation, so significant ozone-induced ultrafine particle production is very unlikely. Direct measurements in real-life room scenarios are consistent with these conclusions. A potential exception is the cleaning material limonene, which has an unusually high ozone interaction cross-section; in the far-UVC context, turning off far-UVC lights during cleaning with limonene products would be reasonable.

Sulfur-doped Eosin-B (SDE-B) photocatalysts were synthesized for the first time utilizing sublimed sulfur (S₈) as a dopant in an in situ thermal copolymerization technique. Sulfur doping not only increased Eosin-B (E-B) absorption range for solar radiation but also improved fixation and oxygenation capabilities. The doped sulfur bridges the S-S bond by substituting for the edge bromine of the E-B bond. The improved photocatalytic activity of SDE-B in the fixation and oxygenation of NAD⁺/NADP⁺ and sulfides using solar light is attributed to the photo-induced hole of SDE-B's high fixation and oxygenation capacity, as well as an efficient suppression of electron and hole recombination. The powerful light-harvesting bridge system created using SDE-B as a photocatalyst works extremely well, resulting in high NADH/NADPH regeneration (79.58/76.36%) and good sulfoxide yields (98.9%) under solar light. This study focuses on the creation and implementation of a sulfur-doped photocatalyst for direct fine chemical regeneration and organic transformation.

Natural products are favored in the study of skin photodamage protection recently. Isoquercetin, namely 3-O-glucoside of quercetin, can be isolated from various plant species. In present research, the protective effect of isoquercitrin on UVB-induced injury in cells and mice skin were investigated. Our study reveals that 400 μM of isoquercitrin exhibits the best viability on UVB-irradiated HaCaT cells, and beneficial effects against oxidative stress UVB-induced in skin tissue by decreasing the levels of reactive oxygen species (ROS) and malondialdehyde (MDA), and simultaneously enhancing the activity of superoxide dismutase (SOD). Additionally, isoquercitrin was identified as an anti-inflammatory agent by reducing the level of COX-2 by Western blot analysis, and inflammatory cytokines such as IL-6, IL-1β, and TNF-α by ELISA, and UVB-induced epidermal thickening evidenced by H&E staining. It also effectively prevented UVB-induced collagen fibers from degradation identified by Masson staining. Isoquercitrin significantly inhibited MAPK pathway by downregulating the levels of AP-1, MMP-1, MMP-3, phospho-p38, phospho-JNK, phospho-ERK, cleaved caspase-9, cleaved caspase-3, and JAK2-STAT3 pathway by western blot analysis. In conclusion, isoquercitrin pretreatment protected mice skin from UVB irradiation-induced injury effectively, and the underlying mechanism may involve MAPK and JAK2-STAT3 signaling pathways.

Little is known about how sun exposure may affect the maternal skin barrier during pregnancy when many hormonal and physiological changes occur. In this longitudinal observational study, 50 pregnant women were recruited at 18-24 weeks' gestation, 25 in summer-autumn, and 25 in winter-spring. At three time points in pregnancy at 18-24, 28-30, and 36-38 weeks' gestation, participants completed a validated sun exposure questionnaire and had skin permeability and surface pH measured on the volar forearm. We identified an association between increased sun exposure and increased skin permeability at 18-24 weeks' gestation (β = 0.85, p = 0.01). Lower transepidermal water loss (decreased skin permeability), mean = 12.1 (SD = 5.1) at 28-30 weeks' gestation was observed, compared to mean = 12.6 (SD = 4.0) at 18-24 weeks' and mean = 13.7 (SD = 8.5) at 36-38 weeks' gestation (n = 27, β = -1.83, p = 0.007). Higher skin pH readings, mean = 5.80 (SD = 0.58) were found at 28-30 weeks' gestation, compared to mean = 5.25 (SD = 0.62) at 18-24 weeks' and mean = 5.47 (SD = 0.57) at 36-38 weeks' gestation (n = 27, β = 0.40, p = 0.004). These gestational fluctuations remained after adjusting for Fitzpatrick skin type, season, and sun exposure. We observed gestational fluctuations in both skin permeability and skin pH, with 28-30 weeks' gestation being a significant point of difference compared to mid- and late-pregnancy periods.

