Journal of Photochemistry and Photobiology最新文献

Skin cells present many endogenous photosensitizers (ePS) that interact with light, generating oxidizing species, causing molecular damage in proteins, lipids, and nucleic acids, and consequently triggering cellular and organelle malfunction. Several cell lines with terminal differentiation are susceptible to accumulating non-digestible pigments, such as lipofuscin or melanin-lipofuscin. Besides being hallmarks of aging, both pigments can work as photosensitizers, increasing and expanding the toxicity of sunlight to the range of visible light (VL, 400–700 nm). In here we review the literature to describe the mechanisms by which the photosensitized oxidation reactions induced by VL cause DNA damage. We aim to provide the mechanistic background needed to improve the current strategies of photoprotection.

Photoreaction of pyrene 1 with methyl cinnamate 15a gave a photocycloadduct 16a at 4,5-position of pyrene stereoselectively. Oxidation of 16a using DDQ yielded a pyrenocyclobutene derivative 18a. Functional group conversion of the ester moiety of 18a resulted in the synthesis of carboxylic acid 19, alcohols 20 and 21, sulfonate 23, and methylenecyclobutene 24. Diels–Alder reactions of 18a with electron-deficient alkenes or alkynes 25a–f afforded cycloadducts, pyrenocyclohexenes 26a–c and pyrenocyclohexadienes 26e, f stereoselectively in good yields. Thermal reactions of pyrenocyclobutene-linked electron-deficient alkenes 22a, b produced 4-benzyl-5-alkenylpyrenes 29a, b via ring cleavage followed by 1,5-hydrogen transfer.

Owing to its low energy, visible light (VIS) was previously considered to have no photobiological effects and research was focused on the ultraviolet (UV) end of the solar spectrum. However, the discovery that exposure of skin to VIS leads to clinical changes in skin reminiscent of those of UV led to a reassessment of its effects. Driving our understanding have been cell and tissue-based models that permit a thorough dissection of the molecular events in skin cells following exposure to specific wavelengths and intensities of VIS. Here we explore how these models have been used to understand the cutaneous impact of VIS and identify substances that protect skin from its damaging effects.

Although the treatment currently recommended for snakebite accidents is serum therapy using antivenom, a need for adjunctive therapy associated with serum therapy for treating the local effects caused by snakebites is an effort of the WHO to reduce local signals and symptoms. Photobiomodulation with laser or LED therapy is one of the primary examples of adjuvant therapy to serum therapy to lessen these local effects caused by snakebite envenoming. For this purpose, the project aims to study the action of photobiomodulation with LED therapy in isolated thioglycolate-elicited macrophages stimulated with Bothrops jararacussu venom (BjV) and isolated bothropstoxins BthTX-I and BthTX-II focusing on cell dead mechanism such as necrosis and apoptosis, mitochondrial membrane potential, and cytokines [Interleukin (IL)-1β, IL-10, IL-6], and [tumor necrosis factor (TNF)-α] and lipid mediator [prostaglandin (PG)E₂] liberation. Briefly, thioglycollate-elicited macrophages were harvested from Swiss male mice incubated with BjV or BthTXs irradiated or not with LED, and the following parameters were analyzed: necrosis and apoptosis, mitochondrial membrane potential, cytokines, and lipid mediator liberation. Herein, results showed that LED therapy was able to decrease necrosis cell death, caspase-3 activity, and TNF-α liberation. In addition, LED therapy induces mitochondrial membrane potential and modulates gene expression of lipid mediators. In conclusion, the data of this study support the use of phototherapy as an adjuvant therapeutical approach in combination with serum therapy to mitigate the local effects resulting from snakebite envenoming.

Wound healing involves a series of cellular and molecular processes to heal injured tissue. Growth factors such as vascular endothelial growth factor (VEGF), and signalling pathways such as phosphatidylinositol 3-kinase, protein kinase B, and mammalian target of rapamycin (PI3K/AKT/mTOR) are essential in wound healing. VEGF is linked to intracellular signalling pathways including PI3K/AKT/mTOR, which controls cell growth, metabolism, proliferation, apoptosis, and protein synthesis. During photobiomodulation (PBM), low-level light in the visible red and near-infrared (NIR) spectrum is employed to promote healing, and reduce pain, inflammation, and oedema. Several studies demonstrate that PBM enhances cellular survival, proliferation, migration, and viability in vitro, however, the exact cellular and molecular mechanisms responsible for these benefits have not yet been identified. The aim of this review is to explore the effects of PBM on the PI3K/AKT/mTOR signalling pathway in wound healing.

