Journal of photochemistry and photobiology. B, Biology最新文献

The effect of simultaneous application of tert-butyl hydroperoxide (tBHP) and polychromatic near-infrared (NIR) radiation on bovine blood was examined to determine whether NIR light decreases the susceptibility of red blood cells (RBCs) to oxidative stress. The study assessed various exposure methods, wavelength ranges, and optical filtering types. Continuous NIR exposure revealed a biphasic response in cell-free hemoglobin changes, with antioxidative effects observed at low fluences and detrimental effects at higher fluences. Optimal exposure duration was identified between 60 s and 15 min. Protective effects were also tested across wavelengths in the range of 750–1100 nm, with all of them reducing hemolysis, notably at 750 nm, 875 nm, and 900 nm. Comparing broadband NIR and far-red light (750 nm) showed no significant difference in hemolysis reduction. Pulse-dosed NIR irradiation allowed safe increases in radiation dose, effectively limiting hemolysis at higher doses where continuous exposure was harmful. These findings highlight NIR photobiomodulation's potential in protecting RBCs from oxidative stress and will be helpful in the effective design of novel medical therapeutic devices.

Hepatic fibrosis (HF) is caused by persistent inflammation, which is closely associated with hepatic oxidative stress. Peroxynitrite (ONOO⁻) is significantly elevated in HF, which would be regarded as a potential biomarker for the diagnosis of HF. Research has shown that ONOO⁻ in the Golgi apparatus can be overproduced in HF, and it can induce hepatocyte injury by triggering Golgi oxidative stress. Meanwhile, the ONOO⁻ inhibitors could effectively relieve HF by inhibiting Golgi ONOO⁻, but as yet, no Golgi-targetable fluorescent probe available for diagnosis and assessing treatment response of HF through sensing Golgi ONOO⁻. To this end, we reported a ratiometric fluorescent probe, Golgi-PER, for diagnosis and assessing treatment response of HF through monitoring the Golgi ONOO⁻. Golgi-PER displayed satisfactory sensitivity, low detection limit, and exceptional selectivity to ONOO⁻. Combined with excellent biocompatibility and good Golgi-targeting ability, Golgi-PER was further used for ratiometric monitoring the Golgi ONOO⁻ fluctuations and screening of ONOO⁻ inhibitors from polyphenols in living cells. Meanwhile, using Golgi-PER as a probe, the overexpression of Golgi ONOO⁻ in HF and the treatment response of HF to the screened rosmarinic acid were precisely visualized for the first time. Furthermore, the screened RosA has a remarkable therapeutic effect on HF, which may be a new strategy for HF treatment. These results demonstrated the practicability of Golgi-PER for monitoring the occurrence, development, and personalized treatment response of HF.

Large scale outbreaks of infectious respiratory disease have repeatedly plagued the globe over the last 100 years. The scope and strength of the outbreaks are getting worse as pathogenic RNA viruses are rapidly evolving and highly evasive to vaccines and anti-viral drugs. Germicidal UV-C is considered as a robust agent to disinfect RNA viruses regardless of their evolution. While genomic damage by UV-C has been known to be associated with viral inactivation, the precise relationship between the damage and inactivation remains unsettled as genomic damage has been analyzed in small areas, typically under 0.5 kb. In this study, we assessed genomic damage by the reduced efficiency of reverse transcription of regions of up to 7.2 kb. Our data seem to indicate that genomic damage was directly proportional to the size of the genome, and a single hit of damage was sufficient for inactivation of RNA viruses. The high efficacy of UV-C is already effectively adopted to inactivate airborne RNA viruses.