Laser photobiomodulation (LPBM) has been shown to be one of the possible modulating agents of inflammation. Similarly, medicinal plants, such as chamomile (Matricaria recutita) are also used with the same purpose. To evaluate tissue repair in the dorsum of the tongue of rats under topical use of chamomile alone and in association with LPBM. Seventy-five male Wistar rats received a standardized wound on the dorsum of the tongue and were allocated into experimental groups: Control (G1), Chamomile Fluid extract (G2), Chamomile Infusion (G3), Laser (G4), Chamomile Infusion + Laser (G5). Euthanasia was done on days 3, 7, and 14 after surgery. Ulcers were evaluated and measured with a caliper. Sections stained with hematoxylin and eosin and Picrosirius Red allowed evaluation of edema, inflammatory infiltrate, cellularity, and re-epithelialization and characterization of total collagen. Histomorphometric analysis of the percentage of total collagen, the distance from the basal layer to the epithelial surface, and the thickness of the stratum corneum were performed. The G2 and G4 groups modulated the exudative and proliferative phases of inflammation, both clinically and histologically. The G3 and G5 groups did not show significant differences in relation to the G1 group in most of the evaluated parameters. Chamomile fluid extract and LPBM alone showed better clinical and histological responses for tissue repair than the association between these therapeutic modalities. There were differences in the parameters of clinical, histological, and histomorphometric patterns between the experimental groups of the present investigation. The LPBM proved to be superior in the performed analysis.

Photosensitivity can be due to numerous causes. The photosensitivity associated with deficiency of xeroderma pigmentosum type A (XPA) has been previously shown to be associated with excess levels of the lipid mediator platelet-activating factor (PAF) generated by the keratinocyte. As PAF has been reported to trigger the production of subcellular microvesicle particles (MVP) due to the enzyme acid sphingomyelinase (aSMase), the goal of these studies was to discern if PAF and aSMase could serve as therapeutic targets for the XPA deficiency photosensitivity. HaCaT keratinocytes lacking XPA generated greater levels of MVP in comparison to control cells. Mice deficient in XPA also generated enhanced MVP levels in skin and in plasma in response to UV radiation. Use of a genetic strategy with mice deficient in both XPA and PAF receptors revealed that these mice generated less MVP release as well as decreased skin erythema and cytokine release compared to XPA knockout mice alone. Finally, the aSMase inhibitor imipramine blocked UV-induced MVP release in HaCaT keratinocytes, as well as XPA knockout mice. These studies support the concept that the photosensitivity associated with XPA involves PAF- and aSMase-mediated MVP release and provides a potential pharmacologic target in treating this form of photosensitivity.

Cyanobacterium Phormidium lacuna filaments move from dark to illuminated areas by twitching motility. Time-lapse recordings demonstrated that this photophobotaxis response was based on random movements with movement reversion at the light-dark border. The filaments in the illuminated area form a biofilm attached to the surface. The wild-type and the pixJ and cphA mutants were investigated for photophobotaxis at diverse wavelengths and intensities. CphA is a cyanobacterial phytochrome; PixJ is a biliprotein with a methyl-accepting chemotaxis domain and is regarded as a phototaxis photoreceptor in other species. The cphA mutant exhibited reduced biofilm surface binding. The pixJ mutant was characterized as a negative photophobotaxis regulator and not as a light direction sensor. 3-(3,4-dichlorophenyl)1,1-dimethylurea (DCMU) blocks electron transfer in PS II. At concentrations of 100 and 1000 μM DCMU, photophobotaxis was inhibited to a greater extent than motility, suggesting that PSII has a role in photophobotaxis. We argue that the intracellular concentrations of regular photoreceptors, including CphA or PixJ, are too small for a filament to sense rapid light intensity changes in very weak light. Three arguments, specific inhibition by DCMU, broad spectral sensitivity, and sensitivity against weak light, support photosynthesis pigments for use as photophobotaxis sensors.