Introduction

Both UVB and UVA rays induce biological damages in the epidermis and the dermis that contribute to photo-carcinogenesis and photoaging. In the present study, the photoprotective effect of 2 ISO standard sunscreens, P3 (Sun Protection Factor [SPF]15) and P6 (SPF40) and of an SPF50+ labeled commercial sunscreen product was tested in reconstructed skin tissues exposed to increasing doses of UV Solar Simulated Radiation (UV-SSR). UV-induced damages were evaluated using several biological markers, including DNA lesions in the presence or absence of sunscreen protection.

Method

T-Skin™ model samples (EPISKIN), composed of a fibroblast-populated dermal equivalent and a fully differentiated epidermis, were protected with the test sunscreens (1.3 mg/cm² topically applied on molded polymethyl methacrylate plate) before being exposed to increasing UV doses (0 – 2.5 – 5 - 25 – 40 J/cm²). Twenty-four hours after exposure, tissues with and without sunscreen protection, were analyzed for skin viability and morphology, DNA lesions (cyclobutane pyrimidine dimer) and inflammatory mediator quantification. Results were compared to untreated exposed tissues using a Wilcoxon non-parametric test.

Results

For untreated tissues, UV-SSR exposure induced a dose-dependent decrease in epidermal and dermal viabilities, an increase in release of proinflammatory cytokines and matrix metalloproteinases and were associated with morphological damages at doses as low as 5 J/cm². DNA lesions were even detected at the lowest dose of 2.5 J/cm², and their number increased with the UV-SSR dose. In the samples protected with sunscreens, these abnormalities were partially or totally prevented with P6 providing a better protection compared to P3, and the SPF50+ sunscreen showing a trend for better protection than P6, for example against DNA damage.

Conclusions

This study demonstrates that photoprotective effects of different sunscreens can be discriminated and ranked on reconstructed skin tissues (T-Skin™ model) exposed to UV-SSR. Showing significant differences between the reference products P3 and P6 in line with their respective SPF values, such study allows the evaluation of epidermal and dermal damages at the tissue, cellular and molecular levels. It thus opens the way to a new model of integrated assessment of sunscreens. In line with its labeled 50+ SPF, the commercial test product confirmed its improved protection especially on DNA damage prevention.

A lot of effort has been given to the development of nontoxic ternary semiconductor nanoparticles that could act as photocatalyst NIR-I (750–850 nm) or NIR-II (1000–1400 nm) optical windows. This is due to their good stability, high optical absorption coefficient, and desirable band gap that absorbs well within the solar spectrum. CuInS₂ is one of the ternary sulphide semiconductors, which has been considered to be a highly promising photocatalyst. The properties are attributed to its high optical absorption coefficient. In this study, copper indium sulphide (CuInS₂) nanoparticles were synthesized by a microwave irradiation route using copper(II) bis (N-methyl-N-ethanol dithiocarbamate) and In(III) tris (N-methyl-N-ethanol dithiocarbamate) as a precursor complexes. The copper(II) complex was varied in two different ratios (3:1 and 2:1) to determine the best synthesis regime. Then, the effect of the varying ratios on the crystalline structure, morphology, and optical properties of the CuInS₂ was studied by using X-ray diffraction (XRD), scanning and transmission electron microscopy (SEM and TEM), and absorption spectroscopy. The microscopic analyses revealed that the CuInS₂ nanoparticles have similar spherical grain-like shapes whose sizes range between 10.3–50.1 nm. The increase in the concentration of copper(II) complex also altered the band gap energy, given 2.87 and 1.61 eV for CuInS₂(3:1) and CuInS₂(2:1) respectively. The photocatalytic activities of the nanoparticles were determined for the degradation of Tetracycline (TC) under visible light irradiation. The effects of process parameters such as photocatalyst dosage and initial concentration of TC were investigated to establish the optimal performance of the CuInS₂ nanoparticles. The experimental data showed a higher TC degradation percentage for CuInS₂(2:1) (95 %) compared to CuInS₂(3:1) (90 %), indicating its high potential as a photocatalyst for the degradation of TC in aqueous solution.