Autophagy participates in the regulation of ferroptosis. Among numerous autophagy-related genes (ATGs), ATG5 plays a pivotal role in ferroptosis. However, how ATG5-mediated ferroptosis functions in UVB-induced skin inflammation is still unclear. In this study, we unveil that the core ferroptosis inhibitor GPX4 is significantly decreased in human skin tissue exposed to sunlight. We report that ATG5 deletion in mouse keratinocytes strongly protects against UVB-induced keratinocyte ferroptosis and skin inflammation. Mechanistically, ATG5 promotes the autophagy-dependent degradation of GPX4 in UVB-exposed keratinocytes, which leads to UVB-induced keratinocyte ferroptosis. Furthermore, we find that IFN-γ secreted by ferroptotic keratinocytes facilitates the M1 polarization of macrophages, which results in the exacerbation of UVB-induced skin inflammation. Together, our data indicate that ATG5 exacerbates UVB-induced keratinocyte ferroptosis in the epidermis, which subsequently gives rise to the secretion of IFN-γ and M1 polarization. Our study provides novel evidence that targeting ATG5 may serve as a potential therapeutic strategy for the amelioration of UVB-caused skin damage.

The deprotonation of O6 within the S₃ state marks the final deprotonation event before the formation of oxygen‑oxygen bond interactions and eventual production and release of dioxygen. Gaining a thorough understanding of this event, from the proton acceptors involved, to the exfiltration pathways available, is key in determining the nature of the resulting oxygen species, influencing the mechanism through which the first oxygen‑oxygen bond forms. Computational analysis, using BS-DFT methodologies, showed that proton abstraction by the local Glu189 residue provides consistent evidence against this being a viable mechanistic pathway due to the lack of a stable product structure. In contrast, abstraction via W3 shows an increasingly stable oxo-oxo product state between r[O5O6] = 2.1 Å & 1.9 Å. The resulting oxo-oxo state is stabilised through donation of $\beta$ electron character from O6 to Mn1 and $\alpha$ electron character from O6 to O5. This donation from the O6 lone pair is shown to be a key factor in stabilising the oxo-oxo state, in addition to showing the initiation of first O5-O6 bond.

The cytotoxic of α-Ag₂WO₄ synthesized in different morphologies (cuboidal (AW-C), hexagonal rod-like (AW-HRL) and nanometric rod-like (AW-NRL) was analyzed to understand the impact of morphological modulation on the toxicity of 3 T3 cell lines in the dark and when photoactivated by visible light. Pathways of toxicity were examined, such as parameters and electrostatic interaction, uptake, ion release and ROS production. Cytotoxicity was observed for all samples after reaching concentrations exceeding 7.8 μg/mL. Uptake tests demonstrated that the samples were not internalized by cells, likely due to their negative surface charge. AW-NRL exhibited autophagy in the absence of light and during photoactivation, primarily attributed to its ability to generate singlet oxygen. Analyzing intercellular ROS and RNS production, AW-HRL induced an increase in NO through exposure to photo-generated hydroxyl radicals, while AW-NRL showed increases only at non-photoactivated concentrations and AW-C did not exhibit increases. Interestingly, in the dark, these cells showed a low propensity for apoptosis, with late apoptosis and necrosis being more pronounced. When photoactivated, this behavior changed, revealing predominantly apoptotic and late apoptotic cell death. There is a need for an understanding of how morphology can alter the biological properties of α-Ag₂WO₄ to predict and optimize its effects on cellular responses.

In this study, for the first time, red LED light radiation was applied to the fermentation process of table olives using the Negrinha de Freixo variety. Photostimulation using LED light emission (630 ± 10 nm) is proposed to shorten and speed up this stage and reduce time to market. Several physical-chemical characteristics and microorganisms (total microbial count of mesophilic aerobic, molds, yeasts, and lactic acid bacteria) and their sequence during fermentation were monitored. The fermentation occurred for 122 days, with two irradiation periods for red LED light. The nutritional composition and sensory analysis were performed at the end of the process. Fermentation under red LED light increased the viable yeast and lactic acid bacteria (LAB) cell counts and decreased the total phenolics in olives. Even though significant differences were observed in some color parameters, the hue values were of the same order of magnitude and similar for both samples. Furthermore, the red LED light did not play a relevant change in the texture profile, preventing the softening of the fruit pulp. Similarly, LED light did not modify the existing type of microflora but increased species abundance, resulting in desirable properties and activities. The species identified were yeasts - Candida boidinii, Pichia membranifaciens, and Saccharomyces cerevisiae, and bacteria - Lactobacillus plantarum and Leuconostoc mesenteroides, being the fermentative process dominated by S. cerevisiae and L. plantarum. At the end of fermentation (122 days), the irradiated olives showed less bitterness and acidity, higher hardness, and lower negative sensory attributes than non-irradiated. Thus, the results of this study indicate that red LED light application can be an innovative technology for table olives production.