Epidemiological evidence indicates that damage to DNA/RNA initialized by ultraviolet (UV) radiation is associated with skin cancer. Wavelength dependence of DNA photodamage was proposed as early as 1990s and demonstrated later on. Unraveling the photo-activated dynamics involved in related reactions is essential. However, studies aimed at uncovering the wavelength dependent excited state dynamics in canonical pyrimidine nucleosides have not received enough attention. In this work, excitation wavelength dependent excited state dynamics of 2′-deoxy-thymidine (dThd) and oxy-uridine (Urd) are investigated in acetonitrile solutions by femtosecond broadband transient absorption spectroscopy. Varying the excitation wavelength leads to a significant difference in the branching of the excited state population at the Franck-Condon (FC) region, resulting higher fluorescence quantum yield with 285 nm pump but higher triplet state quantum yield under 267 nm excitation. Based on our results, a vibronic coupling regulated excited state relaxation mechanism is proposed. This mechanism information is important for understanding the formation of harmful photoproducts for DNA/RNA with different wavelength UV excitations.

Introduction

Temporomandibular disorders (TMD) are considered the most common complaint associaetd with orofacial pain. A treatment approach for TMD is photobiomodulation auriculotherapy, however, a method that which still requires studies mainly with pulsed frequency.

Objective

To evaluate the feasibility of conducting a randomized clinical trial using pulsed frequency photobiomodulation auriculotherapy and determine the relevant sample size.

Methods

The study was a controlled randomized pilot study. Twenty one volunteers with TMD were randomized into experimental and placebo groups. The evaluation periods were pre-intervention and again after four weeks. The instruments used for the assessment were axis I (mandibular movement measurements [MMM]) and axis II (Graded Chronic Pain Scale [GCPS], Jaw Functional Limitation Scale [JFLS-8], The Patient Health Questionnaire [PHQ-4], and Generalized Anxiety Disorder [GAD-7]) from Diagnostic Criteria for Temporomandibular Disorders (DC/TMD). Mann–Whitney and Wilcoxon tests were used for comparison of groups. The intervention protocol was performed once a week for foour weeks.

Results

The GCPS question about “pain at this exact moment” indicated lower values for the treated group compared to the placebo group (U = 15.50; p = 0.005) after the intervention. The calculation of the total sample was 22 volunteers. The JFLS-8 variable showed no difference between the groups and the sample calculation ranged from 39 to 281 volunteers. The MMM showed no difference between the groups, and the calculation of the necessary sample ranged from 27 to 2.317. The variable PHQ-4 (U = 21.00; p = 0.02) and GAD-7 (U = 20.00; p = 0.02) showed differences between groups with type I error. The required sample was 22 volunteers for PHQ-4 and 25 for GAD-7.

Conclusion

We conclude that this study is feasible and that the required sample should be 11 volunteers for each group in the GCPS subitem “pain intensity at this exact moment”. We were able to find results for this GCPS subitem. However, for other variables we need 25 volunteers for GAD7 and 22 volunteers for PHQ-4. Other variables, such as JFLS-8 and MMM, made it impossible to conduct these scales for future studies.

Agents that cause double-strand breaks (DSBs) of DNA via radical formation have been demonstrated to be effective in treating cancer because DSBs result in cellular apoptosis. Light-responsive agents for the treatment of cancer have been of interest for decades because they afford the ability to spatially control chemical reactions limiting the effects by controlling the area of illumination. Alkylcobalamins, which are structurally related to Vitamin B₁₂ (B₁₂), produce radicals with very high quantum yields when illuminated with green light (approximately 530 nm). Cancerous cells uptake alkylcobalamins to a greater extent than healthy cells because these rapidly dividing cells have an increased demand for B₁₂. Tethering two cobalamins with a propyl group results in a complex that causes true DNA DSBs in a light-mediated manner.