Ultraviolet-B (UV-B) irradiation has been reported to cause oxidative stress and inflammation-mediated skin photo-damage. Furthermore, mitochondrial dynamics have been implicated to play a critical role in these processes. For the first time, we describe in this study how UVB-induced aberrant mitochondrial dynamics and inflammation interact in primary human dermal fibroblasts (HDFs). Our findings demonstrated that UV-B irradiation induced -impairment in mitochondrial dynamics by increasing mitochondrial fragmentation in HDFs. Imbalanced mitochondrial dynamics lead to the activation of NFкB and pro-inflammatory cytokines. The current study further aimed to investigate the protective effect of Naringenin (a naturally occurring flavonoid isolated from Sea buckthorn fruit pulp) against UV-B-induced mitochondrial fragmentation and inflammation in HDFs and Balb/c mice. Although Naringenin has been shown to have anti-inflammatory and antioxidant potential, its effects and mechanisms of action on UVB-induced inflammation remained unclear. We observed that Naringenin restored the UV-B-induced imbalance in mitochondrial fission and fusion in HDFs. It also inhibited the phosphorylation of NFкB and reduced the generation of pro-inflammatory cytokines. Naringenin also alleviated UV-B-induced oxidative stress by scavenging the reactive oxygen species and up-regulating the cellular antioxidant enzymes (Catalase and Nrf2). Topical application of Naringenin to the dorsal skin of Balb/c mice exposed to UV-B radiation prevented mitochondrial fragmentation and progression of inflammatory responses. Naringenin treatment prevented neutrophil infiltration and epidermal thickening in mice's skin. These findings provide an understanding for further research into impaired mitochondrial dynamics as a therapeutic target for UV-B-induced inflammation. Our findings imply that Naringenin could be developed as a therapeutic remedy against UVB-induced inflammation.

With the rapid development of nanotechnology, various functional nanomaterials have shown exciting potential in biomedical areas such as drug delivery, antitumor, and antibacterial therapy. These nanomaterials improve the stability and selectivity of loaded drugs, reduce drug-induced side effects, realize controlled and targeted drug release, and increase therapeutic efficacy. The increased resistance to antifungal microbicides in medical practice and their side effects stimulate interest in new therapies, such as Photodynamic Therapy (PDT), which do not generate resistance in microorganisms and effectively control the pathology. The present study aimed to evaluate, in vitro, the efficacy of photodynamic therapy on Candida albicans using 1,9-Dimethyl-Methylene Blue (DMMB) as photosensitizer, red LED (λ630), and nanoencapsulation of DMMB (RL-NPs/DMMB) using rhamnolipids produced by Pseudomonas aeruginosa to evaluate if there is better performance of DMMB + RL particles compared to DMMB alone via the characterization of DMMB + RL and colony forming count. The tests were carried out across six experimental groups (Control, DMMB, RL-NPs, RL-NPs/DMMB, PDT and PDT + RL-NPs/DMMB) using in the groups with nanoparticles, DMMB (750 ng/mL) encapsulated with rhamnolipids in a 1:1 ratio, the light source consisted of a prototype built with a set of red LEDs with an energy density of 20 J/cm². The results showed that applying PDT combined with encapsulation (RL-NPs/DMMB) was a more practical approach to inhibit Candida albicans (2 log reduction) than conventional applications, with a possible clinical application protocol.

The effects of UVA on the skin are well documented in the literature.

Sunscreens were originally developed to protect against erythema and consequently against UVB. Even today, most sunscreens on the market provide much higher UVB than UVA protection.

By looking at the transmission profile of 3 different sunscreens on the market and making a theoretical calculation, we show that users in the past and even today are being exposed to a huge amount of UVA in a silent way.

This is what we define as silent UVA.

There is a need to develop a new generation of sunscreens with higher UVA protection to reduce Silent UVA exposure.